Cardiac Cases - SD

Introduction

Hello, my name is Jason Matthew Fields.

I am the director of the Emergency Ultrasound Fellowship at Thomas Jefferson University in Philadelphia, Pennsylvania.

This lecture is on some cardiac cases that will help reinforce some of the principles talked about in the cardiac and IVC lectures.

We are going to discuss some cardiac cases to help reinforce some of the principles of cardiac ultrasound.

90% of diagnosis of this is just simply taking a look grossly at the heart, especially for those people new to this.

Pathology is sometimes very easy to see and doesn't require too much advanced skills.

With this example that I'm showing here on my title slide, just simply taking a quick look at this, hopefully you realize that this is something not quite right here.

You can see on the mitral valve here a large hyperechoic mass.

This was a case of endocarditis.

It's very easy to see.

We're going to start pretty simple and kind of work our way up.

Case 1: Cardiac Tamponade

This first case is a 64-year-old guy with end stage renal disease who comes in with worsening dyspnea on exertion and a syncopal episode earlier today.

He is tachycardic and he is hypotensive, and you get an EKG on the patient.

On initial glance, it doesn't seem to be too diagnostic, except when you look down at the rhythm strip, you see this kind of undulating pattern that we call electrical alternans.

You are concerned about cardiac tamponade, and you can take out your ultrasound machine to see if this is the case.

When you put the ultrasound probe on the patient's chest, you're rewarded by seeing a large circumferential effusion as well.

You can see that there is the right ventricle is kind of smushed.

It's a little bit hard to tell in this example just because of the fact that there's so much movement, but you just grossly look at that right ventricle, and it's purely concerning that there is such a large intrapericardial pressure that is causing an impaired relaxation of that right ventricle.

Then finally you see the heart swinging on its axis.

These are all findings that you would expect to see in cardiac tamponade.

When you look at a parasternal view, it's a little bit easier to visualize the free wall of the RV.

Again, in this example, there's a lot of movement of the heart, but what you're looking for is impaired relaxation during diastole of the RV.

Typically, the RV would relax symmetrically.

Whenever there's increased pericardial pressure, it often causes a little bit of a serpiginous shape to the RV free wall, or like a little bit of scalloping kind of pattern.

That's often when you see that, that's often a tip off to cardiac tamponade.

The next step I would say is to take a look at the IVC, or the inferior vena cava.

This is a nice extra data point to have and help confirm your diagnosis.

In the case of cardiac tamponade, you would expect for there not to be very much IVC collapse.

This is just showing where to place the probe to do the subxiphoid approach to looking at the inferior vena cava.

You place the probe in the midline with the pointer pointed towards the patient's head and just scan to the right of midline to see the longitudinal view that's demonstrated here.

Here we see that the fact that there's no IVC collapse or that the IVC is plethoric, and we also see that there's dilated hepatic veins.

This tells us that the patient's intravenous pressure is very high, consistent with cardiac tamponade.

Whenever you're looking at cardiac tamponade, you want to try and make sure that you take a look at the subxiphoid and apical four chambers, because this generally offers the best visualization of pericardium and of the right ventricle.

I often tell people who are trained that there are three steps to diagnosing this.

Three simple steps.

One, identify the pericardial effusion.

You can't have tamponade without the effusion.

Two, look for chamber collapse.

With early diastolic RV collapse being the most sensitive finding.

Being able to differentiate early diastolic RV collapse is a little bit more challenging and takes practice.

Start simply by just looking at the ventricles and seeing does a ventricle look smushed or not.

Three, look at the IVC.

A filled plethoric IVC supports the diagnosis of tamponade, and underfilled IVC does not necessarily rule out tamponade, but suggests the patient's hypotension will be that much more likely to respond to fluids.

Cardiac tamponade, the first step is to give fluids, so that you're always going to do that.

Even when you see a filled IVC, that doesn't mean that the patient doesn't need fluids, because these patients need very high filling pressures to overcome the intrapericardial pressure and maintain their cardiac output.

Continue to give fluids.

Just as an aside, inferior vena cava is talked a lot about in literature as being a surrogate for volume status, but we have to remember that there are other things that can cause an IVC to be dilated or small.

Namely tricuspid regurg, pulmonary hypertension, heart failure, mitral valve stenosis, and sometimes people have an idiopathic enlarged IVC.

Likewise, small IVCs, while they are often caused by dehydration and being intravascularly underfilled, that can also be caused by IVC compression.

IVC stenosis, or just idiopathic, we have a small IVC.

Case one was cardiac tamponade.

We are going to discuss ultrasound guided pericardiocentesis in a different lecture.

Case 2: Pulmonary Embolism

The second case is a 64-year-old male with a history of metastatic renal cell carcinoma who presents with dyspnea on exertion, and a syncopal episode.

He has tachycardic hypotensive, and his pulse ox is low.

This patient's really not a diagnostic dilemma.

Most clinicians would say that this patient always has a high suspicion for something like a pneumonia or a pulmonary embolism.

We get the chest x-ray, and that's clear.

Now we're really concerned about a pulmonary embolism.

Of course, nothing simple and clinical.

In the clinic or in the emergency department, this patient has a contrast allergy.

We can't get a PE study, a CT scan to rule out PE.

As often the middle of the night and getting a VQ technician might be difficult, and the patient's also unstable.

We need to make some real time critical decisions at the bedside.

Namely, the question is going to be whether we start heparin and whether we give thrombolytic therapy.

The ultrasound can be very useful in situations like this.

We take a look at this patient's heart, and when we look at this immediately, we often might think, oh, we've got the probe flipped the wrong way because the LV, the left ventricle appears to be on the left side of the screen, where the right ventricle should be.

But in fact, this is actually just a very enlarged RV.

We talk about normal ratios of RV to LV.

Typically people say 0.6 is the size, is the ratio size that is normal.

Whenever you get up to one, then you've got significantly enlarged RV.

Another finding that we see is a paradoxical diastolic septal motion.

Typically, during diastole, when the ventricles are starting to fill, they're at their lowest pressure.

When this happens, the LV usually has a higher resting pressure and the septum will bow towards the RV.

When you have pulmonary hypertension from a PE, the RV pressure is higher.

The septum bulges over towards the LV during diastole.

You can tell when diastole occurs, 'cause you can see those valves opening, and that's when filling's starting.

It's right when filling's starting.

You see the septum bow over into the LV.

When you look at this in short axis, this is, you can also see this by flattening of the interventricular septum.

People also call this a D sign and the short axis.

Another finding you might see is the McConnell sign.

The McConnell sign is an interesting contraction pattern that occurs in pulmonary embolism.

What happens is you see a normal apical contraction pattern with a hypokinesis or a decreased mid RV contraction pattern.

There are a lot of people aren't exactly sure why this occurs.

Some theories are that the RV, the apex of the RV is somewhat tethered to the LV, and the LV is still normally contracting.

That gives it that appearance that kind of pulling the apex over.

Some people also think that there might be some relative ischemia to the mid RV, so that's causes the kinesis.

Also in these examples we see very enlarged RVs.

We also see the diastolic paradoxical septal motion very nicely, especially in this example.

It's very diagnostic of pulmonary embolism.

Finally, one other finding that you might see in pulmonary embolism that's kind of an icing on the cake, but also very difficult to diagnose with transthoracic echo is you may see, as you see this debris kind of flopping in this right ventricle, you may see an RV thrombus, obviously, that would, if you're able to visualize this and identify it, then you clinch the diagnosis.

In pulmonary embolism, the possible findings include RV enlargement, paradoxical septal motion, McConnell sign, and a dilated IVC is usually seen unless the patient's severely dehydrated.

You may find an RV thrombus.

You should remember though that echo is a cardiac ultrasound has a low overall sensitivity for pulmonary embolism.

Why is this?

This is because most pulmonary emboli are submassive and do not cause significant right heart strain.

Therefore, no findings, no abnormal findings on cardiac ultrasound.

The sensitivity is higher, massive pulmonary embolism, when thrombolytic therapy may be indicated.

The way I think about it is if your patient is sick, tachycardic, hypotensive, and hypoxic from a pulmonary embolism, then findings of RV strain will be present, are highly likely to be present.

If your patient is stable, and you suspect pulmonary embolism, because the patient has some pleuritic chest pain or something else, then bedside echo would likely be normal.

You can't really rule it out with doing this.

As an adjunct, you can always do a DVT study at the bedside to give yourself additional data points and potentially rule in the diagnosis if you find a DVT.

Case 3: Heart Failure vs. COPD

Our third case is a 65-year-old male with a history of obesity, heart failure, and COPD who presents with acute dyspnea.

He's in respiratory distress, and he has a limited lung exam with distant breath sounds, some wheezing and some rales.

Very difficult to clinically distinguish whether this could be COPD or heart failure as the primary etiology of the patient's dyspnea, and essentially, which therapies you're going to give Lasix, nitroglycerin and BiPAP and admit to a CCU, or you're going to give nebs steroids and admit to a MICU.

Cardiac ultrasound can be very useful, along with IVC and lung ultrasound to help figure this out.

First you can look at the heart and take a look at the patient's ejection fraction.

Overall, visual appearance of the heart.

Here we see a very enlarged, dilated chambers suggestive of a dilated cardiomyopathy.

We also see that the patient's heart is squeezing very minimally, almost, we might estimate this at about 10%, or even less.

This helps us establish that this patient does indeed have fairly significant heart failure.

We can then look at the IVC, and I like to think of this as the sonographic equivalent of looking for right-sided heart failure, JVD and peripheral edema, and a dilated IVC.

Here we do see a dilated IVC, this plethoric with minimal to no respiratory variation.

This suggests that the patient's right sided pressures are very high.

Finally, we can take a look at the lung and this is done by placing the probe in the midclavicular line and scanning down from rib space to rib space and looking in between at the pleura.

On the right we have one normal lung exam with your skin subcutaneous tissue rib shadows here and here.

In between the rib shadows you see your parietal pleural line, so echogenic and below that you have air.

Therefore, you start to get reverberation artifacts of this interface between the parietal and visceral pleura.

There's your initial pleura line, and there's a reverberation artifact to that.

Now, whenever you have fluid in the lung, you get this different type of artifact, reverberation artifact, that's called comet tails, or some people call it the strobe lights.

Those go from the top of the pleural line all the way down to the bottom of the screen.

Whenever you have a lot of these, that's diagnostic of pulmonary edema.

Basically this tells us that this patient, the combination of these strings tells us the patient is definitely in heart failure.

In heart failure, you have depressed ejection fraction, a cardiomyopathy, you can, you may see a cardiomyopathy such as in the large or dilated, or you might see left ventricular hypertrophy, a dilated IVC.

If you look at the lungs, you may see B-lines or comet tails.

You may ask yourself, I'm not a cardiologist, can I really estimate a left ventricular ejection fraction?

Multiple studies have demonstrated strong agreement between EPs, emergency physicians with a basic amount of cardiac ultrasound training and cardiologists when estimating LVEF.

It's easy to learn.

You just need to start simple and kind of work your way up.

I suggest becoming comfortable with the extreme states first, let me show you a couple examples.

Short axis is a good way to learn this.

If you focus on this left ventricle and look at the percentage of change in volume that occurs from end of diastole to end of systole, you see that there's a very large amount of squeeze.

It's almost in the range of 80%.

Look at another example.

Also good symmetrical squeeze in this left ventricle, not quite as much as the last example.

This one is probably estimated about 60 to 65%.

Just a normal ejection fraction.

Look at a third example, and you can see the squeeze is significantly less.

People call this depressed ejection fraction, maybe in the range of 30 to 40%.

In this example, it's severely depressed.

There's not very much squeeze at all here.

Gonna be the range of 10%.

Put those all together to kind of give you a sense of how easy it is to see the difference between the different states.

The top left, we have the hyperdynamic one and the top right, we have a normal one.

In the bottom left, we have a depressed ejection fraction, and in the bottom right we have a severely depressed ejection fraction.

Also, in just kind of a gross view, you can quickly establish that the patient may have a cardiomyopathy in this example, or left ventricular hypertrophy, just by simple kind of gross look at the ventricular walls.

You can also measure them and establish the patient has left ventricular hypertrophy.

Case 4: Chest Pain and Possible STEMI

In the fourth case, we have a 74-year-old male who presents with chest pressure and shortness of breath, the patient's tremulous and diaphoretic, and we're unable to get a good quality EKG.

However, there's appearance of maybe some ST segment elevations, V one and V two.

But it's poor quality, and a situation that's commonly faced in the emergency department.

This has significant implications.

If this is truly an ST elevation MI, the patient will benefit from cath lab activation.

Recently cath lab activation has been something of debate, as to who should activate the cath lab.

More places are veering towards emergency department cath lab activation.

But sometimes there still needs to be communication with the cardiologist.

Many times there may be disagreements as to whether the cath lab should be activated or not.

It's very difficult when you don't have clear objective evidence.

Is there anything else that can sometimes help us establish whether this patient's having true ischemia to their ventricle.

Ultrasound can be useful for this.

If we took a look at this patient, we can see that the patient has an akinetic septum.

Whereas the other walls, the RV free wall and the other walls of the left ventricle seem to be contracting very nicely.

This is consistent with ischemia to the septum.

There is a caveat to this in that you don't know if this is a new finding or if this patient had a previous infarct, so you have to take it with a grain of salt and apply it to the patient's clinical history.

If the patient is a healthy patient that's never had any medical problems, then you would think that this is likely a new finding.

But it could be an old finding, but seeing this in light of a consistent EKG can help you push you towards the correct therapies.

Case 5: Syncope

Our fifth case, we have a 42-year-old female who comes in after a syncopal episode.

She looks well.

Her labs, EKG, and chest x-ray are very normal.

She wants to leave.

She's a very busy person and wants to get on with her normal life.

But there shouldn't really have much risk factors for a poor outcome from syncope, but you think you hear kind of an odd heart sound, maybe like an odd plop on cardiac auscultation.

It makes you a little bit wary of letting this lady leave.

Maybe to help convince her to stay, you maybe should just take a look at her heart and see if you see anything.

In this case, you're well rewarded because that plop is actually a myxoma in the left atrium plopping through the mitral valve annulus.

A very high risk patient to be discharging.

Not that I would say that every patient with syncope should get a cardiac ultrasound, but certainly studies have shown that patients that have cardiac risk factors, and abnormal cardiac exams or EKGs, can benefit from an echo.

Left atrial myxoma is most common cardiac tumor.

It's more common in women.

It can cause mechanical obstruction or even embolize.

When it prolapses through the mitral valve, tricuspid valve, and like as in this example, it can cause valve damage and destroy the annulus.

Sudden death occurs in 15% of cases and it can be operative or resected.

A nice pickup in this case.

Case 6: Cardiac Arrest Triage

In our final case six, you're working in a small community emergency department when the nightmare scenario occurs that three patients are brought in and all in cardiac arrest.

You can begin a ACLS simultaneously for all three, but all three are in asystole.

After five minutes, you realize you do not have the resources to continue a ACLS in all three patients without endangering other patients in the emergency department.

The question is, who do you triage your resources for.

The patients may have varying age and risk factors, but let's just say for argument's sake that these three patients are fairly identical in age and in past medical history.

It's difficult to determine which one has the best chance of survival, if any of them do.

There was a study looking into this question, to figure out what the outcome in cardiac arrest patients found to have cardiac standstill on the bedside emergency department echo, if that can predict who survives, and in fact, it did.

In the study of 169 patients with cardiac standstill, none survived to emergency department discharge.

That might sound like a no brainer, but it's actually very clinically important to realize that you can take a do an ultrasound and if you see cardiac standstill that's suggests that the patient's not going to recover.

You can abort your therapy and ACLS and triage your resources to the other patients that actually have a chance of survival.

Of the patients that did have return of circulation all had some cardiac activity on ultrasound.

This is an interesting finding.

It's only one study, but there is a multicenter study going on currently to help see if this pans out.

Let's get our ultrasound for these three patients.

Patient number one, we take a look and we see pretty much no squeezing of the left ventricle in this example.

Cardiac standstill and our patient's unlikely to recover.

Our second patient, again, we see cardiac standstill and the patient is probably not going to recover here.

The third patient, we do actually see some mild contraction pattern.

A little bit is hypokinetic, but there is something there.

If we also notice, we can see that that RV is fairly small, suggesting the patient's underfilled.

In this case, I would continue ACLS and even give more fluids if I haven't been giving them already, as the patient looks slightly hypovolemic.

All right, that's the end of this lecture.