Pericardium and Extra-Cardiac Structures: Anatomy and Pathology

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Pericardium and Extra-Cardiac Structures

Anatomy and Pathology

Enrique Pantin and F. Luke Aldo

There are so many things surrounding the heart that no one pays attention to!

It is all about the heart though, so who cares about all that other stuff. Right? Wrong!

Like a lot of things in life, we forget that it is not about the “prima donna”, but about the team! After all, there is no “I” in team, but wait a second, there is a “ME”. Alright, never mind, let’s move on!

The Pericardium

image

The aortic root (“B” in the image above) is one of the structures the pericardium covers, so if the root decides to rupture, well that patient is so out of luck… cold and dead! As in ruptured aortic root dissection with exsanguination into the pericardial sac→pericardial tamponade→that light at the end of the tunnel…

There is a club composed by the “extra-cardiac structures team” whose members can be seen by TEE most of the time but they are not too happy with the lack of credit. Everybody talks about the heart, but what about us?

These are all members of the “extra-cardiac structures team”, they are the majority, but this still sounds like a dictatorship by that narcissistic heart!

As the TEE probe is advanced through the esophagus and into the stomach we can image several structures besides the heart.

image Starting from the esophageal entrance we can see the main neck vessels (the carotid arteries and internal jugular veins)

image In the esophageal upper 1/3, we can see part or all of the arch vessels

image In the mid 1/3 of the esophagus, the trachea creates a blind spot, and we miss the distal ascending aorta, proximal arch, and proximal to mid left pulmonary artery, but we can see:

image In the lower 1/3 of the esophagus, we can see:

image From the transgastric window we can see:

Because the esophagus, our magic TEE window, is all the way in the back of the chest, we decided to do a drawing from the esophageal perspective. Then we took the back of our drawing away, including the spine and rest of the bones, and applied some crude “X-ray” views to see what lies in front of it. This is probably the only time the esophagus finished first in a coronal view anatomical race. Congratulations Mr. “E”!

L = left and R = right; PA = pulmonary artery, P = pulmonary veins, H = heart, L = liver, S = spleen, and K = kidney.

image

How can we see fluid on TEE?

In a transgastric mid-short-axis view below, we can see lots of stuff besides the heart!

image

There are very few important questions about the extra cardiac structures in the fast-paced world of anesthesiology and acute care. Usually questions include:

The rest is by far secondary, technicalities we really don’t care too much about! After all, we are here to diagnose cardiac abnormalities and things that can immediately affect cardiac function, not to determine if the patient had filet mignon or penne a la vodka for dinner last night!

The Pericardium—we are back here again!

image Is 1–2 mm thick.

image Is difficult to see by echo unless there is fluid on both sides of it or it is very thickened.

image Can elicit some extra brightness on echo like it has its own light.

image Has two layers (fibrous and serous).

image Serous layer has visceral and parietal aspects:

image

image The layers extend a couple of centimeters, incorporating the aorta and main pulmonary artery.

image Confines the total volume the heart can handle at one time creating a closed volume relationship among all cardiac chambers.

image This limited volume relationship is the basis for the changes seen during effusions and restrictive or constrictive pericarditis.

image There is normally a bit of pericardial fluid or “oil” (normally 5 to 10 ml and rarely up to 50 ml) that lubricates the heart so it can dance without causing too much noise. Just like a car engine needs motor oil, so does the engine of the human body. Luckily, we don’t need oil changes every 3000 miles!

image When the oil is too thick because the sac gets inflamed (pericarditis) or if the sac gets stiff, the pericardial layers rub as the heart moves and make some weird noises.

image When the oil level is too high, we call this a pericardial effusion.

image Several types of “oil” can fill the pericardial space:

image Excess “oil” can be due to:

image Pericardial effusion, like everything in medicine, we like to grade it, but there are no prizes, and the higher the grade AND speed of accumulation the worse!

image

image Pericardial-cardiac filling pressures are intimately related to breathing.

image Normally during SPONTANEOUS inspiration there is a drop in intrathoracic and intrapericardial pressure. This facilitates right-sided filling, right ventricle stroke volume and a drop in blood flow out of the pulmonary veins, resulting in decreased left ventricular stroke volume.

image Normally during SPONTANEOUS expiration, intrathoracic and intrapericardial pressures increase causing a drop in right ventricular filling and stroke volume. This provides more space to the left ventricle and causes the squeezing of blood from the lungs into the left ventricle, resulting in an increased left ventricular stroke volume.

image This cyclic variation in stroke volume during SPONTANEOUS breathing results in a less than 10 mmHg of inspiratory systolic systemic pressure drop during normal conditions.

image If this systolic blood pressure variation exceeds 10 mmHg it is called “pulsus paradoxus”. During conditions that increase respiratory effort (COPD, acute asthma, etc.), hypovolemia, or tamponade this pressure variation is greatly exaggerated.

image During MECHANICAL ventilation, the intrathoracic pump-sucking effect created by the negative pressure during SPONTANEOUS inspiration is lost and things get much worse for the blood pressure if there is tamponade. During MECHANICAL ventilation, the ventilation-pericardial pressure/cardiac filling relationship is reversed and the inspiratory thoracic pump is GONE! All this stuff is easily seen if the patient has an arterial line (top tracing) and also if left ventricular filling patterns are measured using PWD (middle tracing) through the mitral valve. “I” = inspiration; “E” = expiration.

image

image Normally the respiratory variation for tricuspid inflow velocity (this is proportional to ventricular filling) is less than 25% and for mitral less than 15%. This is all very scientific, but it is better just to do simple math: symptoms + 2D echo finding = diagnosis.

image Cardiac chamber collapse during diastole is diagnostic of tamponade. Usually tamponade is a clinical diagnosis with imaging support, but sometimes chamber collapse can be seen before symptoms are clearly seen. If a patient had a thick right ventricle, collapse may be absent, despite having tamponade.

image If the pericardial sac gets stiff, due to inflammation, tissue infiltration, or calcification, then it can affect the heart motion and filling causing restrictive and/or constrictive pericarditis. It is very hard to “see” pericardial sac thickening, stiffness, or calcification by echo and most of the time we just see the effect of the stiffness on the heart.

image CT and MRI are better diagnostic tools for pericardial layer imaging, especially if there is no associated effusion.

The Aorta

image Is the strongest tube we have, and one of the longest.

image Has six segments starting at the aortic valve annulus (annulus located between “A” and “B” in the aortic figure), with a diameter of about 3 cm, the sinus of Valsalva (at “B”), sinotubular junction (area connecting segments “B” and “C”), ascending aorta (“B”+“C”, 5 cm long), arch (segment “D”, from origin of innominate artery to end of left subclavian artery), and descending aorta (segment “E”, starting after left subclavian, and “K” ligamentum arteriosum and continuing to the descending thoracic and abdominal aorta).

image The “aortic root” includes the aortic annulus up to the proximal ascending aorta, and is included in the pericardial sac.

image The ascending is contained, with the pulmonary artery trunk, in the pericardial sac and can be divided into the root with its sinus of Valsalva, sinotubular junction, and ascending aorta.

image The aorta ends at the level of the 4th lumbar vertebra with about 1.75 cm in diameter as it bifurcates into the common iliac arteries.

image The coronary arteries are the only branches of the ascending aorta.

image The arch gives origin to the innominate artery, left carotid and left subclavian, although there are many anatomical variations that these vessels can have.

image The descending aorta gives origin to intercostals and some abdominal branches that often can be seen by TEE, like the celiac trunk, superior mesenteric artery, and sometimes even the renal arteries.

image

image The descending thoracic aorta in long-axis view looks like an evenly sized black tube and it should have a smooth inner surface:

image CT and MRI provide excellent views of the aorta, its branches, and of all extra cardiac structures, but they require IV contrast. Additionally, the MRI/MRA requires lots of time. CT and MRI are also both very “difficult” to do in the operating room!

image TEE can give a quick assessment of almost the entire aorta, from origin to upper/mid abdomen. It is best to start your exam at the aortic valve annulus and to try to follow the aorta all the way to the belly.

image

image It is best to examine the aorta in a short-axis view. This will prevent you from missing something. Once an area of concern is identified then a long-axis exam can add valuable information, such as length of the pathology, which can help reconstruct a 3-D mental view of the problem. We can actually do real-time 3-D views as well with some machines.

image We are not going to give you the TEE multiplane angles “recommended”. Instead you should try to:

image follow the aorta as you move from the aortic root to the ascending

image once you lose the ascending aorta view, due to tracheal interposition between the aorta and esophagus, turn the TEE probe to the patient’s left (if you are standing at the head of the bed) to find the proximal descending aorta

image once you find the descending aorta, by pulling/withdrawing the TEE probe you reach the aortic arch

image after you have given a good look at the arch, try to find the arch vessels, especially the left subclavian which is easily seen in the distal arch. Make sure you do not pull the probe out of the patient while looking at arch branches—we have done that!

image then, while reinserting the probe, try to follow the aorta down to its most distal aspect in the abdomen

image sometimes the aorta can be tortuous and you must “follow” it by turning the probe

image other times the aorta just disappears when you are following it distally—it’s OK—these are just segments of the aorta that have a poor echo window. In this situation, just prevent the probe from turning left or right and continue to advance distally until the aorta reappears

image NEVER advance the probe if you feel abnormal resistance.

Aortic aneurysm, dissection, and atheroma are the 3 big things. The good thing is that we know what these things look like in the anatomic specimen. With TEE it is only black-and-white images.

Aortic Aneurysm

image An aneurysm is a dilation greater than 1.5 times the normal size for that structure.

image The ascending aorta is much larger than the aortic root and sinotubular junction in the image below…what could this be? Yes, you are correct an aneurysm it is!

image

image Sometimes we don’t know what the normal size is, but comparing to other areas of the same structure usually gives us a hint that things are bigger than they should be!

image Aneurysms can be isolated or associated with a cardiovascular problem like HTN, aortic valve disease (AS/AI/bicuspid aortic valve), Marfan’s, etc.

image Ascending aortic dilation can cause secondary aortic valve insufficiency as well.

image Aneurysms greater than 5 cm or a rapidly growing (>5 mm/year) are often used as indications for surgery. These are most commonly CT- or MRA-based diagnosis.

image Patients with Marfan’s or other connective tissue disorders usually have other cardiovascular anomalies. Thus a complete exam must be done.

image Aneurysm of the sinus of Valsalva, like in any other portion of the aorta, can also occur. Depending on which sinus is affected, it can rupture into the right atrium (most commonly) or distort the annulus and cause aortic valve insufficiency.

Aortic Dissection

image Dissection occurs when a breach in the intima allows pressurized blood to separate the intima from the medial layers. In the image below note the double wall in the ascending aorta, typical of dissection.

image

image Blood can propagate proximally, distally, or both between the intima and medial layers.

image Can present as a clearly separated layer with a flow-like pattern, often with several entry/exit points connecting the “true” and “false” lumens (so called “fenestrations”).

image Sometimes it is difficult to find the “true” lumen, and color flow Doppler can help in finding these fenestrations and define which one is the perfusing lumen and which is not.

image The “true” lumen usually expands with systole and has a regular shape (from circular to a flat tube).

image Dissections can also present as an intramural hematoma (5–10%) and they must be differentiated from a smooth-layered atheroma. Intimal layered calcifications (in the wall, below the plaque) and close observation of the surface usually help distinguish the plaque from intramural hematoma, where calcifications, if present, are in the intimal layer of the hematoma.

image Dissection can be localized or diffuse, and occasionally it can present as an intimal tear without dissection.

image Another way dissections can occur is of iatrogenic origin (cardiac catheterization, post aortic cannulation, etc.), or when an ulcerated atherosclerotic plaque suffers penetration into the intimal/medial layer.

image Dissections are classified as Stanford A or B (SA or SB) or DeBakey I, II, or III (DB1, DB2, or DB3) types.

image

image Surgery of an aneurysm or a dissection:

Aortic Plaque

Aortic plaque or atherosclerosis is a common finding in our older or vascular patients.

image Hypertension, diabetes, smoking, high cholesterol, and poor diet (usually a Western diet; i.e. most of us!!!! I’ll take a Big Mac and fries please. Oh and can you supersize that! STAT!) are all risk factors.

image Plaque is often located in the arch and descending aorta, and is less common in the ascending aorta.

image The most common site for plaque in the ascending is the right sinotubular junction area and if calcified will give a nice black shadow (see image below), as the ultrasound is pretty bad at penetrating through calcium. As a result of the echo “shadow”, we are not able to see beyond the calcification. If we want to see what “lies beneath”, we will need to find this through alternative imaging angles.

image

image Atheromas can take almost any shape and size, sometimes artistic, mostly very scary! They can be flat, round, mountain looking, pedunculated, mobile or not, as well as calcified or not.

image In this long-axis view of the descending thoracic aorta a large atherosclerotic plaque can be seen, yes! that white blob attached to the inner surface of the aorta.

image

image The bigger and more mobile they are, the higher risk for stroke and embolic phenomena there is.

image We should define these plaques by their location, size (measure from base to highest point), and if mobile or not.

image Aneurysm, dissection, and plaque can overlap in the same patient making its management more complicated.

Aortic Trauma

Aortic trauma is a distinct problem from dissection, but with the potential of acute death as well—as opposed to chronic death? I tell you, my partner was a bit sleepy when he wrote this stuff….

image Most commonly occurs after blunt chest trauma, usually due to high-speed impact.

image The aorta has several areas where it is relatively fixed (annulus to heart, neck vessels, descending thoracic aorta fixed by intercostals) to the chest and other areas where it is mobile (ascending and arch).

image The aorta can rotate and twist at the aortic root, can bend at the arch vessel area, and at the ligamentum arteriosum area.

image The aorta most commonly breaks at the root, arch vessel area, or at its fixture at the ligamentum arteriosum area.

image If the transection is complete, kaput you are DEAD!

image Partial transections are what we see, and CT is the primary diagnostic mode because it is part of the usual trauma workup.

image TEE can miss small tears in the arch and ligamentum area as they are difficult to see with TEE due to tracheal interposition. Anyway aortic shape disruption, adventitial hematoma, small evagination of the wall, intraluminal hematoma, small flaps or tears can be seen.

image If you don’t see anything by TEE, but there is strong suspicion of a transection, then a CTA or angiogram (much less used these days) must be done.

image Aortic trauma can also be present with rupture of any other cardiac structures: sinus of Valsalva into the right atrium, traumatic atrial-septal defect, rupture of a papillary muscle (tricuspid or mitral), aorto-caval fistula, etc.

Pulmonary Artery

Why do we care?

image It can tell us a bit about the chronic pulmonary vasculature strain it suffers with chronic severe mitral regurgitation, pulmonary hypertension (primary or secondary to asthma, COPD, etc.), acute or chronic pulmonary embolism, etc. In all chronic cases it gets BIG, and we don’t mean fat, but dilated like a nice round Italian sausage.

image Did you know that a pulmonary embolism is one of the most common causes of sudden unexpected intraoperative cardiac arrest?!? But of course you knew! The other common causes include acute myocardial ischemia, arrhythmias, tamponade, and severe hypovolemia. ALL, but arrhythmias can have its diagnosis “assisted” by TEE.

image As a rule made by us, the right (“R”) and left (“L”) pulmonary artery should be 2/3 the diameter of the main pulmonary artery (“P”), and the main PA and SVC (“S” = short-axis superior vena cava) should be 2/3 of the ascending aorta (“A” = short-axis ascending aorta). This “2/3” rule also applies to many other chambers and tubes in the heart.

image In the image below, take note that the main PA has a similar diameter to the ascending aorta, probably because there is some chronic abnormality occurring with the PA.

image

image Sometimes we get lucky and can see an embolus occluding the main or proximal PA branches, but most of the time we just see signs of right ventricular strain. In cases of pulmonary embolism, signs include PA dilation, RV dysfunction, RV dilation (“R”), tricuspid insufficiency, dilated RA, bulging of the interatrial septum to the left, and flattening of the interventricular septum (the so-called “D”-shaped left ventricle (“L”) or a really squashed LV!).

image

Now what? We looked at the tubes going out of the heart. Now it’s time for the incoming pipes.

Superior Vena Cava, Inferior Vena Cava, and their Cousins the Hepatic Veins

Once you get a nice 4-chamber view from the mid-esophageal window, center the right atrium (“R”) in the middle of the screen and multiplane to about 90 degrees. Most of the time you will get a nice bicaval view with the SVC at the right of the screen and the IVC at the left of the screen. If you multiplane a bit more, to around 120–140 degrees, you will see the “modified bicaval view” like the beautiful one we got below.

In this modified bicaval view, we can see the left atrium (“L”), the interatrial septum and its thinner/thinner area (the fossa ovalis), the right atrium (“R”), the SVC (“S”), the IVC (“I”), the entrance of the coronary sinus (“C”), and the right atrial appendage with its typical broad base (“A”). The tricuspid valve (“T”) can also be partially seen, as well as some of the right ventricle (“RV”).

image

If we advance the probe into the stomach following the IVC, we will see the hepatic IVC (“I”) and the hepatic veins (“H”). Normally the IVC is less than 2.5 cm in diameter. The hepatic veins can be used to assess the inflow venous pattern as they lay parallel to the Doppler beam and thus make it easier to evaluate with PWD or color flow Doppler.

image

The hepatic venous flow:

image Like the pulmonary venous flow, has 3 main waves, the “S”, “D”, and “A” waves.

image Place the pulsed wave Doppler cursor, also called the “gate” or “sampling volume”, 1 cm into the hepatic vein. Then we press the PWD button and voila, a waveform for the hepatic venous flow is displayed:

image “S” wave corresponds to ventricular systole. During this time, the area of the heart with the closed tricuspid and mitral valves (aka the base of the heart; I’d like to ask a few questions to the person who named this!) is pulled down and a suction effect facilitates forward flow to the atria

image Next the valves open and the “D” wave (diastolic) occurs as the atrial blood volume emptying into the ventricles makes room for more blood to move into the atria

image Finally, when atrial contraction occurs the “A” wave (atrial) is generated because most of the blood is pumped into the ventricles, but some is pumped retrograde into the hepatic or pulmonary veins. This causes the “A” wave to inscribe below the baseline. Yes, you figured it out! This is the so-called atrial flow reversal and it is totally normal.

image

image In cases of severe tricuspid or mitral regurgitation, because the valve is incompetent, blood flow is pumped into the atrium during ventricular systole and from there into the hepatic or pulmonary veins. The normal forward flow of the “S” wave is seen as totally blunted or even reversed and inscribed below the baseline. This tells us that blood is going into the hepatic or pulmonary vein in ventricular systole instead of coming out of them and into the atria. It’s pretty neat that we are able to follow blood flow in real time without having to cut the heart open!

Well, well we are not done, but from here on it is much easier!

image The azygos vein, trachea, thymus (in children), and spine can be seen, but add very little in acute care.

image For fun we can see the stomach and its contents thus having an idea if there is some significant gastric content.

image From the gastric window, the liver and spleen are easily identified.

image Within the liver, the inferior vena cava has a normal diameter change with respiration, suggestive of normal CVP.

image The right kidney and the hepato-renal space (Morrison pouch), as well as the subdiaphragmatic area, will show any fluid accumulation in the right upper quadrant.

image We leave the lung and pleural space for last.

image TEE exam is never complete if we do not look at the left and right pleural spaces

image lung can be seen with its typical aerated pattern

image if there is lung atelectasis or condensation it looks like liver. Remember?

image pneumothorax is much more difficult to diagnose and we will leave that for you to research!

image pleural effusions are easy to see, but we need to look for them. The best view to start looking for pleural effusions is in the descending aorta short-axis view. Anything we see in this location, we will know belongs to the left chest, as seen in the following image. This is a short-axis view of the descending aorta with normal lung (“L”), atelectatic lung which looks very similar to the liver in echo (“A”), pleural effusion (“E”), and the chest wall with the ribs and all (“C”).

image

image After we are done with the left chest we have two options, you can just rotate to the right at the level of the atria until you find a right effusion or normal lung. You could also simply find the liver and pull the probe straight back from there until you see the right lung. Be careful not to pull out so much or the TEE probe will come out of the patient’s mouth!

Now it is your turn to grab that TEE probe and start trying to find all the cool stuff we talked about. Lots of extra-cardiac stuff and many things to see, some more important than others, but all fun!

Bibliography

Armstrong WF, Ryan T. Feigenbaum’s echocardiography, 7th edn. Philadelphia: Lippincott Williams & Wilkins, 2009.

Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22:1–23.

Brown JM, O’Brien SM, WuChangfu, et al. Isolated aortic valve replacement in North America comprising 108,687 patients in 10 years: changes in risks, valve types, and outcomes in the society of thoracic surgeons national database. J Thorac Cardiovasc Surg. 2009;137:82–90.

Isolated aortic valve replacement in North America comprising 108 687 patients in 10 years: Changes in risks, valve types, and outcomes in the Society of Thoracic Surgeons National Database.

Kisslo JA, Adams DB. Doppler Evaluation of Valvular Stenosis #3 <http://www.echoincontext.com/doppler03.pdf>

Mathew J, Swaminathan M, Ayoub C. Clinical manual and review of transesophageal echocardiography, 2nd edn. New York: McGraw-Hill Professional, 2010.

Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr. 1999;12:884–900.

Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and the Task force on valvular regurgitation, developed in conjunction with the American College of Cardiology, Echocardiography Committee, the Cardiac Imaging Committee Council on Clinical Cardiology, the American Heart Association, and the European Society of Cardiology Working Group on Echocardiography. J Am Soc Echocardiogr. 2003;16:777–802.

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