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Clinical Manual and Review of Transesophageal Echocardiography, 2e

Chapter 22. TEE in the Critical Care Unit

Jordan Hudson; Andrew Shaw

TEE in the Critical Care Unit: Introduction

In addition to its role as an intraoperative diagnostic tool, transesophageal echocardiography (TEE) has
been shown to be increasingly useful in the critical care setting. Patients in the critical care unit may have
impaired cardiac function due to comorbidities or as a result of their critical illness. Indeed, cardiac
dysfunction is one of the most common causes of hemodynamic instability and death in critically ill
patients.1 Unlike many other diagnostic modalities available to the intensivist, TEE is minimally invasive
and can be rapidly performed at the bedside. It can be used to provide valuable information on cardiac
function, guide resuscitation and management, and diagnose a wide range of pathologies that may have a
negative impact on the critically ill patient (Table 22–1). TEE was initially applied in the intensive care unit
(ICU) for the postoperative evaluation of unstable cardiac surgery patients. However, TEE has also been
shown to be beneficial in the general ICU setting, changing management in up to two-thirds of cases.2,3 In
addition to the fact that the use of echocardiography has a positive impact on the management of patients
in the general ICU,4 there is also evidence to support its therapeutic impact and its value in predicting
mortality.5 Surprisingly, despite all these advantages, echocardiography is still not yet available in most
ICUs, being largely limited by the availability of trained providers.5

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Table 22–1. TEE Diagnoses in the Hemodynamically Unstable Patient.

Acute myocardial infarction

Cardiac tamponade

Aortic dissection

Valvular dysfunction

Endocarditis

Source of embolism

Pulmonary embolus (central)

Pleural e usion

From Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of
echocardiography—summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). J Am Coll Cardiol.
2003;42(5): 954-970.

Indications
The indications for TEE, as previously discussed in this manual, also apply to critically ill patients. The ACC/
AHA/ASE guidelines define hemodynamic instability and suspected aortic dissection as class I indications
for echocardiography in the ICU (ACC/AHA/ASE 2003 guidelines) (Table 22–2). Acutely ill trauma patients
should also undergo an echocardiographic evaluation if they are suspected to have cardiac tamponade or
aortic injury. The most common indication for which TEE is performed in the ICU is hemodynamic
instability, followed by endocarditis, assessment of ventricular function, aortic pathology, and
miscellaneous others.2

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Table 22–2. Recommendations for Echocardiography in the Critical Care Unit.

ACC/AHA/ASE Class I Recommendations for Echocardiography in the Critically Ill

1. The hemodynamically unstable patient

2. Suspected aortic dissection (TEE)

ACC/AHA/ASE Class I Recommendations for Echocardiography in the Critically Injured

1. Serious blunt or penetrating chest trauma (suspected pericardial e usion or tamponade)

2. Mechanically ventilated multiple-trauma or chest trauma patient

3. Suspected pre-existing valvular or myocardial disease in the trauma patient

4. The hemodynamically unstable multiple-injury patient without obvious chest trauma but with a
mechanism of injury suggesting potential cardiac or aortic injury (deceleration or crush)

5. Widening of the mediastinum, postinjury suspected aortic injury (TEE)

6. Potential catheter, guidewire, pacer electrode, or pericardiocentesis needle injury with or without signs of
tamponade

TTE versus TEE

In the general population, transthoracic echocardiography (TTE) is typically the first modality used, as it is
noninvasive and more widely available. In the ICU population, however, up to one-half of mechanically
ventilated patients cannot be imaged adequately via TTE.6 Barriers to adequate TTE imaging include
mechanical ventilation with positive end-expiratory pressure, wounds and dressings, and body habitus. In
addition, many ICU and trauma patients may be too unstable to be positioned in the le lateral decubitus
position for TTE imaging. In a study comparing TTE to TEE in patients with unexplained hypotension in the
ICU, TTE images were inadequate in over 60% of cases, while TEE provided new, clinically significant
diagnoses in 28% that were not seen by TTE.7 The American College of Cardiology deems TEE a reasonable
first test (versus TTE) in patients who are intubated, recently postoperative, or who have chronic
obstructive pulmonary disease (COPD) or chest wall abnormalities, which may impair TTE examinations.8

In addition, there are certain structures and pathologies that are best visualized using TEE. These include
the mitral valve, prosthetic valves, great vessels, and atria, as well as endocarditis and intracardiac thrombi
(Table 22–3).8,9 This is particularly important in trauma patients who may be at risk of cardiac tamponade,
aortic injuries, and traumatic valvular disruption or septal defects. Finally, TEE is indicated in critically ill
patients requiring echocardiographic evaluation in whom TTE images are inadequate.

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Table 22–3. Indications for TEE.

TEE should be first choice

1. Endocarditis

2. Prosthetic valve dysfunction

3. Mitral valve anatomy before and a er mitral valve repair

4. Aortic dissection

5. Le atrial thrombus

6. Aortic dissection

7. Posterior structures in congenital heart disease

TEE superior to TTE

1. Mechanically ventilated

2. Hemodynamically unstable

3. Chest trauma

4. Postoperative

5. Cardiac tamponade

6. Central pulmonary emboli

7. Suspected intracardiac source of embolus

8. Assist devices (IABP, LVAD, RVAD)

IABP, intra-aortic balloon pump; LVAD, le ventricular assist device; RVAD, right ventricular assist device.

Complications
As with TEE in the general population, transesophageal echocardiography has a very low incidence of
complications in critical care patients.2,10 Excluding feeding tube dislodgement, TEE had a complication
rate of 2.6% in a review comprising 2508 examinations in the ICU.2 The most common complications
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included oropharyngeal mucosal lesions (0.7%), hypotension (0.6%), and coughing (0.3%). TEE should not
be performed in any patient with esophageal perforation or in whom esophageal pathology or other
comorbidities prevent safe and atraumatic insertion of the TEE probe.

TEE Evaluation of the Critically Ill Patient

Patient Preparation
Prior to performing a TEE examination, appropriate equipment for airway management, suctioning, and
resuscitation should be available. Standard monitoring should be used including pulse oximetry, invasive
or noninvasive blood pressure monitoring, and continuous electrocardiogram. It may be beneficial to have
a second physician present to assist with management during the examination of hemodynamically
unstable patients.

For elective TEE examinations, the patient should fast for 4 hours prior to the procedure to facilitate gastric
emptying. Topical anesthesia with aerosolized or viscous local anesthetic should be performed prior to
probe insertion. Judicious sedation may be used at the intensivist's discretion, depending on the patient's
clinical presentation. Small titrated doses of benzodiazepines and/or opioids are commonly used, with
reversal agents readily available.

For emergent TEE, gastric contents should first be suctioned via orogastric or nasogastric tube if in situ. In a
patient with cardiopulmonary instability and an unsecured airway, endotracheal intubation prior to TEE
may be clinically indicated. While TEE can be an invaluable tool for diagnosis, its use should not delay
appropriate resuscitation and management of the unstable patient.

Imaging
Many TEE studies in the ICU are performed to facilitate diagnosis and management of an unstable patient,
or to rule out a specific disease such as tamponade or endocarditis. Thus, while a comprehensive TEE exam
as described in the ASE/SCA guidelines should be performed in all cases,11 the intensivist performing
echocardiography should initially focus the exam based upon the patient's clinical status and suspected
diagnosis. The following is a brief summary of the intensivist's echocardiographic approach to various
clinical presentations and diagnoses—a thorough discussion of each topic can be found in earlier chapters.

Hemodynamic Instability

Hypovolemia and Preload Assessment

Significant hypovolemia is seen on TEE as decreased le ventricular (LV) filling and commonly
demonstrated by obliteration of the LV cavity (“kissing” papillary muscles) in the transgastric (TG)
midpapillary short-axis (SAX) view. However, systolic cavity obliteration may also occur in the setting of
reduced a erload and/or increased ejection fraction in 20% of cases, and may not reflect hypovolemia.12
Furthermore, visual detection of small (< 10%) yet potentially important changes is di icult and more
objective measurements of LV volumes are required, especially in patient with compromised ventricular
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function (see Chapter 21). A le ventricular end-diastolic area (LVEDA) in the TG SAX view less than 6.3
cm2/m2 (women) or 7.5 cm2/m2 (men) could be consistent with hypovolemia as these values define the
lower limits of normal in subjects under general anesthesia.13 Unfortunately, there is a wide range of
normal values and as a consequence, visual estimation of LV volume is limited to the extremes—cavity
obliteration or marked ventricular dilation.

Despite the fact that pulmonary artery occlusion pressure (PAOP) does not accurately reflect preload or
volume responsiveness, it is still used as supportive criterion for the diagnosis of acute respiratory distress
syndrome and heart failure. Noninvasive estimation of PAOP is feasible using TEE-derived simple Doppler
variables, but not in every patient. In fact, Vignon and colleagues14 prospectively assessed the ability of
TEE to predict PAOP in mechanically ventilated patients with a pulmonary artery catheter. In the initial
group of patients, the correlations between simple Doppler variables and PAOP were better in patients with
depressed LV systolic function than in those with normal LV systolic function. PAOP 18 mm Hg or less could
be predicted by an E-wave/A-wave ratio greater than 1.4, E-wave deceleration time greater than 100
milliseconds, atrial filling fraction greater than 31%, and systolic fraction of pulmonary venous flow greater
than 44%. In a second group, these cuto values were prospectively validated and the utility of color M-
mode Doppler flow propagation velocity (Vp) and the maximal early diastolic velocity of the lateral mitral
annulus by tissue Doppler (E′) were assessed. An E/E′ ratio less than 8 and an E/Vp ratio less than 1.7 were
predictive for PAOP 18 mm Hg or less, but the predictive value of these variables was not di erent from the
“simpler” pulsed Doppler variables.14

Regional Wall Motion Abnormalities

A thorough survey of the le ventricle using the midesophageal (ME) four-chamber, two-chamber, and
long-axis (LAX) views, as well as the TG basal, midpapillary, and apical SAX views allows the intensivist to
identify regional wall motion abnormalities. It is important to examine each segment for thickening as well
as motion, and to observe each segment in multiple views. Comparison with previous echocardiographic
exams is helpful to determine whether any abnormalities are new or pre-existing. A new regional wall
motion abnormality is consistent with myocardial ischemia. Although the sensitivity for ischemia detection
by TEE is established, the specificity and implications of a transient wall motion abnormality are less clear
(see Chapter 21).

Le Ventricular Function
Contractility can be inferred from the le ventricular ejection fraction (LVEF). There are several methods by
which TEE can estimate the LVEF, including fractional area change, visual assessment, Simpson's rule, area-
length method, and three-dimensional (3D) modeling. Cardiac output can be calculated using the
continuity equation from the LV outflow tract area and velocity-time integral. These techniques are
described in earlier chapters. It is also important to note the presence of associated le ventricular
hypertrophy or dilatation.

Right Ventricular Function

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Although right ventricular function can be more di icult to quantify than le ventricular function, it is
possible nonetheless to identify patients with impaired RV performance. Acute right ventricular
dysfunction in the critically ill patient may signify pulmonary embolus, acute pulmonary hypertension, or
right coronary artery disease. The right ventricle is a thin-walled structure; thus, RV thickening should not
be used to quantify function. Tricuspid annular displacement toward the RV apex in the ME four-chamber
view, fractional area change in the TG short-axis view, and 3D imaging can all be used to quantify RV
function. Other signs of RV dysfunction include flattening of the septum (creating a “D-shaped” le
ventricle) and right ventricular enlargement.

Diastolic Function
Impaired cardiac filling can cause cardiac failure in the setting of normal systolic function. Diastolic
dysfunction di ers from systolic dysfunction in pathophysiology and therapeutic approach; therefore, this
diagnosis is important for the intensivist in planning management. A clinical finding of acute cardiogenic
pulmonary edema, in the presence of normal systolic function by TEE, is highly suggestive of diastolic
dysfunction.15 Diagnosis of diastolic dysfunction with TEE requires the use of pulsed-wave Doppler of
mitral inflow and pulmonary venous flow (see Chapter 12). However, Sadler et al16 confirmed the load
dependence of the pulsed-wave Doppler parameters used to evaluate LV diastolic properties. The abrupt
preload reduction induced by ultrafiltration in ICU patients with renal failure significantly decreased E-
wave maximal velocities and the E/A ratio because A-wave velocities remained una ected. Both the
isovolumic relaxation time and E-wave deceleration time were significantly prolonged by volume
reduction. Also, changes in the pulmonary vein D wave paralleled that of mitral E wave, and the S/D ratio
increased a er hemodialysis. Therefore, conventional pulsed-wave Doppler parameters to identify
transient LV diastolic dysfunction in clinical settings characterized by abrupt changes in loading conditions
should be interpreted with caution.17 On the other hand, E′ velocity from the lateral mitral annulus may be
less preload dependent.17

Valvular Function
Each valve should be examined for stenosis and regurgitation, as well as abnormalities such as vegetations,
thickening, calcification, and prolapse. While valvular lesions may cause hemodynamic instability, their
presence may also have implications for management. Severe tricuspid regurgitation, for instance, may
result in spurious measurements of cardiac output using thermodilution. Mitral regurgitation may occur as
a result of ischemic disease and papillary muscle rupture. Aortic stenosis may be associated with
secondary diastolic dysfunction as a result of ventricular remodeling.

Cardiac Tamponade
In the intensive care unit, cardiac tamponade may occur following cardiac surgery, traumatic injury,
pericardial e usion, or as a result of myocardial infarction with wall rupture. Rarely, tamponade may occur
as a complication of central venous line placement or other procedures. Clinically, cardiac tamponade may
present with Beck's triad of hypotension, elevated jugular venous pressure, and mu led heart sounds.
However, the absence of these symptoms does not exclude the diagnosis of tamponade, as lesser volumes
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or chronic accumulation may present with more subtle clinical findings. TEE is highly sensitive and specific
in the detection of pericardial tamponade, with accuracy greater than 99%.9 Pericardial fluid can o en be
detected in the TG midpapillary SAX, TG LAX, and ME four-chamber views (Figure 22–1). Restriction of
cardiac filling and equalization of pressures between the le and right heart may manifest via flattening of
the interventricular septum, decreased le ventricular end-diastolic volume, decreased LV size during
inspiration, and diastolic posterior motion of the RV.

Figure 22-1.

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Acute (A) and chronic (B) pericardial e usions (asterisk).

Miscellaneous
Other causes of unexplained hypotension that may be diagnosed with TEE include pulmonary embolus,
hypertrophic obstructive cardiomyopathy, and intracardiac thrombus.

Pulmonary embolus is not normally seen with TEE, with the exception of central emboli involving the
pulmonary trunk or main pulmonary arteries. Echocardiographic signs suggestive of pulmonary embolus
include new-onset RV dilatation and dysfunction, acute tricuspid regurgitation, and elevated right-side
pressures, in the appropriate clinical context.

Hypertrophic cardiomyopathy may result in dynamic obstruction of the le ventricular outflow tract (LVOT)
in up to 25% of patients. This obstruction may be intermittent, and is typically exacerbated by
hypovolemia, tachycardia, increased contractility, and decreased a erload. In the ME four-chamber and ME
aortic valve (AV) LAX views, le ventricular hypertrophy is o en seen, particularly septal hypertrophy.
Diastolic dysfunction is common in this population. Le ventricular outflow obstruction can cause high
flow velocities in the LVOT, increased LV pressures, and a dagger-shaped pattern of flow on pulsed-wave
Doppler or continuous-wave Doppler of the outflow tract.

Intracardiac thrombi can be seen in patients with ventricular aneurysm, dilated cardiomyopathy,
coagulopathic states, and dysrhythmias. Thrombi appear as echogenic, mobile masses that may be freely
floating or attached to a cardiac structure, and may mimic intracardiac tumors. Clinically, pulmonary or
systemic thromboembolic disease may arise as a result.

Hypoxemia
TEE can be a useful diagnostic tool in the critically ill patient with unexplained hypoxemia. Causes of
hypoxemia that can be detected with TEE include le ventricular failure, valvular pathology, cor
pulmonale, pulmonary hypertension, pulmonary vein stenosis, central pulmonary embolus, right to le
shunts, and pleural e usions (Figure 22–2).18

Figure 22-2.

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Right pleural e usion (asterisk).

Echocardiographic findings consistent with pulmonary hypertension include right ventricular dilatation
and dysfunction. In the presence of tricuspid regurgitation, the pulmonary artery systolic pressure (PASP)
can be estimated by the modified Bernoulli equation (PASP = 4(VTR)2 + CVP, where VTR is the maximal flow
in m/s of the tricuspid regurgitant jet and CVP is central venous pressure). Pulmonary vein stenosis is an
uncommon cause of pulmonary hypertension whose incidence has been increasing as a result of
transcatheter radiofrequency pulmonary vein isolation for the treatment of atrial fibrillation.

Right-to-le shunts may also cause unexplained hypoxemia in the ICU in patients with elevated right heart
pressures. Shunts may be intracardiac (patent foramen ovale, atrial septal defect, ventricular septal defect)
or intrapulmonary. Intracardiac shunting can be detected with color-flow Doppler, or by the venous
injection of agitated saline for contrast.

Endocarditis
Febrile patients in the ICU may require evaluation for the presence of endocarditis. In these patients, TEE is
the gold standard for noninvasive assessment of endocarditis, with a sensitivity of 88% to 98%.19–21 In
contrast, TTE has a sensitivity of 58% to 62%.19,21 TEE should be performed to rule out endocarditis in
patients with a high index of suspicion and a negative TTE, for suspected prosthetic valve endocarditis, in
patients with bacteremia of unknown source (or refractory to antibiotic therapy), and to assess
complications of known endocarditis.22

Echocardiographic signs of infective endocarditis include vegetations on valves, cardiac structures, or

devices; dehiscence of prosthetic valves; new onset of valvular regurgitation; and abscesses.23 Vegetations
on native or prosthetic valves occur most commonly on the atrial side of the mitral and tricuspid valves and
the ventricular side of the aortic and pulmonary valves (Figure 22–3). Vegetations are frequently oscillatory,

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moving in sync with the cardiac cycle and valvular motion. Repeat TEE examinations are o en necessary
over the course of treatment to assess for complications of infective endocarditis and the disappearance of
vegetations.

Figure 22-3.

Mitral valve endocarditis (arrow).

Embolic Source
In the patient with unexplained stroke or peripheral embolic disease, TEE may be helpful to identify
intracardiac sources of emboli. These include le -side intracardiac thrombi, endocarditis, tumors, aortic
atheromatous disease, and right-side masses in the presence of a right-to-le shunt. Patients with
indwelling peripherally inserted central catheter (PICC) lines are at increased risk of catheter-associated
thrombus (Figure 22–4), occurring in 15% of cases in a recent prospective study.24 Prior to elective
cardioversion of patients with atrial fibrillation or flutter, TEE may be indicated to rule out the presence of
thrombi in the le atrium, le atrial appendage, and le ventricle.20 Patients with a history of atrial
dysrhythmia greater than 48 hours who are not therapeutically anticoagulated are at increased risk of
thrombus development and stroke following cardioversion.

Figure 22-4.

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PICC line thrombus (arrow) with 2D (A) and 3D (B) imaging.

Trauma
TEE is of particular value in the unstable trauma patient, particularly those with blunt or penetrating chest
trauma. In such patients, TTE is most o en unsatisfactory due to contusions, wounds, subcutaneous
emphysema, mechanical ventilation, and/or di iculty with positioning. Patients with traumatic chest injury
are at risk for aortic dissection and injury, myocardial contusion and acute dysfunction, traumatic

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ventricular septal defect, cardiac tamponade, and hemothorax, all of which can be visualized by TEE. TEE
should not be performed if esophageal perforation is suspected.

Aortic Dissection
While angiography remains the gold standard for diagnosis of aortic injury in the trauma patient, it is time-
consuming and requires transportation of a patient who may be hemodynamically unstable. TEE can be
performed safely and rapidly at the bedside or in the operating room.25 The diagnostic accuracy of TEE in
patients with suspected acute traumatic aortic injury is comparable to helical computed tomography (CT)
but TEE was more sensitive for injuries involving the intimal or medial layers of the thoracic aorta.26 TEE
may miss lesions in the distal ascending aorta and proximal aortic arch due to the interposition of the air-
filled trachea between the aorta and the TEE probe.

In a patient with suspected aortic injury, careful inspection of the ascending aorta, aortic arch, and thoracic
aorta should be performed. Echocardiographic signs of aortic dissection or disruption include presence of
an intimal flap (Figure 22–5), turbulent blood flow in the aorta, evidence of low flow in the aorta visible as
spontaneous echo contrast or “smoke,” aortic aneurysm, and thrombus.25

Figure 22-5.

Aortic dissection flap (arrow) with color-flow Doppler imaging.

Summary
TEE is a minimally invasive diagnostic tool that can provide valuable information rapidly and can be
performed at the patient's bedside. TEE is increasingly being used by critical care physicians, particularly in
hemodynamically unstable and trauma patients. The information obtained from a TEE examination by a
skilled operator will o en lead to important management changes, as well as alert the intensivist to new

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diagnoses. Lastly, it is likely that the advent of real-time 3D imaging will only extend the usability of TEE for
intensive care physicians.

References

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