Category: 4. Cardiac Ultrasound (Echo) Pathology

Cardiac Tamponade occurs when the pericardial pressure exceeds the pressure of the right atrium or right ventricle leading to decreased preload of the left ventricle and eventually a drop in cardiac output/blood pressure. It is considered an obstructive type of shock.

Recall that cardiac tamponade is more dependent on the rate of pericardial fluid accumulation versus the actual size.

On physical exam you may see Beck’s Triad defined as hypotension, jugular venous distension, and muffled heart sounds. You can also detect pulsus paradoxus as well. However, other diagnoses can cause false positives for these findings including severe COPD, tension pneumothorax, or other causes of obstructive shock.

Point of Care Ultrasound can offer a more definitive diagnoses of pericardial effusion and cardiac tamponade.

Ultrasound Findings of Cardiac Tamponade:

Using transthoracic echocardiography (TTE) you can see if the pericardial pressure exceed the right atrial or right ventricular pressures.

Since the lowest pressures in the heart is the right atrium, the first echo sign you will see of cardiac tamponade is right atrial systolic collapse.

The second echo sign you will see in cardiac tamponade is right ventricular diastolic collapse.

Either of these signs are considered positive echocardiographic signs of cardiac tamponade.

Note: Keep in mind that there is a difference between echocardiographic and clinical cardiac tamponade. Echocardiographic cardiac tamponade just exams to see if the right heart (RA or RV) are affected, the echo can’t tell if your patient is actually hypotensive. Clinical cardiac tamponade requires the patient to be hypotensive and in shock. Even though the echocardiographic signs of cardiac tamponade will usually correlate clinically with a hypotensive patient, it is not always the case.

A Pericardial Effusion is when there is a collection of excess fluid within the pericardial cavity. When enough pressure builds up from a pericardial effusion, it can turn into Cardiac Tamponade.

Patients with Pericardial effusion will typically present with exercise intolerance, tachycardia, pleural friction rub, tachypnea, shortness of breath, and chest pain. The causes of a pericardial effusion can be from various causes including pericarditis, myopericarditis, uremia, malignancy, infections, rheumatologic, etc.

An important point you must remember about Pericardial effusions is that is it not just based on size, the deleterious effects of pericardial effusions are actually more dependent on how quickly a pericardial effusion accumulates rather than it’s size.

In the figure below, a rapidly accumulating pericardial effusion can increase the pericardial pressures significantly and lead to cardiac tamponade despite a relatively small size. Conversely, an end-stage renal disease patient can have a chronic pericardial effusion that slowly accumulates with over 200-400 ml with no hemodynamic consequences.

Ultrasound Findings of Pericardial Effusion:

• The parasternal long-axis and subcostal four-chamber views are typically favored for inspection of pericardial effusions
• The Descending aorta is a distinguishing landmark used to distinguish between a Pericardial Effusion and a pleural effusion
• A pericardial effusion will appear anterior to the descending aorta whereas a pleural effusion will appear posterior to the descending aorta.

The cardiac ultrasound image below shows both a pericardial effusion (anterior to the descending aorta) and a pleural effusion (posterior to the descending aorta).

Pericardial effusion vs Pericardial Fat Pad

Being able to determine the difference between a Pericardial Effusion and a Pericardial Fat Pad is important as they may have similar sonographic appearances.

• Pericardial fat pads are usually located anteriorly and can usually be seen on the Parasternal Long Axis view.
• Pericardial fat pads are usually not completely anechoic and can appear to have striations.
• Lastly, pericardial fat pads can usually be seen to move with the motion of the heart.
• If you are in doubt, ask another more experienced POCUS user to look at it or order a formal echo to clarify if needed.

A Pulmonary Embolism is a blood clot that has dislodged from a distal site which has lodged into one of the pulmonary arteries. Predominantly the clot originates from a deep vein thrombosis (DVT) in the lower extremities where it will travel in the venous circulation, enters the right side of the heart, and eventually into the pulmonary arteries. Learn how to perform DVT Ultrasound here.

Considering the rapid onset/timing of a Pulmonary embolism, patients typically show symptoms or complain of chest pain, shortness of breath, cough, hemoptysis, or even syncope. Risk factors include cancer, oral contraceptive (OCP) or hormone replacement therapy (HRT), immobility, and recent travel.

Here are the different types of pulmonary embolism you may encounter:

• Submassive Embolism– Submassive (or intermediate-risk) PE refers to those patients with acute PE without systemic hypotension but with evidence of either right ventricle (RV) dysfunction or myocardial necrosis. RV dysfunction is characterized by RV dilation, hypokinesis, or elevation of brain natriuretic peptide (BNP); myocardial necrosis is suggested by elevated troponin. There is evidence that these patients may possibly benefit from “half dose” thrombolytic therapy.
• Massive Pulmonary Embolism-Massive (or high-risk) PE is a term used to designate patients with right ventricular dysfunction and sustained hypotension (systolic blood pressure <90 mmHg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE). These patients may benefit from thrombolytic therapy.
• Saddle Embolism-A Saddle is a large pulmonary embolism that straddles the bifurcation of the pulmonary trunk, extending into both the left and right pulmonary arteries. Although it only occurs in about 2-5% of all pulmonary embolism, Saddle Embolisms can completely obstruct both left and right pulmonary arteries resulting in right heart failure and, unless treatment is prompt, death.

Bedside echo is extremely valuable in risk stratifying patients with pulmonary embolism to see if they may benefit from anticoagulation or thrombolytic therapy.

Ultrasound findings of Pulmonary Embolism:

The most definitive way to diagnose a pulmonary embolism is to directly visualize the clot either in the pulmonary artery itself or as a clot in transit.

Unfortunately directly visualizing a clot in the heart or pulmonary artery is a rare finding. Most of the echocardiography findings for pulmonary embolism are “indirect signs” that evaluate for the dysfunction of the right ventricle from a significant clot burden. Usually, this is seen as an enlarged right ventricle.

The two most common and easy to recognize signs to look for right ventricular dysfunction on echo are the “D Sign” and McConnell’s sign.

The “D Sign” on Echocardiography

• The “D Sign” is an ultrasound/echo finding that shows the left ventricle as a D-shaped structure. It is a result of right ventricular strain causing a shift of the septum towards the left side of the heart.

“McConnell’s Sign” on Echocardiography

• McConnell’s sign is where there is akinesia of the right ventricular lateral wall with hyperdynamic appearance of the right ventricular apical wall.

Patients with Systolic Heart Failure also known as “Heart Failure with Reduced Heart Function (HFrHF)” will commonly present with shortness of breath, orthopnea, paroxysmal nocturnal dyspnea (PND), exercise intolerance, irregular heartbeats, and edema in the bilateral upper and lower extremities. This is usually accompanied by cardiogenic pulmonary edema and B-lines on ultrasound.

One of the most commonly used surrogates in assessing systolic function in these patients is done by measuring the Left Ventricular Ejection Fraction.

Ejection fraction (EF) in percentage is defined as: EF(%) = SV/EDV x 100

Where SV: Stroke Volume and EDV: End Diastolic Volume

Ejection fraction (EF) is basically a percentage, of how much blood the left ventricle pumps out with each contraction. For example, an ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out during each systolic contraction

	Hyperdynamic	Normal	Mildly Reduced	Moderately Reduced	Severely Reduced
Ejection Fraction	>70%	55-69%	45-54%	30-44%	<30%

Measuring Ejection Fraction on ultrasound can be approached either qualitatively or quantitatively. In this post, we will go over the qualitative technique to assess ejection fraction.

Qualitative Approach to Assessing Ejection Fraction:

1. Look at how well the left ventricle walls are moving. Are they coming close to each other during systole?
2. Look at how well the anterior mitral valve leaflet is moving. Is it coming close to the ventricular septum during diastole?

If the left ventricular walls are moving well and coming close together during systole and the anterior mitral valve leaflet is almost touching the septum during diastole then the patient likely has a normal ejection fraction.

Conversely if the left ventricular walls are barely moving during systole and the anterior mitral valve leaflet is barely moving during diastole the patient likely has a low ejection fraction.

Here are cardiac ultrasound (echo) images of patients with different degrees of ejection fraction from hyperdynamic to severely reduced:

Ultrasound of the Inferior Vena Cava (IVC) can be used to estimate the central venous pressure (CVP) of a patient by looking at the size (diameter) and collapsibility of the IVC. This is especially useful when you are trying to evaluate fluid tolerance or the presence of venous congestion in your patients.

Here is a simplified and practical table you can use to interpret your IVC findings.

IVC Size	IVC Collapsibility	Interpretation (CVP)
< 1.5cm	>50% collapsibility	0-5 mm Hg (Low CVP)
< 1.5-2.5cm	>50% collapsibility	6-10 mm Hg
1.5-2.5cm	<50% collapsibility	11-15 mm Hg
>2.5cm	<50% collapsibility	16-20 mm Hg (High CVP)

Adapted from Kircher et al.

The caveat about IVC measurements is that it just gives you a static measurement to estimate the central venous pressure. So all of the limitations of using CVP will also pertain to IVC measurements.

We find it most useful when the IVC either estimates a low CVP or high CVP. The measurements in between can be considered indeterminate and more advanced hemodynamics measurements should be obtained to assess for venous congestion and fluid responsiveness (change in cardiac output)

Using bedside echocardiography (echo) is one of the most useful Point of Care Ultrasound (POCUS) applications. It can help you assess the hemodynamic status of your patients, estimate fluid status, and look for life-threatening causes of shock such as tamponade or pulmonary embolism. In this section, we will show you how to use cardiac ultrasound to help you in your daily practice.