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Cardiovascular disease or CVD, it's kind of sobering, but it remains the number one killer in the United States.
Yeah, it really is.
More deaths than cancer and chronic lung disease put together annually.
Wow.
So understanding the cardiovascular assessment isn't just important,
it's absolutely critical for anyone in healthcare.
Couldn't agree more.
And that's what we're aiming for today.
Think of this as a focus shortcut.
We're hitting the essential assessment pieces for the CV system.
Okay, so from the foundational stuff like anatomy and physiology.
Right, like perfusion and fluid and electrolyte balance.
Those are our core concepts here.
All the way to risk what patients actually tell you, the tests we use and crucially, the safety stuff around advanced procedures.
You mentioned perfusion and fluid electrolyte balance.
And there's a key number tied to perfusion for major organs, isn't there?
The MAP?
That's the one, main arterial pressure.
You really need to keep that MAP between 60 and 70 millimeters of mercury.
That's the sweet spot for keeping kidneys, brain, everything adequately perfused.
Below 60.
Danger zone.
Definitely a danger zone.
So let's start with the engine itself, the heart's mechanics, the cardiac cycle.
Blood flow is pretty straightforward, right?
Right atrium, right ventricle.
Then off to the lungs to get oxygenated.
Back to the left atrium, left ventricle, then boom, out the aorta to the rest of the body.
Exactly.
And this whole cycle has two main parts, diastole and systole.
Diastole, that's the filling part.
Right, relaxation and filling.
And it's actually, the longer phase takes up about two -thirds of the cycle time.
Then systole is the squeeze, contraction and emptying.
And the valves keep everything going the right way, like a little one -way doors.
Perfect analogy.
You've got the AV valves, tricuspid and metral between the atria and ventricles.
And the semilinear valves, pulmonic and aortic, guarding the exits.
Their main job is closing during sister, so blood doesn't slosh backwards.
Precisely.
Prevents regurgitation.
Now, here's a really key detail about timing, especially relevant clinically.
The heart muscle itself, the myocardium, gets its own blood supply mainly during diastole.
When the heart relaxes, resistance in those tiny coronary vessels drops, allowing blood to flow in.
Ah, so if the heart beats too fast, it cuts short that diastolic filling time.
Exactly.
Less diastole means less time for coronary artery perfusion.
That's why very high heart rates can actually be dangerous for the heart muscle itself.
That makes so much sense.
Okay, let's talk output.
Cardiac output.
Formula is heart rate times stroke volume.
Yep.
CO equals HR times SV.
And normally for an adult, we're looking at about three to six liters per minute.
And stroke volume, the amount pumped per beat, depends mainly on two things, two big ones.
Preload and afterload.
Think of preload as the stretch.
It's the volume of blood in the ventricle right at the end of diastole just before it contracts.
That's Starling's law, right?
More stretch equals a stronger contraction.
You got it.
Up to a point, of course.
Stretch it too much, like in heart failure, and it loses efficiency.
And afterload.
That's the pushback.
Perfect word for it.
It's the resistance the ventricle has to overcome to actually eject that blood.
It's directly related to blood pressure and how constricted or relaxed the arteries are.
So if someone has high blood pressure,
their heart has a higher afterload, works harder.
Exactly.
That's why managing hypertension is so key in preventing heart failure.
We use meds to reduce that resistance, reduce the afterload, make the heart's job easier, or diuretics if preload is the main issue, like in fluid overload.
It's amazing how the body regulates blood pressure.
You mentioned three systems.
Yeah, it's a triple check system, almost.
The autonomic nervous system gives you those quick adjustments via baroreceptors, sensing pressure changes.
Like when you stand up too fast.
Right.
Then the kidneys play the longer game with the renin -angiotensin -aldosterone system managing fluid volume and constriction.
And the endocrine system pitches in with various hormones too, all working to keep that MAP stable.
Incredible.
So when this finely tuned system starts having problems, it's often down to long -term issues, the risk factors we need to ask about.
Absolutely.
We usually group them into two buckets,
things you can't change, the non -modifiable ones, like age.
Risk just goes up as we get older, unfortunately.
True.
And gender plays a role.
Men generally have higher risk earlier, but women catch up, especially post -menopause, and have unique risks, like from pregnancy complications.
Ethnicity matters too.
And family history.
That's a big one, isn't it?
If your parent or sibling had early heart disease.
Huge red flag.
A first -degree relative with CVD is a major, major risk factor.
Okay, now the ones we can hopefully do something about, the modifiable factors.
Smoking has to be top of the list.
Number one, definitely.
The tar, nicotine, carbon monoxide, all bad news for the cardiovascular system.
We even quantify it using pack years.
Right.
Packs per day times years smoked.
Important for the record.
And there's a method for helping people quit.
The five A's.
Yeah, the five A's.
Ask about smoking status.
Advise them to quit.
Assess their willingness.
Assist them with resources and
sopens.
Arrange follow -up.
It's a structured way to approach it.
Good framework.
Then there's lack of exercise.
What's the target again?
Aim for about 150 minutes of moderate intensity, or 75 minutes of vigorous intensity exercise per week.
Getting that regular activity makes a big difference.
And obesity BMI over 30.
Linked to everything else, it seems.
Pretty much.
Hypertension, high cholesterol, diabetes.
Obesity is a major driver for all of those.
You know, one factor that maybe doesn't get enough attention is the psychological side.
Stress, anger.
Oh, absolutely.
It's becoming much clearer.
Chronic anger, hostility, depression.
These aren't just feelings.
They physically impact the body through constant sympathetic nervous system activation.
Like keeping the fight or flight system switched on all the time.
Essentially, yes.
That constant flood of stress hormones damages blood vessels, raises blood pressure, affects clotting.
It's a direct physiological hit over time.
Fascinating and scary.
Yeah.
We should also quickly mention adults with diabetes have a much higher risk, right?
Yeah.
Something like two to four times the rate of death from heart disease.
And veterans are another group with specific cardiovascular risk profiles we need to be aware of.
Okay.
So these risks build up.
How do they actually show up?
What do patients complain about?
The clinical manifestations.
Right.
What is the patient experience?
And the number one thing, the absolute top nursing safety priority has to be chest pain or discomfort.
Rule number one, treat it as cardiac until proven otherwise.
Always.
It's potentially life threatening.
You can't afford to dismiss it, but it's not always that classic crushing pain, especially we need to highlight this for women's health.
The triad.
Yeah.
Women often present differently.
Maybe it's a triad of things like unusual fatigue that won't go away.
Just feeling generally unwell, maybe anxiety, shortness of breath, or sometimes discomfort they describe as indigestion or feeling full.
So we need to listen carefully to the words they use, heaviness, pressure, aching, choking, vice -like.
Right.
Any of those descriptions warrant serious investigation.
Beyond pain, shortness of breath dyspnea is another major flag.
There are different types.
Yes.
Important to distinguish.
First is DOE dyspnea on exertion, trouble breathing when you're active.
This is often an early sign of art failure.
And sometimes the only sign in women.
Often, yes.
Then there's orthopnea.
That's difficulty breathing when lying flat.
How many pillows do they need to sleep?
That gives you a clue to severity.
One pillow, two pillows sleeping in the recliner.
Exactly.
And then the really frightening one, PND,
paroxysmal nocturnal dyspnea.
That's waking up suddenly gasping for air.
Yes.
Hours after lying down.
Fluid that's been pooling in the legs and periphery shifts back to the central circulation when they're flat.
The struggling heart can't handle that extra volume suddenly and fluid backs up into the lungs.
Terrifying experience for the patient.
Wow.
And that fluid shift ties directly into weight, doesn't it?
Best indicator of fluid balance.
Absolutely.
Daily weights are key.
And the conversion factor to remember is that a sudden gain of 2 .2 pounds or one kilogram.
Equals about a liter of fluid they're holding on to.
That's why asking about rings feeling tight, shoes not fitting or sock marks being deeper than usual.
Those are practical, useful assessment questions.
Good tips.
What about pain in the legs or arms?
Extremity pain.
Need to figure out if it's arterial or venous.
If they describe cramping, usually in the legs or buttocks, that comes on with walking and gets better with rest or dangling the legs down.
That sounds like intermittent claudication.
Arterial problem.
Not enough blood getting down there.
Right.
Ischemia.
But if the pain is more of an ache that gets worse with prolonged standing or sitting and feels better when they elevate their legs, that's more likely venous insufficiency.
Blood having trouble getting back up.
Okay.
That makes sense.
Now let's move to what we actually see, touch, and hear during the physical exam.
Skin first.
Skin gives you great clues about perfusion.
Look for pallor, paleness in nail beds, palms, inside the mouth.
Cool, pale, maybe moist skin often means poor perfusion or anemia.
And cyanosis.
The blue tinge.
The bluish over sometimes darkened discoloration from low oxygen in the blood.
Important note, in people with darker skin, it might look more like a graying of the tissues, especially around the mouth or conjunctiva.
And there's central versus peripheral cyanosis.
Right.
Central cyanosis like blue lips or tongue usually means a serious lung problem or cardiac shunt.
Peripheral cyanosis like blue fingers or toes is more often about low cardiac output or maybe just being really cold causing vasoconstriction.
Context matter.
Okay.
Pulses and blood pressure.
Let's nail down orthostatic hypotension.
What are the specific criteria?
Okay.
Orthostatics.
You're looking for a drop in systolic BP of more than 20 millimeter HG,
O -R, a drop in diastolic BP of more than 10 millimeter HG.
And then when they go from lying down to sitting or standing.
Correct.
And usually you'll also see the heart rate jump up by 10 to 20 percent trying to compensate.
You check this especially when starting BP meds or if someone reports dizziness.
Got it.
What about listening over arteries like the carotids, brutes?
Brutes.
Those are swishing sounds you hear with your stethoscope.
It means turbulent blood flow, usually because of a narrowed atherosclerotic artery.
But there's a catch.
Yeah, a crucial one.
If the artery gets really blocked, like 90 percent or more, the flow might decrease so much that the brute actually disappears.
So no brute doesn't always mean no blockage.
Good point.
And for checking circulation in the legs, the ABI, ankle brachial index.
Yeah.
Simple calculation.
You take the highest systolic pressure measured at the ankle and divide it by the highest systolic pressure measured in the arm, brachial or artery.
And what do the numbers mean?
Normal is 1 .00 or higher.
If it's less than 0 .9, that suggests some level of peripheral artery disease, maybe moderate.
Less than 0 .5, that's severe vascular compromise.
That leg is in trouble.
Okay.
Now, the main event for auscultation, heart sounds, normal sounds first, S1 and S2.
S1 is the lub, that's the sound of the mitral and tricuspid valves, AV valves.
Closing marks the beginning of systole, best heard at the apex, the bottom tip of the heart.
And S2 is the dub.
Yep.
Closure of the aortic and plamonic valves, the semi -lunar ones, marks the end of systole, beginning of diastole, usually a bit shorter, sharper, best heard at the base, the top of the heart.
Then we get the abnormal sounds, the gallops, S3.
S3, the ventricular gallop, sounds like kentakelin.
It can actually be normal in kids or young adults under 35, but hearing it in someone older, that's usually bad news.
Sign of heart failure.
Often an early sign, yeah.
Indicates decreased ventricular compliance, the ventricle is stiff and resisting filling during early diastole.
And S4, the atrial gallop.
Sounds like Tennessee.
This happens late in diastole, just before S1.
It's the sound of atrial contraction forcing blood into a stiff, non -compliant ventricle.
You often hear it in patients with hypertension,
history of MI, or just significant aging.
And murmurs, just turbulence.
Basically, yeah.
Turbulent blood flow usually across a valve that's either narrowed, stenotic, or leaky, regurgitant.
We describe them by where they're loudest, when they happen in the cycle, and their intensity.
There's a grading scale from I, very faint, to V, extremely loud.
Can hear it even with the scope off the chest.
Okay, let's shift to the tests that confirm things.
Lab work first.
If we suspect a heart attack, what's the go -to marker?
Troponin.
Specifically, troponin T and troponin I.
These proteins are released when a heart muscle cells die necrosis.
They are highly specific to heart.
And the key takeaway is?
Any rise in troponin indicates some level of cardiac damage.
Even a small elevation is significant and means increased risk, so we treat those aggressively.
We often get results fast with point -of -care testing right at the bedside or in the EV.
Critical info.
What about baseline risk assessment labs?
Lipids.
Yeah, the lipid panel.
For quick reference goals, we generally want total cholesterol under 200mgdL, LDL, the bad cholesterol, ideally less than 130, or even lower in high -risk folks.
And HDL, the good stuff, we want that above 45 for men and above 55 for women.
And inflammation plays a role too.
HSCRP.
Highly sensitive C reactive protein, yes.
It's a marker of general inflammation in the body, which we now know is deeply involved in atherosclerosis.
Less than 1mgL is low risk.
Over 3mgL is considered high risk for future cardiac events.
All right, now for the big one.
The invasive test.
Cardiac catheterization, often called a heart cath.
The gold standard, really.
Most definitive way to look directly at coronary arteries and heart pressures, but it is invasive.
So safety becomes paramount.
Let's focus right there.
Pre -procedure care.
What absolutely has to be checked.
Allergies are huge, especially to iodine or shellfish because of the contrast dye used.
Kidney function is critical too.
The dye can be tough on kidneys, so we need baseline labs, maybe give extra fluids beforehand.
A function is borderline.
What should we tell the patient they might feel?
Warn them they might feel their heart skip a beat or race for a second when the catheter touches the inside wall.
Also, when the contrast dye goes in, it often causes a warm flushing sensation, like a hot flash.
It's normal, but good to pre -warn them.
Any meds to hold?
Definitely check anticoagulants.
If they're using the femoral artery in the groin for access, drugs like warfarin are usually held for a few days beforehand to reduce bleeding risk.
Check specific orders, obviously.
Okay, it absolutely is.
Critical rescue time.
The patient needs strict bed rest.
The insertion site leg, if femoral access was used, has to be kept straight.
Usually for two to six hours, depends on the type of closure device used at the site.
And monitoring?
Frequent vital signs, like every 15 minutes for the first hour, then maybe every 30.
Checking the insertion site for bleeding or hematoma formation.
And crucially, checking peripheral pulses, color, temperature, sensation in that extremity distal to the site.
Comparing it to the other side.
What if something goes wrong?
What are the immediate red flags we need to jump on?
Okay, critical rescue action alert time.
If the patient reports chest pain, if you see active bleeding from the site or rapidly growing hematoma, or if those distal pulses disappear or the leg becomes cold and pale.
Exactly.
Any of those.
Don't hesitate.
Call the rapid response team or provider immediately.
If it's bleeding, your first action while waiting for help is firm, direct pressure, usually just proximal to the insertion site.
Time is muscle, or in this case, preventing major hemorrhage or limb loss.
Wow.
Intense, but so vital.
Okay, we've really covered a lot of ground here.
From the core mechanics, preload, afterload.
To those non -negotiable risk factors, including the psychosocial ones like chronic anger, which we can't ignore.
Recognizing subtle symptoms like that triad in women or the differences between DOE, orthopnea, and PND.
Interpreting physical findings from skin signs to heart sounds like S3 and S4.
And wrapping up with those critical safety protocols around cardiac cath, a really comprehensive sweep.
It is.
And you know, just as a final thought,
the heart isn't just a pump.
Symbolically, culturally, it's tied to our very existence, our emotions, our survival.
Right.
So when someone gets a serious cardiovascular diagnosis, it hits hard on many levels.
Exactly.
Denial is a pretty common, even normal initial reaction.
It's a defense mechanism.
But when that denial stops someone from following their treatment plan, taking beds, changing diet, quitting smoking.
Then it becomes maladaptive.
Dangerous.
Precisely.
It crosses a line.
And it makes you think, how do patients and their families cope with the immense stress of managing a condition that requires such a fundamental life changes?
Well, it's a huge challenge that goes way beyond just the medical facts.
That's a really powerful point to end on.
Something for all of us to reflect on in our practice.
Indeed.
Well, thank you for joining us for this deep dive into the cardiovascular assessment.
Hopefully it's been helpful.
Absolutely.
Thanks everyone for listening.