Chapter 17: Peripheral Vascular System

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Welcome back to the Deep Dive.

Today, we are shifting gears just a little bit.

We are entering what we like to call the last minute lecture zone.

Your panic zone.

Definitely the panic zone.

Exactly.

We know exactly who you are, who's listening to this right now.

You're a medical student, maybe a nursing student, maybe a PA student.

You are staring down the barrel of a massive vascular exam or maybe step one is looming over you like a giant storm cloud and you just had that sinking feeling that you don't actually know exactly where the propyteal artery is.

Or, and I think this is even more important, why you should care where it is in the first place.

Right.

And you definitely, definitely do not have time to sit down and read 40 pages of incredibly dense small print text.

So we're going to do the heavy listing for you.

We are.

Today, we are laser focused on a single, I would say, biblical text of medicine, base guide to physical examination and history taking.

We're in the 13th edition and we're dissecting chapter 17, the peripheral vascular system.

This is the plumbing of the human body.

It's the whole network, arteries, veins, and the often forgotten lymphatics.

And I'll be honest with you, when I first look at this chapter, my first thought was, okay, pipes, fluid goes out, fluid comes back.

How complicated can it be?

Right.

Seems simple enough on the surface.

But as we really dug into the source material, I realized this is actually one of the most high stakes systems you can possibly touch.

Yeah.

It's quiet, it's hidden, but when it fails, whether that's a clot in the leg or an aneurysm in the belly, it is absolutely catastrophic.

It is.

It isn't just plumbing.

It is the supply chain and the waste management system for every single cell in your body.

And so the mission for this deep dive is, well, it's pretty simple.

We're going to methodically break down this chapter.

We're going to visualize the anatomy so you don't have to just memorize it by rote.

Okay.

We're going to explain the physiology, the why behind the movement of all these fluids.

And then we're going to walk you through the physical exam, literally hand placement by hand placement.

So here is the roadmap for you, the listener.

We are following the chapter structure exactly.

So if you happen to have the book open, you can follow along, but trust me, you won't need it.

We start with the three systems that's arterial, venous, and lymphatic.

Then we're going to move to the health history, the specific questions that can unlock the diagnosis.

And finally, the physical exam and those special techniques like the ankle brachial index, which I know for a fact shows up on every board exam ever written.

Oh, it's a favorite.

And we will wrap up with how to document it because the golden rule of medicine applies here more than ever.

If you didn't write it down, you didn't do it.

Absolutely.

Yeah.

Okay.

Let's dive in section one, anatomy and physiology.

And we're starting with the arteries.

Now Bates opens with a diagram.

It's figure 17 to one.

And it blew my mind a little bit.

I was pictured an artery as just a simple rubber tube, but the text shows it's actually a complex multi -layered organ.

It is an organ.

That is absolutely the right way to think about it.

It has three concentric layers and you have to know them because each one has a different job and more importantly, a different way of failing.

Let's peel it like an onion then from the inside out.

The layer that's actually touching the blood is the intima.

The intima.

So this is the inner lining and it's just a single continuous layer of what are called endothelial cells.

Now for a long, long time, doctors just thought this was, you know, kind of like the Teflon coating on a frying pan to smooth surface to let blood slide by.

Right.

Nose stick.

Exactly.

But Bates really emphasizes that it is metabolically active.

This layer is a chemical factory.

It synthesizes substances that regulate clotting, that control blood flow, that manage inflammation.

It's not passive at all.

And this is where the trouble begins, isn't it?

Yeah.

This is ground zero for atherosclerosis.

This is ground zero.

The source material describes atherosclerosis as a chronic inflammatory disease and it starts right there in the intima.

You get an injury to those endothelial cells, maybe from smoking, maybe you have high blood pressure, maybe high blood sugar from diabetes.

That insults the intima.

And once it's injured, it stops being nonstick.

It becomes sticky.

Sticky for what, specifically?

For cholesterol.

Specifically, the bad kind, the LDL particles, they start to seep into the wall and they stick to that injured area.

And then, and this is the part the text describes so vividly, the body sends in the cleanup crew.

Monocytes.

Monocytes, exactly.

They are a type of white blood cell.

They come in from the blood, they burrow into the wall, they turn into macrophages, and they try to eat the LDL cholesterol to clean up the mess.

But they get a little too greedy.

They eat too much.

They gorge themselves.

They get so full of this fatty material that they transform into what the text calls foam cells.

That is such a gross, but I have to say, incredibly memorable image.

Foam cells.

It is vivid, isn't it?

And these foam cells start to pile up inside the artery wall.

And that accumulation is what forms the very first stage of plaque, which is called a fatty streak.

Then, to make matters worse, smooth muscle cells migrate in from the deeper layer to try and cover up the mess.

They form a fibrous cap over it.

So you've got this lump of fat and cells with a cap on it bulging into the artery.

That's your plaque.

That whole drama, the plaque, the blockage, the eventual heart attack or stroke when that cap ruptures, it all starts in that microscopic inner layer, the intima.

Wow.

Okay, so that's the lining.

The drama happens there.

What is wrapped around the intima?

That's the media.

The middle layer, this is all about smooth muscle.

It also has elastic fibers, elastin.

This is the layer that does the heavy lifting, quite literally.

What do you mean by that?

Well, arteries are high -pressure vessels.

They have to expand every time the heart pumps, that's systole, to absorb that energy.

And then they have to recoil when the heart relaxes, that's diastole, to keep the wave of blood moving forward.

It's that recoil that maintains your diastolic blood pressure.

The media provides that contractile power and that essential elasticity.

So intima is the lining,

media is the muscle and the elastic.

What's on the very outside?

The adventitia.

You can think of this as the casing.

It's tough connective tissue.

It holds the nerve fibers that help control the artery.

And it holds something really cool called the vasovasorum.

The vasovasorum.

I looked this up.

It sounds so, I don't know, Roman.

It translates to vessels of the vessels.

It's a great term.

And think about why it exists.

The wall of a large artery, like the aorta, is so thick that oxygen from the blood flowing inside the tube can't diffuse all the way out to the outer layers.

Oh, I never thought of that.

The wall itself needs to be fed.

Exactly.

The outer wall would starve.

So the artery needs its own tiny blood supply to feed its own wall.

Those tiny little vessels, the vasovasorum, live in the adventitia and they burrow into the media to keep it healthy.

That is just wild.

The pipe has its own plumbing.

Yeah.

Okay.

So we have the layers.

Now let's talk about the geography of the system.

The text describes a sort of hierarchy of arteries from big to small.

Right.

It's a branching system, just like a tree.

You start with the aorta.

That's the trunk of the tree.

It's highly elastic because it has to take the full tremendous brunt of the heart's pumping action.

Then you branch off into medium -sized muscular arteries.

Think of things like the coronary arteries feeding the heart or the renal arteries feeding the kidneys.

And then smaller and smaller.

Down to the arterioles.

And Bates gives these a very specific name.

It calls them the resistance vessels.

Why that specific term resistance vessels?

Because they are the gatekeepers of your blood pressure.

Their smooth muscle tone, how tight or how relaxed they are, determines the total resistance to blood flow in your entire body.

So if they all clamp down.

If all your arterioles tighten up at once, your blood pressure skyrockets.

That's hypertension.

If they all relax and dilate, your blood pressure plummets.

They are the control valves for the entire system.

And at the very end of the line, we have the capillaries.

The end of the line.

The capillaries are just microscopic.

We're talking seven to eight microns in diameter.

That is barely the width of a single red blood cell.

In fact, red blood cells have to like squeeze through them in single file.

Wow.

And structurally they're different, right?

They're missing a layer.

They are.

They have no media, no muscle layer.

It's just a single layer of endothelium that Intimu talked about.

And that's it.

Why would they lose the muscle?

Seems like a design flaw.

It's a design feature.

The goal here isn't transport anymore.

It's exchange.

You want the wall to be as thin as humanly possible so that oxygen and nutrients can diffuse out into the tissues and CO2 and waste can diffuse back in.

If it had a thick muscle layer, that diffusion couldn't happen efficiently.

It's all about form following function.

If that makes sense.

Yeah.

Okay.

Before we leave the arteries, there is one last concept in this anatomy section that feels, I don't know, kind of hopeful.

Collateral circulation.

Nature's bypass.

It's an amazing concept.

Explain that to me.

Okay.

So if you have a blockage, let's say a big atherosclerotic plaque in a major artery,

the body isn't totally helpless.

There are these things called anastomoses, which are basically connections between branching networks of smaller arteries.

So like back roads on a map.

That's a perfect analogy.

If the main highway is blocked, these small back roads can dilate and even increase in size over time to carry the blood around the blockage.

So the body literally rewires its own plumbing.

It tries to.

Now it takes time and it definitely has its limits.

It's not a perfect solution, but it's the reason someone can have a totally blocked femoral artery and still have a viable leg with a pulse at the foot.

The collaterals are doing the work.

That's incredible.

Okay.

Let's get practical.

We're in the exam room.

We need to find these arteries.

We need to feel the pulse, the text lists specific pulse points.

I want to run through these because knowing where to put your fingers is like half the battle.

Let's start with the arms.

In the arms, you have three major pulses you need to know.

First, the brachial artery.

You find this at the bend of the elbow, the area called the anticubital fossa.

The landmark you're looking for is the biceps tendon.

You want to feel for your fingers to be just medial to that tendon.

Medial to the biceps tendon.

Okay.

Then you have the radial artery.

Everyone knows this one.

You find it on the lateral flexor surface of the wrist.

It's the checking your watch pulse.

Easy enough.

What about the ulnar?

The ulnar is on the medial flexor surface, but Bates puts a bit of a warning label on It says that overlying tissues often obscure it.

The bottom line is, it's much, much harder to feel than the radial.

You often can't.

And why do we even have two arteries in the wrist?

Why the redundancy?

It's a safety mechanism.

The text mentions these arterial arches in the hand.

The radial and ulnar arteries actually connect in the palm to form these loops or arches.

That means if you, say, get a deep cut and slice your radial artery, the ulnar artery can still supply blood to the entire hand through those arches and keep your fingers alive.

Okay.

That's smart design.

Let's move down to the abdomen.

Figure 17 to 4 in the book.

This feels like a scarier area to be examining.

It is.

The main player here, obviously, is the abdominal aorta.

You can palpate pulsations from it in the epigastrium, that upper middle part of the belly.

But Bates makes a really critical point here about what you can't feel.

The branches off the aorta.

Right.

The abdominal aorta has three massive unpaired branches that feed the gut.

You've got the celiac trunk, the superior mesenteric artery, and the inferior mesenteric artery.

Together they feed your stomach, your liver, your spleen, and all 20 plus feet of your intestines.

And there's no way for us to feel them on an exam?

No.

They are way too deep inside the abdomen.

But you have to know they're there.

You have to keep them in your mental model of the patient's anatomy because if they get blocked, you get something called mesenteric ischemia.

And what is that?

It's basically a heart attack of the gut.

The bowel tissue loses its blood supply and starts to die.

It's a massive surgical emergency with a very high mortality rate.

So even though you can't touch them, you have to think about them.

Okay.

That's a sobering thought.

Finally, let's go to the legs.

This is really the bread and butter of the peripheral vascular exam.

Four key pulses.

Four key pulses.

Yeah.

Start at the top.

The femoral artery.

The landmark here is very precise.

You want to be below the inguinal ligament, midway between the

superior iliac spine.

That's the pointy part of your hip bone.

And the symphysis pubis, which is the pubic bone in the middle.

Midway between the hip bone and the pubic bone.

Exactly.

And you have to press deeply, especially in larger patients.

Then as you move down the leg, you get to the popliteal artery.

This is behind the knee.

We'll talk a lot more about the technique for finding it later.

But anatomically, it's just a continuation of the femoral artery.

And then down in the feet?

Two main pulses in the foot.

You have the posterior tibial or PT.

This is found just behind the medial malleolus, that big ankle bone on the inside of your foot.

Okay.

Behind the inner ankle bone.

Mm -hmm.

And then the dorsalis pedis or DP.

This is on the top of the foot.

The landmark is the extensor tendon of the big toe.

You find that tendon, you want to be just lateral to it.

Just lateral to the big toe tendon.

I'm definitely writing that one down.

Okay.

Let's switch systems.

That's a good overview of the arteries.

Now for section two,

the veins.

Yeah.

This is a totally different engineering problem here.

The text calls them thin -walled and highly distensible.

What does that really mean?

Okay.

So think of arteries as high -pressure fire hoses.

They're thick, they're muscular, they're resistant.

Veins, on the other hand, are more like low -pressure storage bags.

They're very stretchy.

They can hold up to two -thirds of your total circulating blood volume at any given time.

They act as a reservoir for blood.

But they have a huge problem that arteries don't really have to deal with, and that's gravity.

Right.

If you're standing up, the blood in your feet has to climb a meter, maybe more straight uphill to get back to your heart.

How does it do that without just sliding right back down?

It's got to be the valves.

Unidirectional valves.

They are literally built into the inner lining of the veins.

They look like little leaflets.

They open to let blood flow up toward the heart, and then they snap shut if blood tries to fall back down with gravity.

And Bates makes a big distinction between two venous systems in the legs,

the deep and the superficial.

This seems really important for understanding blood clots.

It is absolutely critical.

The deep veins, these are things like the femoral vein and the popliteal vein, are buried deep within the muscle.

They're well supported by fascia and muscle tissue, and they carry about 90 % of the venous return from the legs.

And that's where the bad clots happen.

That's where the dangerous clots happen.

A deep vein thrombosis, or DVT.

It's dangerous because the flow in these big veins is high, and if a piece of that clot breaks off, it can be swept straight up to the lungs.

And the superficial ones are different.

Totally different.

These are just under the skin in the subcutaneous fat.

The tissue support around them is poor.

This system includes the great saphenous vein.

The text points out that this is the longest vein in the entire body.

It is.

It runs from the top of the foot all the way up the medial side of the leg and empties into the femoral vein up in the groin.

Because it's superficial and has poor support, it's the one that you typically see forming varicose veins.

And interestingly, because it's long and easily accessible,

it's the vein that is most often harvested for coronary bypass surgery.

Oh really?

So they take a vein from the leg to fix a clogged artery in the heart?

Frequently, surgeons will literally strip it out of the leg, flip it upside down so the valves don't cause a problem, and use it to bypass a clogged coronary artery.

Wow.

So we have deep veins and superficial veins.

How are they connected to each other?

They're connected by what are called perforating veins.

You can think of them like rungs on a ladder connecting the superficial system down into the deep system.

They have valves too, and they ensure that blood flows in the right direction, from superficial to deep, not the other way around.

And there's one more mechanism mentioned in the text to help fight gravity.

The venous pump.

The calf muscle pump.

This is such a cool mechanism.

When you walk, your calf muscles, the gastrocnemius and soleus, they contract.

That contraction squeezes the deep veins that are running through the muscle.

And because of all those one -way valves, the blood can only go one way when it's squeezed up.

So walking, just the simple act of walking, literally pumps blood back to your heart.

Which explains perfectly why sitting on a plane for 10 hours can cause your ankles to swell up.

The pump is turned off.

The pump is off.

The fluid just pools in your lower legs because that mechanical pump isn't working to send it back uphill.

That makes so much sense.

Okay, let's hit the third system.

The lymphatics.

The unsung hero of the vascular system.

It really seems like the body's drainage system.

It's the body's drainage ditch.

That's a great way to put it.

Think about it.

Arteries push fluid out into the tissues to feed the cells.

Veins use pressure gradients to suck most of it back up, but they're not perfect.

They don't get all of it.

The lymphatic capillaries are designed to pick up the leftovers, the excess fluid, the plasma proteins that are too big to get back into the veins, and any cellular debris that the veins missed.

And it's also a huge part of the immune system, too.

Huge.

The lymph nodes act as filters.

As that fluid, now called lymph, flows back toward the heart, it passes through these chains of lymph nodes.

And inside the nodes are immune cells that engulf bacteria, viruses, and debris.

It's like a water treatment plant before the water gets dumped back into the river of the bloodstream.

Now, unlike arteries and veins, we usually don't feel the lymphatic vessels themselves, but we can feel the nodes.

Bates points out some specific palpable nodes we need to check in a vascular exam.

Right.

In the arm, the key one to check is the epitrochlear node.

Okay.

Where is that exactly?

It's on the medial surface of the arm, about three centimeters above the elbow.

You find it in the groove between the biceps and triceps muscles.

And should we be able to feel it?

In a healthy person.

Absolutely not.

If you can feel a node there, it's a red flag.

It drains the ulnar side of the forearm, and so the fourth and fifth fingers.

It could mean a local infection there, like from a cat scratch, or it could be a sign of something more systemic, like lymphoma or HIV.

Okay.

So a palpable epitrochlear node is always abnormal.

What about in the legs, the inguinal nodes?

These are in the groin, and Bates splits them into two distinct groups, the horizontal group and the vertical group.

What's the difference in what they do?

It's all about what they drain.

The horizontal group is high up, right below the inguinal ligament.

They drain the superficial lower abdomen, the buttocks, and the external genitalia, including the anal canal, perineum, and vagina.

But, and this is a classic board question, they do not drain the testes.

Oh, that's a key distinction.

Where do the testes drain?

The testes drain internally, way up into the abdomen, following the path they descended.

So testicular cancer does not show up in the inguinal nodes.

Good to know.

And the vertical group?

They cluster a bit lower down, near the upper part of the great saphenous vein.

They drain pretty much the entire leg.

So the rule is, infection in the foot.

Check the vertical nodes.

An infection or lesion on the skin of the lower belly.

Check the horizontal nodes.

Okay, before we move to the clinical part of this, we have to talk about transcapillary fluid exchange.

It's figure 1710 in the book, and it really explains the why behind swollen ankles.

This is the Starling equilibrium.

At its core, it's a balance of forces,

a push and a pull.

Push and pull, okay.

Right.

Inside the capillary, you have hydrostatic pressure, which is basically just blood pressure.

It's the force that pushes fluid out of the capillary and into the surrounding tissue.

That's the push, what's the pull?

The pull is colloidal osmotic pressure, or oncotic pressure.

It's caused by proteins, mainly albumin, that are floating in the blood.

These proteins are too big to leave the capillary, so they act like little sponges sucking fluid back in.

So in a healthy person, the push and the pull basically balance each other out?

Mostly.

There's a slight net push out, which is what the lymphatic system is there to clean up.

But if you break that delicate balance in a big way, you get edema.

Give me an example.

Okay.

If you have heart failure, your venous pressure is very high.

That backs up all the way into the capillaries, so your hydrostatic pressure, the push, is too high.

Fluid leaks out, edema.

What about the pull?

If you have liver failure, your liver can't make enough albumin protein.

Now your oncotic pressure, the pull, is too low.

Fluid stays out in the tissues, edema.

Or if your lymphatics are blocked, like after surgery or radiation, the drain is clogged.

Fluid piles up, lymphedema.

And that leads directly to the difference between pitting and non -pitting edema, right?

Exactly.

Pitting edema, where you poke the swollen area and the dent stays for a while, that's usually from excess water and salt.

It's mobile fluid.

Think heart failure, kidney issues, venous insufficiency.

Non -pitting edema is usually a sign of lymphedema.

The fluid that's leaked out is very rich in protein.

And over time, it causes the tissue to become fibrotic, hard, and thick.

It doesn't move when you press on it.

Okay.

That is the foundation.

We've got the anatomy and the physiology down.

Check.

Now let's go to section four, the health history.

We're talking to the patient.

What are the key questions we need to be asking?

The whole goal of the history really is to figure out, is this pain vascular,

or is it musculoskeletal, or is it neurologic?

Because my leg hurts can mean 20 different things and you have to be the detective.

So how do we start to tell the difference?

You have to focus on two things, perfusion and exertion.

Vascular pain, specifically arterial pain, is all about supply and demand.

The muscles need a certain amount of oxygen to walk.

If the arteries are clogged with plaque, the supply of oxygen can't meet the demand of walking.

The pain comes on with exertion and goes away with rest.

This is the textbook definition of intermittent claudication.

That's the term, correct.

It comes from the Latin word claudicare, which means to limp.

The classic story is the patient who says, I can walk one block and then I get this terrible cramp in my calf.

I have to stop for five or 10 minutes.

The pain goes away completely.

Then I can walk another block and the pain comes right back.

It's predictable.

But the text gives a pretty big warning here.

Yeah.

Do not rely solely on that classic story.

It explicitly states that only about 10 % of patients with peripheral arterial disease, or PAD, have that textbook presentation.

It says, up to 60 % are completely asymptomatic.

They have the disease, but no symptoms.

And many others just have atypical leg pain, so you have to dig deeper.

There's a box here, box 17 -2, titled warning signs.

It's a checklist of red flags for PD.

What are some of the big ones?

Okay.

So you want to ask about any fatigue, aching, numbness, or pain that limits walking.

You want to ask about any poorly healing or non -healing wounds on the feet or toes.

And a really big one, pain at rest.

This is a huge red flag.

Pain at rest sounds really bad.

It is ominous.

If the leg hurts when the patient is just lying in bed, it means the blood flow is so critically low that it can't even sustain the tissue at rest.

That's a state called critical limb ischemia.

That leg is an imminent danger of dying and needing amputation.

Wow.

There's another symptom listed here that I found completely fascinating,

food fear.

Ah, yes.

This points us back to those abdominal arteries, the mesenteric arteries.

If those arteries are blocked, the gut can't get enough blood to do the work of digesting food.

So every single time the patient eats, they get terrible cramping abdominal pain.

It's essentially angina of the stomach.

So they just stop eating to avoid the pain.

They become terrified to eat, and so they lose a lot of weight.

If you have an elderly patient with unexplained weight loss and belly pain that happens, 30 minutes after every meal, you have to think about vascular disease.

Okay.

What about the veins?

If we're worried about a DVT, a blood clot, what are we asking?

For DVT, we're looking for swelling, and it's usually unilateral, meaning in just one leg.

We ask about pain or tenderness, often in the calf, and then we have to ask about risk factors.

The text lists the big ones.

Immobilization,

recent major surgery, prolonged travel, and cancer.

And for clots in the upper extremity, in the arms?

The biggest risk factor there by far is having a central venous catheter, a PICC line, a port, a dialysis catheter, or having a pacemaker.

Anything that threads a wire or a tube into the central veins can cause inflammation and lead to a clot.

And just to be clear, why are we so paranoid about DVT?

Because of the risk of a PE, a pulmonary embolism.

If that clot in the leg or arm breaks loose, it rides the elevator up the vena copper, goes through the right side of the heart, and then slams into the pulmonary arteries in the lungs, blocking blood flow.

It can be instantly fatal.

The text says that up to 20 % of people who have a DVT will develop a PE.

That's a huge number.

The history is done.

We have our suspicions.

Now it's time to actually touch the patient.

Section 5, the physical examination.

And Bates suggests a very systematic top -down approach.

Don't just jump around.

Start with the carotids, then do the arms, then the abdomen, and then finish with the legs.

And what's the single golden rule of the whole exam?

Compare side to side.

Always, symmetry is your best friend.

Humans are mostly symmetrical.

If the left arm is cool and pale and the right arm is warm and pink, you have a diagnosis right there before you do anything else.

Perfect.

Let's start with the arms.

Inspection and palpation.

Okay, so you're looking at the size of the arms, any swelling,

any prominent venous patterns.

You look at the color of the skin, the color of the nail beds.

Then you move to palpation.

You feel for the radial pulse and you feel for the brachial pulse, medial to the biceps tendon.

And as we're feeling these pulses, we need to be grading them.

There is a scale in box 17 to 3 that every single student needs to memorize.

It feels a little counterintuitive at first.

It does.

It's a 0 to 3 plus scale.

0 is absent.

You can't feel it even with a daubler.

1 plus is diminished.

It feels thready, weak.

2 plus is brisk or expected.

This is the normal pulse.

And 3 place is bounding.

It feels like it's punching your fingertips.

You might see this in aortic regurgitation or severe anemia.

So normal is 2 plus cote.

That's the part that trips people up.

Usually you think of normal as being, I don't know, 100 % or the max score.

Right.

But in this scale, 2 plus is your target.

If you write in your note, radial pulse is 2 plus bilaterally.

You are communicating to everyone else who reads it.

Everything is fine here.

Okay, moving down to the abdomen.

A key part of this exam is screening for in AAA an abdominal aortic aneurysm.

How do we do that with our hands?

Okay, so you start by feeling for the aortic pulsation in the epigastrium.

But don't just feel it thumping up and down.

You need to assess its width.

Place the palms of your hands on either side of the pulsation and gently press inward until you feel the lateral edges of the aorta.

In a normal adult, it should be no wider than 3 centimeters.

And if it feels wider than that?

If it feels like a pulsating grapefruit in there, you are feeling an aneurysm until proven otherwise.

This is a critical screening skill, especially in older men who have a history of smoking.

Okay, now for the main event, section 6.

The legs.

Bates is very, very specific about the preparation for this part of the exam.

Yes.

You absolutely cannot do a proper vascular exam through a pair of jeans.

You cannot do it through socks.

The patient must be supine.

They should be draped.

The genitalia are covered for modesty.

But the legs must be fully exposed from the groin all the way to the toes.

Socks off.

Socks off.

That should be the number one rule of the vascular exam.

It absolutely is.

You can miss so much.

From ulcers between the toes to changes in skin color if the socks are on.

So inspection, the socks are off.

What are we looking for?

First and foremost, symmetry.

Does one calf look more swollen than the other?

If it does, get a tape measure.

Bates gives us a hard number here.

A difference of more than 3 centimeters in circumference between the calves is highly suggestive of a DVT.

Three centimeters.

That's a good objective cutoff.

It is.

Then you look at the veins.

You may need to have the patient stand up for a moment.

Varicose veins might be invisible when they're lying down because they drain with gravity.

Standing fills them up and makes them pop out.

Okay.

And then look at the quality of the skin.

Is it brown and leathery around the ankles?

That's a sign of chronic venous insufficiency called stasis dermatitis.

Is the skin shiny, thin, and hairless?

That's a classic sign of arterial insufficiency.

The hair follicles die from lack of blood flow.

Okay.

Now for palpation.

We have to find those four pulses we talked about.

Femoral, popliteal, DP, and PT.

Let's talk technique.

The popliteal is notoriously legendarily difficult.

The popliteal is the boss fight of pulses.

It's buried deep in the popliteal fossa.

So technique number one.

The patient is supine.

You flex their knee slightly to relax the muscles.

Then you place the fingertips of both of your hands so they meet in the midline behind the knee.

And you press deeply trying to compress the artery against the bone.

And if that doesn't work?

Technique number two.

If that fails, flip the patient over.

Put them in the prone position on their stomach.

Flex their knee to 90 degrees.

This relaxes the hamstrings even more.

Then press your thumbs deeply into the fossa.

That prone tip is gold.

I have definitely seen that work when nothing else does.

What about the foot pulses, the DP, and the PT?

Sometimes they just feel like they're not there.

It can be tricky.

A common mistake is pressing too hard.

These are small vessels.

You can easily obliterate them with your thumb.

Use a light touch.

Move your fingers around.

And Bates offers a very humble but important tip.

Don't mistake your own pulse for the patient's.

Oh, I have definitely done that.

You're feeling around and you think, wow, this patient has a heart rate of 90.

Oh, wait, I just had an espresso.

It happens to everyone.

If you're ever unsure,

feel your own carotid pulse with one hand while you're feeling the patient's foot pulse with the other.

If the beats don't match up, you know you're feeling the patient.

That's a great pro tip.

We also have to check temperature.

Yes.

And you want to use the bats of your fingers.

The dorsal aspect of your hand is much more sensitive to subtle temperature changes than your calloused fingertips.

You run your hands down both legs simultaneously from thigh to foot, comparing one side to the other.

And what are we looking for?

Asymmetry.

If you hit a line of demarcation, a place where the warmth abruptly stops and the leg becomes ice cold, you have just found the level of the acute arterial blockage.

And edema.

How do we test for pitting edema properly?

You have to press firmly and for long enough.

Use your thumb.

Press for at least two seconds.

Don't just give it a quick poke.

And check in a few spots.

The dorsum of the foot, behind the medial malleolus, and over the shin.

And there's a grading scale for this too.

Yes.

The one plus to four plus scale.

One plus is barely detectable.

A slight depression.

Two plus is a bit deeper.

Maybe a four millimeter pit that rebounds in about 15 seconds.

Three plus is a deep six millimeter pit.

And it takes around 30 seconds to rebound.

And four plus is a very deep eight millimeter pit that stays there for well over 30 seconds.

Okay.

One last thing on palpation.

Tenderness.

I remember being taught the Holman sign in school.

You sharply dorsiflex the foot.

And if the calf hurts, it's a sign of a DVT.

And Bates is here to tell you, and everyone listening to please stop doing that.

Really?

Just throw it out.

It is officially discredited.

Even Holman himself who first described it later said it was unreliable.

It is neither sensitive nor specific.

You can have a massive DVT with no Holman sign.

And you can have a positive Holman sign just from a pulled muscle.

Do not rely on it for diagnosing a DVT.

Myth officially busted.

Section seven.

Special techniques.

These are the high yield skills that often get tested.

First up, the ABI.

The ankle brachial index.

If you take only one clinical skill away from this deep dive, learn how to do an ABI.

It is the definitive non -invasive bedside test for PAIDI.

So what's the concept behind it?

It's a simple ratio.

You are comparing the systolic blood pressure in the ankle to the systolic blood pressure in the arm.

In a healthy plumbing system with no blockages, the pressure at your ankle should be the same, or actually even slightly higher than the pressure in your arm.

Why higher?

Because of the reflection of the pressure wave off the smaller, more resistant vessels in the legs.

But if there is a significant blockage in the leg arteries, the pressure downstream from that blockage at the ankle will drop significantly.

So how do we actually measure it?

You need a Doppler probe, that's the little handheld ultrasound stick that makes the whooshing sound, and a regular blood pressure cuff.

The patient needs to lie flat for about 10 minutes to get a stable baseline.

You measure the systolic pressure in the brachial artery of both arms.

You use the higher of those two numbers as your denominator.

You move the cuff to the ankle and measure the systolic pressure in both the DP and the PT arteries in both ankles.

For each leg, you take the higher of the two ankle pressures.

That's your numerator.

The math.

You divide the highest ankle pressure for that leg by the highest arm pressure you measured earlier.

Ankle pressure divided by arm pressure.

Right.

And then you interpret the number.

If the ratio is between 0 .90 and 1 .40, that is considered normal.

If it is less than 0 .90, that is diagnostic for PID.

And if it is less than 0 .50, that indicates severe PAD.

What if you get a really huge number, like greater than 1 .40?

That's a trap.

Doesn't mean you have super arteries.

It means the arteries in the ankle are heavily calcified and stiff, and you can't compress them with the blood pressure cuff.

So you get a falsely elevated reading.

You see this often in patients with long -standing diabetes or end -stage renal disease.

The result is considered non -compressible, and the test is uninterpretable.

Got it.

Low is bad, but too high is an artifact.

Next special technique, the Allen test.

This is for the hand.

This is safety 101.

Before you stick a needle into someone's radial artery -like for an arterial blood gas draw, or before a surgeon harvests that artery for a bypass graft, you absolutely must ensure the ulnar artery is patent.

You have to know the hand has a reliable backup blood supply.

Walk us through the steps.

It's a bit like a magic trick.

It is.

Okay, step one.

Ask the patient to make a very tight fist.

This squeezes the blood out of the palm, making it blanch.

While their fist is clenched, you use your thumbs to compress both the radial and the ulnar arteries at the wrist.

Occlude them completely.

Ask the patient to open their hand.

It should look pale and white.

The ghost hand.

Now, the reveal.

You release your pressure on only the ulnar artery while keeping the radial artery compressed.

What should happen then?

If the ulnar artery is working properly, the palm should flush bright pink within three to five seconds.

That's a positive or normal Allen test.

If the hand stays pale and white for more than five seconds, that means the ulnar artery is blocked or inadequate.

Do not puncture that radial artery because you might be cutting off the only significant blood supply to the hand.

Okay, section eight.

Documentation and clinical reasoning.

We've gathered all this data from the history and the exam.

How do we put it all together and communicate it?

Let's start with ulcers.

Table 17 before in the book compares arterial, venous, and neuropathic ulcers.

This is classic exam material.

How do we tell them apart at the bedside?

It's all about the location, the look, and the feel.

Let's break it down.

These happen because of a severe lack of blood flow.

So they typically occur at the most distal points.

The toes, the foot, maybe the shin.

The ulcer itself looks punched out with pale edges.

The base may be black or necrotic, which is gangrene.

And crucially, they are intensely painful.

And if you feel for pulses, you won't find any.

That makes perfect sense.

No blood, tissue dies.

It hurts a lot.

Exactly.

Now, venous ulcers.

These happen because of chronic high pressure and pooling of blood in the veins.

So they occur in the area most affected by that pooling, usually around the ankle, especially the medial malleolus.

They are typically shallow, large, with irregular borders.

The surrounding skin is often brown and pigmented from chronic inflammation.

They are wet, they ooze, and the leg is zydematous.

And the pulses are present, but you might have to dig through all that swelling to feel them.

And the third type.

Neuropathic ulcers.

These are the classic diabetic foot ulcers.

They happen at pressure points, the bottom of the foot, the ball of the foot, places where a person puts weight.

They're often surrounded by a thick callus.

And the key feature, the thing that makes them so dangerous, is that they are painless.

The patient has neuropathy, so the nerves are dead.

They can have a deep hole in their foot and not even know it.

That breakdown is absolutely essential.

Arterial equals dry, painful, no pulse on the toes.

Venous equals wet, brown on the ankle with a pulse.

And neuropathic equals pressure point, callus, and painless.

That's a perfect summary.

If you can remember that, you'll be able to differentiate them 90 % of the time.

Finally, let's talk about screening for this stuff.

We want to catch vascular disease early before it causes a catastrophe.

What did the National Guidelines say?

For PAD, it's a little bit debated.

The USPSTF, the US Preventive Services Task Force, says there is currently insufficient evidence to screen the general asymptomatic population.

But the major cardiology societies, like the AHA and ACC,

they recommend doing a screening ABI in people who are at high risk.

And who is high risk?

Anyone over 65, anyone over 50 who has risk factors like smoking or diabetes, and anyone with a known atherosclerotic disease elsewhere, like in their heart or carotids.

And what about for AAA, the abdominal aortic aneurysm?

This one is much clearer and is a grade B recommendation from the USPSTF.

They recommend a one -time screening ultrasound for all men aged 65 to 75 who have ever smoked.

Ever smoked.

What's the definition of that?

The official definition is having smoked more than 100 cigarettes in their lifetime.

100 cigarettes.

That's just five packs.

That is a very low bar.

It is.

The takeaway is basically, if you are a man over 65 who was ever a smoker, you should get screened with an ultrasound.

The data shows it clearly cuts mortality from ruptured aneurysms by about 50%.

We have traveled from the microscopic intima all the way to the popliteal fossa and then to the national screening guidelines.

This has been a marathon.

It's a very dense chapter.

But think about what we've covered.

We aren't just memorizing lists of pulses or facts.

We're building a complete mental model of the body's plumbing.

And for my final thought, the thing that I really keep coming back to through this material is the silent nature of so much of this vascular disease.

It's haunting, isn't it?

It really is.

You can have a five centimeter ticking time bomb of an aneurysm in your belly, or you can have 80 % blockage in the arteries of your legs.

And you can feel absolutely nothing.

You feel totally fine.

Until the moment you try to run for a bus and your legs give out.

Or until the moment the aneurysm ruptures.

That is precisely why the physical exam matters so much.

That simple palpation of the belly, that careful check of the pedal pulses.

It might be the only warning that patient ever gets.

You, the examiner, are the early warning system.

These aren't just boxes to check on a form or maneuvers to get through for a grade.

They are life -saving investigations.

Well said.

Now go out there and find those pulses.

Thank you so much for trusting the Last Minute Lecture Team with your study time.

We sincerely hope this helps you crush your exam and even more importantly, take better care of your future patients.

See you next time.