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23 Infective Endocarditis
a
305
Fig. 23.4 Normal variantsExamples of normal anatomic
variants that are easily confused for vegetation. (a) Chiari
network, which appears as a lamentous structure stretching across the right atrium (yellow arrows). Seen on TEE in
the midesophageal bicaval view on the left side and in the
inverse 4 chamber view on the right. (b) Lambl’s excrescence (red arrow), which appears as a thin lamentous
structure on the aortic valve. Seen on TTE in the parasternal
long axis view. (c) Fibroelastoma on the aortic valve (blue
arrow), seen on TEE in the midesophageal long axis view
Left-Sided Endocarditis
those with structural valve abnormalities, such
as severe valvular sclerosis or congenital val-
Left-sided endocarditis refers to infection of the
mitral valve, aortic valve, and any associated
structures in the left atrium or left ventricle. It
constitutes the majority of infective endocarditis cases. Patients who are at higher risk include
vular disease. The presenting symptoms may
be nonspecic and include symptoms from
systemic septic embolisms such as stroke, ischemic limb, renal infarcts, or splenic infarcts.
Septic emboli can also seed vascular walls and
306
F. Li and S. Nikravan
form mycotic aneurysms, most commonly in
the cerebral vessels. Vegetations >10mm are an
indication for urgent surgical intervention [13].
Endocarditis that is inadequately treated can lead
to heart failure from severe valvular regurgitation and volume overload. Patients with baseline
altered mental status, moderate to severe heart
failure, endocarditis due to bacteria other than S.
viridans, or who receive medical therapy without valve surgery have an increased six-month
mortality [2]. Following diagnosis with leftsided endocarditis, the initial series of diagnostic
imaging and testing should be followed by more
complete imaging for systemic embolic events
using modalities such as whole-body computed
tomography (CT) or cerebral magnetic resonance imaging (MRI) [14].
In mitral valve endocarditis, vegetations are
most commonly seen as mobile masses on the
left atrial side of either leaet. With progression
of disease, valvular destruction occurs, leading
to severe mitral regurgitation (Fig. 23.2, Video
23.10). Acute onset of severe mitral regurgitation may lead to dyspnea from ash pulmonary
edema, volume overload of the left ventricle,
and development of pulmonary hypertension.
Patients with severe mitral regurgitation or heart
failure require urgent surgical management. In
cases with small, isolated valve lesions where
mitral valve repair is feasible, valve repair
instead of valve replacement may lead to better outcomes compared to valve replacement.
However, this may not be an option for patients
with extensive valvular destruction or perivalvular destruction. Unrepairable valves can be
replaced with a bioprosthetic or mechanical
prosthetic valve replacement [14, 15].
Vegetations in aortic valve endocarditis are
most commonly on the left ventricular side of the
valve. As with mitral valve endocarditis, aortic
valve endocarditis can present with evidence of
systemic emboli. Abscess formation and spread
into the perivalvular space is more common in
aortic valve endocarditis and can lead to complete heart block due to the proximity of the aortic valve annulus to the atrioventricular node
(Fig. 23.1a, b) [16]. Perivalvular spread can
involve the aorto-mitral curtain, the brous space
that separates the aortic root from the anterior
mitral leaet, and from there spread to the mitral
valve. Acute severe aortic regurgitation from
valve destruction or perivalvular stula formation causes a sudden elevation in left ventricular
end-diastolic pressure. This can lead to cardiogenic shock from a sudden reduction in cardiac
output, elevated left atrial pressure, and pulmonary edema. Early surgical intervention in aortic
valve endocarditis improves outcomes compared
to medical management alone and can prevent
some of the late sequelae of aortic endocarditis.
Indications for surgery are similar to those for
mitral valve endocarditis [17, 18].
Right-Sided Endocarditis
Right-sided endocarditis refers to infection of the
tricuspid valve, pulmonic valve, and associated
right atrial and ventricular structures. It constitutes the minority of endocarditis cases and is
only seen in 5–10% of all cases. Risk factors for
right-sided endocarditis include intravenous drug
use and the presence of venous or intracardiac
hardware such as intracardiac devices and central
venous catheters. Structural valve abnormalities
remain a risk factor but are less common in the
tricuspid and pulmonic valves. Of the common
causes of right-sided endocarditis, intravenous
drug use is the most common, and 2–5% of intravenous drug users develop endocarditis every
year [19, 20]. With the ongoing opioid epidemic
in the United States, the incidence of intravenous
drug use-related endocarditis is likely to also
increase. The mechanism of seeding is direct
bacterial seeding from contamination of injected
substances and skin ora. In addition, illicit drugs
can be mixed with diluents or chemical contaminants, which cause valve thickening, prolapse,
and regurgitation [19]. Successful treatment of
this patient population involves not only medical
and surgical management but also treatment of
the underlying addiction. Addiction specialists
should be engaged early in the treatment course
since relapse and reinfection rates are high.
Right-sided endocarditis related to intracardiac
devices is becoming more common as the number
23 Infective Endocarditis
307
of implanted devices increases with the aging
patient population. Intracardiac devices include
pacemakers, implantable cardioverter debrillators (ICD), and cardiac resynchronization therapy
(CRT) devices. The risk of endocarditis rises with
the complexity of the device, with ICDs being at a
higher risk than pacemakers and CRT devices having the highest risk (Fig.23.5a). Patients who have
had a device replacement or revision are also at
higher risk [21]. Other indwelling venous hardware that have been reported as sources for endocarditis include central lines used for inpatient care
and chronic indwelling lines used for outpatient
infusion therapy [22]. In addition to direct infection of the central line, a brin sheath may form
around long-term central line catheters and remain
after catheter removal, serving as a site for vegetation formation [19].
As in left-sided endocarditis, presenting
symptoms are often nonspecic and consistent
with bacteremia. Septic emboli from the right
side of the heart cause pulmonary symptoms
such as dyspnea rather than symptoms of systemic embolism, which is rare unless there is a
structural abnormality allowing paradoxical
embolism. Valvular destruction and severe valvular regurgitation lead to right heart volume overload and failure, which can be exacerbated by
increased afterload from heavy pulmonary
embolic burden. Additional evaluation with
imaging should focus on detection of pulmonary
complications such as pulmonary embolisms,
abscesses, and infarcts [19, 20].
The tricuspid valve is involved in 90% of
right-sided endocarditis (Fig. 23.5b, Video
23.11). Isolated native pulmonic valve endocarditis is rare, constituting only around 5% of cases.
Although uncommon, infection of the Eustachian
valve, interventricular septum, and right ventricular free wall has been reported [19]. Intravenous
antibiotic therapy is the rst-line treatment for
right-sided endocarditis and is preferred for
patients who use intravenous drugs, as the risk of
reinfection is high. Patients with devices should
have the device, leads, or catheters removed
urgently, since those are presumed to be infected
even if vegetation is not visualized on imaging.
Reimplantation of new devices should be delayed
until the completion of antibiotic therapy and
conrmation that the infection has resolved.
Indications for surgical intervention on the tricuspid valve include vegetations >20 mm, right heart
failure from severe tricuspid regurgitation, persistent infection despite adequate medical therapy, perivalvular complications, and recurrent
emboli. Valve repair is possible in cases with limited valve damage and has been recommended
for patients who use intravenous drugs, as this
reduces the amount of prosthetic material that
can be later re-infected. When valve reconstruction is not possible, valve replacement is performed with either a bioprosthetic or mechanical
valve. Outcomes between the two types of valves
have been comparable [19, 20, 23].
Prosthetic Valve Endocarditis
Surgical and minimally invasive transcatheter
prosthetic valves are increasingly common, and
with that comes an increase in prosthetic valve
endocarditis. Early infection after implantation is
caused by direct seeding of the prosthetic material from intraoperative contamination or hematogenous spread. These infections have a
mortality rate of as high as 70%. Late infection
more closely resembles native valve endocarditis,
since exposed prosthetic materials are protected
by endothelialization. Compared to native valve
endocarditis, prosthetic valve endocarditis is
more difcult to diagnose and has an overall
worse prognosis [3, 24]. Presenting signs and
symptoms are often atypical, and imaging is
often negative or indeterminate. In addition,
echocardiographic assessment of prosthetic
valves is challenging due to shadowing from
prosthetic material and postsurgical changes that
can be difcult to distinguish from endocarditis.
TEE has a sensitivity of 86–94%, superior to that
of TTE, and should be used for all cases of suspected prosthetic valve endocarditis. Prosthetic
valve endocarditis tends to be associated with
perivalvular complications such as abscess formation, conduction abnormalities, and stulae.
Vegetations are more common on mechanical
valves and can be seen directly on the occluders
308
F. Li and S. Nikravan
a
b
Fig. 23.5 Right sided endocarditisRight sided endocarditis can occur on native structures or on intracardiac
devices, which are most often inserted into the right
heart. (a) Large mass on a pacemaker lead (red arrow).
or on support material. Bioprosthetic valves present with either regurgitant or stenotic lesions,
with or without visible vegetations [24]. Valve
dehiscence and associated new perivalvular leak
can result from the high incidence of perivalvular
complications (Fig.23.1c, Video 23.3) [3].
Seen on TTE in the apical 4 chamber view. (b) Tricuspid
mass in a patient with a history of intravenous drug use
(yellow arrows). Seen in TEE midesophageal 4 chamber
view on the left and RV inow outow view on the right
Prosthetic valve endocarditis often cannot be
eradicated with medical therapy alone, and
most cases require urgent surgical intervention
[3, 24, 25]. Surgical treatment poses several
challenges, such as reentry into the chest,
extensive debridement and reconstruction, and
23 Infective Endocarditis
309
poor tissue quality. Rates for reinfection are
6–15%, and up to 25% of patients require additional surgery [25].
Summary Points
• Diagnosis of endocarditis can be challenging
due to its variable presentation. The modied
Duke criteria incorporate clinical ndings,
laboratory examination using blood cultures,
and echocardiography into one diagnostic
system.
• Both TTE and TEE play important roles in
imaging for suspected endocarditis. TTE
should be used as an initial modality, with
TEE as follow-up imaging in selected cases.
• Direct echocardiographic ndings of endocarditis include vegetations, abscesses and related
perivalvular complications such as pseudoaneurysms and stulas, and new dehiscence of a
prosthetic valve.
• Most endocarditis cases are left-sided. Rightsided endocarditis is more common in patients
who use intravenous drugs and patients with
intracardiac devices.
• Prosthetic valve endocarditis tends to be more
challenging to diagnose and to treat, often
requiring early surgical management.
Questions
1. Which of the below ndings would meet cri-
teria for diagnosis of endocarditis using the
modied Duke criteria?
A. Temperature 38.2, history of IV drug use,
one positive blood culture growing Staph
aureus
B. Temperature 38.5, history of IV drug use,
new-onset severe tricuspid valve regurgitation, two positive blood cultures growing Strep bovis
C. Temperature 38.2, prior bioprosthetic AV
replacement, imaging concerning for
mycotic aneurysm of the ascending aorta
D. Temperature 38.5, prior bioprosthetic AV
replacement, discovery of an early dia-
stolic decrescendo murmur
Answer: B
Explanation: A diagnosis of endocarditis
using the modied Duke Criteria requires the
presence of either two major criteria, one
major and three minor criteria, or ve minor
criteria. Answer B depicts a patient with two
major criteria: evidence of endocardial
involvement with new-onset severe tricuspid
valve regurgitation and two positive blood
cultures growing typical microorganisms,
Strep bovis being the causative organism in
this case. The other choices have concerning
ndings but not the combination of ndings
that would result in a diagnosis of endocarditis using the modied Duke Criteria.
2. Direct echocardiographic ndings of endocarditis include:
A. Echocardiographic evidence of a myxo-
matous mitral valve in a former IV drug
user
B. Echocardiographic evidence of a perival-
vular leak in a patient with a history of a
prior transcatheter aortic valve replacement (TAVR) intervention.
C. Echocardiographic evidence of an aortic
root pseudoaneurysm in a patient with a
prior surgical bioprosthetic aortic valve
replacement
D. Echocardiographic evidence of a bicuspid
aortic valve with a newly diagnosed dia-
stolic murmur
Answer: C
Explanation: Direct echocardiographic
ndings of endocarditis include evidence of
vegetations, abscesses, and other perivalvular
complications such as pseudoaneurysms and
stulas, and new dehiscence of a prosthetic
valve. While a myxomatous mitral valve is a
common valvular abnormality, it is dened as
a degenerative valve disease causing valvular
thickening, prolapse, or even ail in some
cases. Despite the abnormal nding, it is not a
direct echocardiographic nding of endocarditis. Similarly, although abnormal, perivalvular leaks can be seen in patients with prior
history of TAVR and are not dened as direct
echocardiographic ndings of endocarditis.
While congenital cardiac abnormalities such
as a bicuspid valve may place a patient at a
higher risk for developing endocarditis, a
bicuspid aortic valve and associated murmurs
310
F. Li and S. Nikravan
are not direct echocardiographic ndings of
endocarditis. Evidence of abscesses and other
perivalvular complications such as pseudoaneurysm are direct echocardiographic ndings
of endocarditis, making answer choice C the
correct answer.
3. Prosthetic valve endocarditis…
A. can present like native valve endocarditis
B. can often be treated medically
C. can easily be ruled out with negative echo-
cardiographic imaging
D. has a lower mortality than native valve
endocarditis
Answer: A
Explanation: When occurring later, pros-
thetic valve endocarditis can present like
native valve endocarditis. Unfortunately, in
many cases prosthetic valve endocarditis
requires more than medical treatment alone
for full eradication and can be challenging to
diagnose with echocardiographic imaging.
For this reason, the mortality rate with prosthetic valve endocarditis is higher than that of
native valve endocarditis.
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10. Habib G, Badano L, Tribouilloy C, et al.
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11. ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/
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13. Mohananey D, Mohadjer A, Pettersson G, Navia J,
Gordon S, Shrestha N, etal. Association of vegetation size with embolic risk in patients with infective
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Cardiac Tamponade
GilAllen andMaryEllenAntkowiak
24
Learning Objectives
1. Describe the pathophysiologic changes found
in pericardial tamponade.
2. Review the echocardiographic ndings of
pericardial tamponade.
Pathophysiology ofPericardial
Tamponade
The normal pericardium is a broelastic sac surrounding the heart. It is lined by smooth pericardial reections: the outer, parietal layer, which
lines the external brous sac, and the inner, visceral layer, which lines the epicardial surface of
the heart. Under normal circumstances, this sac
contains a small amount (~5–15 ml) of serous
uid [1, 2]. Under a variety of pathologic conditions, uid can accumulate in this space, forming
a pericardial effusion. Fluid will typically accumulate dependently at rst in the oblique ssure,
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_24.
G. Allen (*) · M. Antkowiak
Division of Pulmonary and Critical Care, Department
of Medicine, University of Vermont Medical Center
and Larner College of Medicine,
Burlington, VT, USA
e-mail: gil.allen@uvmhealth.org; maryellen.
antkowiak@uvmhealth.org
posterior to the left ventricle. As uid accumulates, it will circumferentially surround the heart.
When uid accumulates gradually, as in chronic
pericardial effusions, the pericardial sac may
have time to stretch and adapt, becoming more
compliant and accommodating large amounts of
uid with minimal clinical impact. In contrast,
rapid accumulation of uid in the pericardial
space does not allow for adaptation in pericardial
compliance, leading to the development of acute
tamponade with signicantly smaller volume
effusions [1, 2].
Whether the accumulation of pericardial uid
occurs gradually or rapidly, cardiac tamponade
occurs when pericardial pressure exceeds intracardiac pressure [1–3] (Fig. 24.1). The rise in
pericardial pressure leads to impaired venous
return to the right-sided cardiac chambers. As
pressure increases, tamponade physiology progresses, leading to right-sided chamber collapse
and reduction in cardiac output. Cardiac output is
further reduced during inspiration in tamponade
physiology. [1–3] While total venous return to
the right-sided cardiac chambers is overall
restricted in the setting of cardiac tamponade, the
drop in intrathoracic pressure that accompanies
inspiration still leads to increased venous return
relative to that during expiration. With severe
elevations of pericardial pressure, the increased
volume of blood returning to the right ventricle
can only be accommodated by septal bowing
towards the left ventricle, leading to impaired left
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_24
313
314
Pericardial Effusion Volume (ml)
Intrapericardial Pressure
G. Allen and M. Antkowiak
ventricular lling. This phenomenon is termed
“ventricular interdependence.” These physiologic
alterations that occur in tamponade manifest clinical and echocardiographic ndings that can be
assessed to aid in the diagnosis of this lifethreatening condition [4].
Rapidly accumulang
pericardial fluid
Fig. 24.1 Accumulating pericardial uid on the horizontal
axis and intrapericardial pressure on the vertical axis, demonstrating how rapidly and slowly accumulating pericardial
uid can achieve conditions of tamponade physiology (when
intrapericardial pressure exceeds intracardiac pressure) at
smaller and larger volumes of pericardial uid, respectively.
This is due to the pericardium having more time to stretch and
accommodate volume when uid accumulates more slowly
Slowly accumulang
pericardial fluid
threshold for
tamponade physiology
Intrapericardial
Pressure
>
Intracardiac
Pressure
Clinical Criteria
Patients presenting with cardiac tamponade will
present with a variety of signs and symptoms
attributable to the pathologic changes that accompany increases in pericardial pressure. The majority of these are nonspecic, including dyspnea,
presyncope, tachycardia, and hypotension. Chest
pain, cough, and dysphagia may also be present.
Advanced cases may present similarly to other
forms of cardiogenic shock, with altered mental
status, cold extremities, jugular venous distension, and renal failure [1, 2]. More specic ndings may alert clinicians to the presence of
cardiac tamponade. Heart sounds may be mufed, and patients with inammatory pericardial
effusions may exhibit a pericardial rub.
Electrocardiograms may show low voltage or
electrical alternans (Fig.24.2 and Supplementary
Videos 24.1 and 24.2) [1, 2]. The clinical nding
most diagnostic of cardiac tamponade is pulsus
paradoxus. Dened as a drop in systolic pressure
of greater than 10 mmHg during inspiration, pul-
sus paradoxus can be detected using sphygmomanometry or via invasive arterial blood pressure
Fig. 24.2 Electrocardiogram consistent with electrical alternans, created by the shifting of the heart’s
electrical axis and/or variable electrical signal impedance across a variable distance of fluid to the chest
wall leads while the heart rocks back and forth within
the pericardial sac of fluid (see Supplementary Videos
24.1 and 24.2 for corresponding echocardiogram
findings)
24 Cardiac Tamponade
315
Fig. 24.3 The top section demonstrates normal and nominal ventricular interdependence under non-restrictive conditions, with negligible respirophasic variation in cardiac
output and systolic blood pressure. The bottom section dem-
monitoring [1–3]. As this drop is the result of the
ventricular independence described in the previous section, it is highly suggestive of a diagnosis
of cardiac tamponade in the presence of a pericardial effusion (Fig.24.3) [4]. There are a variety of conditions that, when present, can prevent
the development of pulsus paradoxus, reducing
the sensitivity of this diagnostic nding [2].
Given the non-specic signs and symptoms of
cardiac tamponade and the challenges encountered in evaluating pulsus paradoxus, echocar-
onstrates the exaggerated ventricular interdependence that
results from the increased restriction of accumulating pericardial effusion, resulting in respirophasic variation in both
cardiac output and blood pressure (i.e., pulsus paradoxus)
diography has become increasingly useful in the
evaluation of patients presenting with pericardial
effusion and concern for hemodynamic compromise. Echocardiography should be considered a
supplementary tool for helping one raise or lower
one’s suspicion that tamponade physiology is
accounting for a patient’s clinical presentation,
but as only some echocardiographic features of
tamponade may be present in any given patient,
cardiac tamponade should always be considered
a clinical diagnosis.