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16 Cardiomyopathies
221
radial, and transverse strain [62]. Assessment of
Diastolic dysfunction utilizes 2016 ASE/EACVI
guidelines [63].
2019 Cirrhotic Cardiomyopathy Consortium
Criteria for diagnosis of Cirrhotic cardiomyopathy includes [61]:
• Systolic dysfunction (Any of the following)
– LV ejection fraction <50%
– Absolute GLS <18%
• ≥3 of the following
– Septal mitral annular early diastolic veloc-
ity (e′) velocity<7cm/s
– Mitral inow early diastolic velocity (E) to
e′ (E/e′)ratio≥15
– Left Atrial Volume Index (LAVI) >34mL/
2
m
– Tricuspid regurgitation (TR) velocity
>2.8m/s
Cardiac dysfunction has been reported in up to
50% of patients with cirrhosis [64]. In the critical
care setting, it is important to acknowledge the
potential for cardiac dysfunction in cirrhotic
patients and its potential contribution to an individual patient’s hemodynamic instability.
Left ventricular noncompaction cardiomyopathy is classied by the European Society of
Cardiology as an unclassied Familial
Cardiomyopathy and by the American Heart
Association as a genetic cardiomyopathy [68,
69]. There are several proposed echocardio-
graphic criteria for the diagnosis of noncompaction cardiomyopathy without a unied diagnostic
consensus [70]. Multiple sources agree on the
presence of apical trabeculations, deep intertrabecular recesses, and identication of a twolayered myocardium with a compact epicardial,
and a noncompacted trabeculated endocardium
as elements of this disorder [71, 72]. A ratio of
noncompacted to compacted myocardium of
>2:1 is considered diagnostic [14]. The left ventricular apex is most affected by trabeculations
with right ventricular and biventricular involvement possible and sparing of the basal level of the
ventricles [66]. Contrast echocardiography,
speckle tracking, and tissue Doppler offer additional modalities which may provide important
information regarding myocardial function.
However, further study is required to establish
the diagnostic validity of these techniques (see
Fig.16.10).
Noncompaction Cardiomyopathy
Noncompaction cardiomyopathy, or left ventricular noncompaction cardiomyopathy, is characterized by excessive trabeculations of the left
ventricle, intertrabecular recesses, and a bilayered myocardium with a compact epicardial layer
and a thickened endocardial noncompacted layer
[65]. An autosomal dominant genetic pattern is
associated with the failure of the myocardium to
“compact” during embryologic development
resulting in a bilayer appearance [66]. Patients
with noncompaction cardiomyopathy present
with evidence of heart failure and are at risk of
mural thrombus formation in the deep intertrabecular recesses. The risk is particularly increased
in those with reduced EF or atrial brillation [66,
67]. Patients are also at risk of conduction abnor-
malities including ventricular arrhythmias associated with sudden cardiac death.
Septic Cardiomyopathy
Septic cardiomyopathy is broadly identied as
acute cardiac dysfunction in the setting of systemic infection and inammation [73]. Common
characteristics include reduced left ventricular
contractility, left ventricular dilatation, and
reduced response to volume infusion. However,
a consensus denition with diagnostic criteria
does not exist [73, 74]. In 1980, septic cardiomyopathy was initially described as an acute
decrease in left ventricular ejection fraction
with dilation during sepsis [73, 75].
Echocardiographic characteristics include
decreased LV ejection fraction which is reversible and normalizes in days, normal or low left
ventricular lling pressure [75]. About 2/3 of
patients have RV dysfunction on evaluation with
RV fractional area change (FAC) with tricuspid
annular plane systolic excursion (TAPSE), and
222
Fig. 16.10 Apical
two-chamber view of a
patient with
noncompaction
cardiomyopathy (see
Video 16.9)
J. C. Klick and R. Carlson
tricuspid annular tissue Doppler imaging (TDI,
and RV wall TDI). LV Diastolic dysfunction is
common and septal relaxation on TDI strongly
predicted mortality in multiple studies [76, 77].
Alterations in preload and afterload during sepsis have a signicant impact on LVEF, introducing concern EF may not be a reliable measure of
cardiac function in a disease state known for
signicant alterations in systemic vascular resistance [73, 78, 79].
Speckle-tracking echocardiography has been
shown to be more sensitive in sepsis in identifying
LV dysfunction. Global longitudinal strain is less
susceptible to alterations in preload and afterload
[79–81]. While Speckle-tracking echocardiography offers potential for improved evaluation of
cardiac dysfunction, the modality has not undergone evaluation with larger, randomized trials
[74]. Despite unclear diagnostic criteria of septic
cardiomyopathy, treatment remains focused on
the treatment of the underlying infection with
supportive management of hemodynamics,
including inotropic support, as the inammatory
state improves [73].
Summary Points
• Cardiomyopathy refers to intrinsic disease of
the myocardium in the absence of coronary
artery disease, hypertension, valvular or con-
genital disease.
• Patients in the intensive care unit may present
with various forms of cardiomyopathy and
their sequelae.
• Bedside echocardiography is a powerful tool
to identify and help manage patients in the
ICU with cardiomyopathies.
• Dilated cardiomyopathy diagnostic criteria
include evidence of left ventricular systolic
dysfunction with EF <45%, and/or fractional
shortening <25% in association with left ventricular end-diastolic dimension >112% corrected for age and BSA.
• Hypertrophic cardiomyopathy manifests left
ventricular hypertrophy with disorganized myocardial architecture in the absence of hypertension or valvular disease. Up to two- thirds of
patients display dynamic outow tract obstruction with evidence of a gradient >30mmHg.
• Restrictive Cardiomyopathy is a cardiac muscle disease characterized by increased stiffness, elevated end-diastolic pressure, and
ultimately diastolic dysfunction of one or both
ventricles. Despite abnormal diastolic lling,
the systolic function of the ventricles remains
preserved.
• Arrhythmogenic right ventricular cardiomyopathy is characterized by progressive brofatty replacement of the right ventricular
myocardium resulting in right ventricular
dilation and dysfunction.
16 Cardiomyopathies
223
• Stress-induced cardiomyopathy manifests as
transient dyskinesis, hypokinesis, or akinesis
with abnormalities in regional wall motion of
the left ventricular wall extending beyond
epicardial vascular distribution usually in the
presence of a stress trigger.
• Cardiac dysfunction has been reported in up to
50% of patients with cirrhosis and can be
identied using echocardiography.
• Noncompaction cardiomyopathy is characterized by excessive trabeculations of the left
ventricle, intertrabecular recesses, and a bilayered myocardium with a compact epicardial
layer and a thickened endocardial noncompacted layer.
• Septic cardiomyopathy is acute cardiac dysfunction in the setting of systemic infection
and inammation. Echocardiography is essential to its identication
Questions
1. A 55-year-old male with a history of hyper-
tension and hypertrophic cardiomyopathy is
admitted to the ICU with severe pneumonia
secondary to COVID-19. The ICU team
decides to intubate him for his progressive
respiratory failure. After the administration of
propofol sedation, he becomes tachycardic
and profoundly hypotensive. The airway is
secured and a bedside POCUS echocardiogram is performed. What would you expect
the continuous wave Doppler prole across
the aortic valve to show?
A. Late-peaking dagger-shaped appearance
B. Early systolic peak with a triangular shape
to the velocity curve
C. Rounded curve with a mid-systolic peak
Answer: A
A late-peaking dagger-shaped appearance to the continuous wave Doppler prole
across the LVOT and the aortic valve is characteristic of dynamic LV outow tract
obstruction, as in SAM. An early systolic
peak with a triangular shape to the CWD
prole is characteristic of mild aortic valve
obstruction, while a rounded curve with a
mid-systolic peak is characteristic of severe
aortic valve stenosis.
2. A 65-year-old female is admitted to the ICU
from the ED after experiencing a “thunderclap” headache and loss of consciousness.
She is diagnosed with a ruptured ACOM
aneurysm and goes to neuro-IR for coiling of
her ruptured aneurysm. Postprocedure she
develops diffuse ST depressions on ECG and
becomes profoundly hemodynamically unstable. Her troponin level is signicantly elevated and your resident calls a STEMI
activation. You perform a bedside TTE and
note that the basal and mid-levels of the LV
are hyperdynamic but the apex is dyskinetic
and “ballooning” circumferentially. There
does not appear to be any LVOT obstruction.
What is the next most appropriate course of
action?
A. Immediate transfer to the cath lab for left
heart catheterization
B. Inotropic support
C. Emergent CT surgery consults for emer-
gent CABG
D. Emergent ECMO consult
Answer: B
This patient is experiencing a stressinduced or Takotsubo Cardiomyopathy. This
is a consequence of a massive catecholamine
surge in the setting of an acute neurologic
insult. The LV wall motion abnormality does
not t any one coronary distribution, hence
there is no role for emergent coronary revascularization. Provided there is no echocardiographic evidence of dynamic LVOT
obstruction, the patient should receive inotropic support. Mechanical circulatory support
should be initiated only if the patient is refractory to inotropic pharmacologic support.
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Aortic Stenosis
ConnorO’Brien andChristopherF.Barnett
17
Abbreviations
AoV Aortic valve
AoV VTI Aortic valve velocity time integral
AS Aortic stenosis
AVA Aortic valve area
CW Continuous wave
DI Dimensionless index
LVOT Left ventricular outow tract
LVOT VTI Left ventricular outow tract
velocity time integral
LVOTd Left ventricular outow tract
diameter
PLAX Parasternal long axis
PSAX Parasternal short axis
PW Pulse wave
SV Stroke volume
Learning Objectives
1. Learn to identify and grade aortic stenosis
2. Learn the methods for grading aortic stenosis
3. Understand the pitfalls for grading aortic
stenosis
4. Learn how to identify aortic stenosis in low
ow states
C. O’Brien (*) · C. F. Barnett
Division of Cardiology and Critical Care Cardiology
Section, Department of Medicine, University of
California-San Francisco School of Medicine,
CA, USA
e-mail: connor.obrien@ucsf.edu
Introduction
Aortic stenosis (AS) is most commonly caused
by restricted opening of the aortic valve (AoV)
leaets. Identication and quantication of AS
can be helpful to understand patient hemodynamics. AS creates an obstruction to outow between
the left ventricle and aorta. As a consequence, left
ventricular stroke volume (SV) is reduced and
left ventricular systolic and diastolic pressures
are elevated so that myocardial oxygen demand
is increased while, simultaneously, coronary perfusion and myocardial oxygen delivery are
reduced.
Using ultrasound to identify and quantify AS
requires an understanding of AoV anatomy, anatomic variants, ultrasound physics as applied to
the measurement of valvular gradients, and
hemodynamic states that can introduce error into
the assessment.
Anatomy oftheAortic Valve
The AoV is composed of three thin leaets with
semilunar attachments arising from a brous
annulus (Fig. 17.1a) [1]. The coronary arteries
originate in the sinuses of Valsalva just inferior to
the sinotubular junction. The names of the aortic
valve leaets and sinuses correspond to the coronary artery that originates from each. The aortic
root is composed of the aortic annulus, sinuses of
© 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_17
229
230
C. O’Brien and C. F. Barnett
ab
Fig. 17.1 Native AoV anatomy. (a) Trileaet AoV
visualized in PSAX by TTE.In this view, the annulus is
a thin, echo bright circular structure. Three, thin leaets
can be seen inserting in the annulus. The dotted line
demarcates leaet edges. (b) AoV in PLAX illustrates
Valsalva, coronary ostia, and proximal ascending
aorta (Fig.17.1b).
How toImage theAortic Valve
withUltrasound
The AoV is best viewed in parasternal long axis
(PLAX) (Fig.17.1b) and short views by transthoracic echocardiography (TTE) (Fig. 17.1a).
Parasternal views offer the shortest transducer to
the relationship between the aortic valve leaets and
annulus with the Sinuses of Valsalva and the sinotubular
junction. LCC left coronary cusp, NCC noncoronary
cusp, RCC right coronary cusp, LVOT left ventricular
outow tract
valve distance and thus the greatest valvular resolution. Excursion of the right coronary and noncoronary cusps is best seen in PLAX (Fig.17.2a).
AS leads to restricted excursion of the cusps,
which can be rst identied in the PLAX
(Fig. 17.2b). In this view, the cause of leaet
restriction and direction of ow acceleration can
also be assessed (Fig.17.2c, d). Rotating to parasternal short axis (PSAX) shows all three leaets
of the AoV en face and can help delineate structural causes of stenosis.
17 Aortic Stenosis
a b
c d
231
Fig. 17.2 (a) Normal, trileaet AoV shown in PLAX.Thin
leaets achieve full excursion nearly opposing the wall of
the aortic root. (b) Sclerotic aortic valve with limited leaet
opening. (c) Normal, trileaet AoV during in peak systole
Causes ofAortic Stenosis
Bicuspid AoV is the most common congenital
cause of AS.Bicuspid AoV disease can be further
divided into true bileaet (Fig. 17.3a) or cusp
fusion in a trileaet valve (Fig.17.3b) [2]. True
bileaet disease is caused by developmental
abnormalities in endocardial cushion migration
[3]. The resultant valve is composed of two, generally equally sized leaets with a single
commissure.
Bicuspid AoV can also be caused by leaet
fusion in a trileaet valve. Similarly, this is
caused by errors in embryological development.
Fusion can occur along any ssure but is most
common between the right and left coronary leaflets (~80%).
Recognizing any bicuspid AoV disease is particularly important because it is associated with
other important cardiac malformations, congeni-
showing laminar ow across the aortic valve. (d) Sclerotic
aortic valve during peak systole showing nonlaminar ow
acceleration across the sclerotic valve orice. NCC noncoronary cusp, RCC right coronary cusp
tal syndromes, abnormalities of aortic tissue that
predispose to aneurysm and dissection.
Calcic disease of the AoV is the most common cause of AoV stenosis [4]. Stenosis is generally mediated by calcication on the aortic side
of the AoV (Fig.17.4a) but can also be subvalvu-
lar. Calcication leads to leaet fusion and
restricts leaet excursion during systole
(Fig.17.4b). Flow acceleration can be identied
through the restricted orice (Fig.17.4c).
Rheumatic disease and endocarditis are less
common causes of aortic stenosis [2]. Rheumatic
disease drives calcication and valvular sclerosis
along the leaet edges, leading to fusion of the
leaet edges commonly creating a triangular
opening in the center of the AoV.Aortic insufciency is a common feature of rheumatic AoV
disease. Rheumatic aortic stenosis rarely occurs
in isolation and should be suspected if rheumatic
disease is seen on the mitral valve. Bulky endo-