Use of echocardiography in icu

USE OF
ECHOCARDIOGRAP
HY
IN ICU
Dr. Nisheeth M. Patel
M. D (Medicine), FCCCM
Consultant Physician & Intensivist

Introduction:
 Echocardiography has evolved to become a
crucial noninvasive imaging modality in the
critically ill patients.
 Its portability, safety, and widespread
availability allow for the rapid diagnosis of life-
threatening cardiac problems and rapid
exclusion of cardiac disease in critically ill
patients.
 These benefits encourage the use of 2D Echo
in ICU on routine day to day basis.

Indications for Transthoracic
Echocardiography in Critical
Care
 Hemodynamics:
 Left ventricular function
 Regional wall motion abnormalities
 Global dysfunction
 Transient dysfunction (sepsis,
ischemic/catecholamine stunning)
 Right ventricular function
 Hypotension
 Pericardial effusion/tamponade
 Assess volume status
 Outflow tract obstruction
 Valvular stenosis/insufficiency

 Hypoxia
 Right ventricular function
 Right ventricular pressure
 Intracardiac/extracardiac shunting
 Pulmonary embolus
 Infections
 Bacterial endocarditis

 Trauma
 Blunt thoracic trauma
 Penetrating thoracic trauma
 General
 Assess proximal ascending aorta—dissection,
hematoma
 Source of murmur
 Source of embolus
 Procedural guidance (especially
pericardiocentesis)

Indications for Transesophageal
Echocardiography in Critical
Care
 Inadequate or non diagnostic transthoracic
echocardiographic images
 Evaluate suspected aortic dissection or trauma
 Evaluate prosthetic valves, especially mitral
 Investigate persistent hypoxemia
 Detect presence of valvular vegetations

 Identify complications of infective endocarditis:
 Abscesses
 Leaflet perforation
 Pseudoaneurysm formation
 Fistulas
 Identify cardiac source of systemic embolus:
 Thrombus in left atrium and left atrial appendage
 Patent foramen ovale/atrial septal aneurysm
 Atheromatous debris of the aorta

 Identify pulmonary embolus in transit
 Characterize intracardiac shunts:
 Atrial septal defect (ASD)
 Ventricular septal defect (VSD)
 Anomalous pulmonary venous connections
 Guide invasive procedures:
 Shunt closure
 Percutaneous balloon valvuloplasty

Diagnostic echocardiography
Clinical findings Cardiac Cause 2D echo findings
Low CO
unresponsive
to inotropes
Valvular disease Any severe stenotic or
regurgitant lesion
Intrinsic cardiac disease HOCM/LVH with LVOTO
Large VSD/ASD
Severe LV/RV
dysfunction
Extrinsic cardiac disease
Cardiac Tamponade
Pericardial effusion
Pericardial disease

Oligouria
Underfilling Low transmitral/tricuspid
velocities
Small ventricular
volumes
Apposition of LV papillary
muscles in systole
Intrinsic cardiac disease Poor LV function, severe
AS
Pericardial disease:
Pericardial
Pericardial effusion,
pericardial tamponade,
pericardial constriction

)
Increased filling
pressures (left-sided)
Impaired LV Increased E > A ratio,
short IVRT
MV disease Significant MS or MR
Increased filling
pressures (right-
sided)
Secondary to left-sided
disease
Significant AS, AR, MS,
MR/LV disease
Impaired RV Reduced TAPSE
TR Annular dilatation or
endocarditis

.
Sepsis/SIRS LV/RV dysfunction Ventricular dilatation,
systolic/diastolic
dysfunction
Source of sepsis masked endocarditis
Endocarditis: Native/prosthetic valve
pacemaker wires
extracardiac ‘endocarditis’
Vegetations
paraprosthetic leaks
aortic root abscess
Pulmonary hypertension
Acute PE Dilated RV, severe TR
Post-pneumonectomy
Displaced heart, increased
pulmonary acceleration
time
Mitral valve disease Significant MS or MR

Failure to wean from
ventilator
Intrinsic cardiac disease
Ischaemia
severe MR
HOCM
LV/RV dysfunction
CVA/embolic event Intracardiac thrombus
LA appendage
RA
apical LV thrombus
Endocarditis
Cyanosis Intracardiac shunting Positive contrast study

Ventricular function
Assessment
 Left ventricle Systolic Function:
 Techniques exist to assess LV function
 measurement of dimensions and volumes in
two/three dimensions
 wall thickness and motion
 assessment of filling patterns
 measurement of myocardial deformation.
 All these measures are variably load and inotropy
dependent; therefore measured values should be
interpreted with caution in the critically ill.

 LV contractility has depended upon linear
measurement of changes in LV internal
dimensions (fractional shortening, FS)
 Differences between systolic and diastolic
areas/volumes in the minor axis (ejection
fraction, EF)
 Normal values of FS/EF are unknown for the
critically ill patient population
 Measured values should be interpreted with
caution in the critically ill.

 Regional functional abnormalities:
 Myocardial thinning (normal 6–12 mm)
 Abnormal motion
(hypokinesis/akinesis/dyskinesis)
 ICU echocardiogram should be interpreted in
the context of the level of inotropic support,
and where abnormalities in contractility
conform to known coronary artery territories,
ischemia/infarction should be suspected.

 Longitudinal axis (LAX) function has three
components:
 Amplitude
 Velocity
 Timing
 Measured using M-mode (mitral annular plane
systolic excursion, MAPSE) (Normal 10-12
mm)
 Velocities of this motion assessed using tissue
Doppler imaging (TDI)

LV diastolic function:
 Derived measures of diastolic function:
 Isovolumic relaxation time (IVRT, normal 70–
110 ms)
 Ratio of peak velocities (E/A, normal 0.75–
1.40)
 E-wave deceleration time (normal 160–
240 ms)
 Normal values are age, inotropy, and filling
dependent, as well as varying with pathology,

A. Pulsed Doppler
echocardiographi
c recording of
mitral inflow
velocity
B. Tissue Doppler
imaging of the
septal or medial
mitral annulus
velocity
C. IVRT
C

 Colour flow propagation velocity (CFPV), as
determined by colour M-mode Doppler
 Measurement to diagnose LV diastolic
dysfunction (Vp<50 cm/s indicating diastolic
disease)

 Tissue Doppler imaging (TDI) of the
myocardium at the base of the heart may
assist in the diagnosis. Here early myocardial
tissue velocities (E′)
 Providing a measure of myocardial relaxation
 E′ of ≥10 cm/s is normal relaxation,
 <10 cm/s is impaired
 <5 cm/s is severely impaired
Normal TDI
velocity

RV systolic function:
 RV is exquisitely sensitive to increases in
afterload and reduction in coronary perfusion
 In the ICU, RV dysfunction is due to:
 secondary to pulmonary disease
 Mechanical ventilation
 LV dysfunction
 A range of techniques is used to assess RV
function, including M-mode, PW Doppler and
TDI.

 Measurement of the longitudinal annular
movement of the RV free wall using M-mode
(tricuspid annular plane systolic excursion,
TAPSE) correlates well
 Normal TAPSE is 2 cm, falling after cardiac
surgery to 1.5 cm
 Any reduction in TAPSE in the setting of
pulmonary hypertension indicates significant
RV dysfunction
 Amplitude of <1 cm implies severe impairment.

 RV diastolic function measurement on same
principles of LV diastolic dysfunction; but its
often unreliable in critical care setting.
 Positive-pressure ventilation may abolish this
pulmonary arterial diastolic wave, making the
diagnosis more challenging.
 Confounding factors include the presence of
LV restriction, elevation of pulmonary arterial
diastolic pressures, tachycardia and
requirement for high ventilatory pressures.

Pericardial Disease:
 Pericardial effusion, cardiac tamponade can be
easily diagnose in critically ill patietns who are
oligouric and having low CO even with inotropes.
 Additional features: swinging heart,
pseudosystolic anterior motion of the MV
demonstration of fixed, dilated caval veins.
 Cardiac Tamopnade on echo:
1. RV early-diastolic collapse
2. RA late-diastolic collapse
3. LA late-diastolic collapse
4. LV early-diastolic collapse
1
• Mild increase in filling
• pressure
2, 3
• Moderate increase in filling
• Pressure
4
• Severe increase in filling
• Pressure

Hemodynamics on Echo in ICU
 It is possible to calculate blood flow at several
levels in the heart and aorta using Doppler
echocardiography.
 Measurements of flow useful in the ICU setting to
derive:
 LV stroke volume, cardiac output, regurgitant
volumes of MR and AR, flow across an ASD or
VSD, valve areas (by continuity principle)
 Response to therapeutic measures such as
intravenous administration of inotropic drugs or
the effect of an intra-aortic balloon pump on
systemic output.

 Stroke volume is calculated as the product of
the cross-sectional area (cm2) of the LVOT and
the TVI (cm) by PW Doppler.
 Cardiac output: Stroke Volume X Heart Rate.

LA pressure (LAP) estimation:
 Combining transmitral Doppler (blood
velocities) with TDI (tissue velocities) has been
shown to improve the correlation with LAP.
 Here, the ratio E/E′ is calculated
 Ratio <10 corresponding to LAP < 15 mmHg
(2 kPa)
 Ratio >15 corresponding to LAP > 18 mmHg
(2.4 kPa)
 Correlation between 11–14 is poor, additional
parameters should be used, generally in
combination.

Pulmonary Art Systolic
Pressure:
 Peak PA systolic pressure is calculated from the peak
Doppler velocity (v) of TR by CW.
 RV pressure = 4 × (peak TR velocity)2
 RV pressure + Estimated RA Pressure = PA systolic
pressure.
 RA pressure Estimation:
 Normal variation or collapse of the IVC with breathing
(>50%) implies normal RA pressure (0-5 mm Hg).
 Partial collapse (<50%) is generally estimated at 5 to
10 mm Hg
 No (or only minimal) change in IVC diameter implies
an RA pressure of 15 mm Hg or more.

 When available, RA pressure can be obtained
directly from a central venous pressure tracing,
which is more accurate
 Care is needed in severe RV dysfunction, as
PASP may be significantly underestimated by
this technique
 In the absence of TR, the pulmonary
regurgitation (PR) trace can be interrogated to
estimate PA diastolic pressure

Volume responsiveness
 Echocardiography allows assessment of
the patient’s volume status,
complementary to invasive hemodynamic
measurements.
 Echocardiographic volume status
assessment:
 Static values (single-measure dimensions
and flows)
 Dynamic indices (variation in flows and
dimensions after dynamic maneuvers)

 Estimation of preload- and volume-
responsiveness using static measurements is
generally unreliable in ICU due to changes in
hemodynamics of critically ill patients .
 LAP does not correlate with volume
responsiveness, but demonstration of
abnormally high pressures with a restrictive
filling pattern should signal caution in volume
resuscitation.
Static parameters

 Indicators of severe hypovolemia in the
critically ill:
 Hyperkinetic LV (in the presence of a normal
RV) with end-systolic cavity obliteration
 LV end-diastolic area <5.5 cm2/m2 BSA
 Small IVC (<10 mm) with inspiratory collapse
(spontaneously breathing patients)
 Small IVC at end-expiration with variable
respiratory change (mechanically ventilated
patients).

Dynamic parameters
 Passive leg raising has been proposed to predict
fluid responsiveness in spontaneously breathing
patients
 Sensitivity and specificity are relatively low
 Confounding factors (intra-abdominal pressure,
hypovolemia, arrhythmia) probably limit its
usefulness in the ICU population.
 Respiratory variations in VTI may be used as an
index of fluid responsiveness.
 Respiratory variation in SVC and IVC dimensions
have been proposed to predict fluid
responsiveness.

 An IVC distensibility index (maximum–minimum/minimum)
>18% (12% normalised to mean value) has been suggested
to predict a significant increase in SV in response to fluid
challenge.
 In contrast, a high SVC collapsibility index (maximum–
minimum/maximum) >36% predicts a positive response to
volume expansion (≥15% increase in SV) with sensitivity 90%
and specificity 100%.
 Prerequisite for interpreting dynamic volume responsiveness:
 Sinus rhythm
 fully mechanically ventilated, with no spontaneous breathing
effort.
 Further, the effects of lung protective ventilatory strategies
may lead to false-negative values

Echocardiography in specific
scenarios:
 ICU echocardiographer must know the potential
pitfalls and coexisting pathologies in order to
make a relevant assessment.
 Myocardial ischaemia/infarction:
 Echocardiography is included in the universal
definition of myocardial infarction (MI), and
suspicion of a mechanical complication of MI is a
class IA indication for echocardiography.
 Extent of infarction/ischaemia should be
demonstrated and complications (MR, ventricular
septal rupture (VSR)/cardiac rupture/RV
infarction) actively excluded.

Acute cor pulmonale:
 Sudden severe increase in RV afterload resulting
in acute RV dilatation and failure.
 Major causes: acute pulmonary embolism and
ARDS.
 Pulmonary embolism (PE)
 Echocardiography provides only indirect signs of
PE:
 Pulmonary hypertension
 signs of RV systolic (septal dyskinesia) & diastolic
overload
 RV free wall hypokinesia
 moderate–severe TR.
 Pre-existing pulmonary hypertension is suggested

Hypoxemia
 Diagnosis and management of hypoxemic
patients on the ICU
 Establishing the differential diagnosis
(cardiogenic vs non-cardiac)
 Assessment of secondary effects of pulmonary
pathology on cardiac performance
 Diagnosis of a low CO state and/or diagnosis
of anatomical shunt (intracardiac or
intrapulmonary).

 Many ICU factors increase right-sided
pressures, leading to right–left intracardiac
shunting across an atrial septal defect/patent
foramen ovale.
 Intrapulmonary shunts are independent of
right-sided pressure, and have been described
in ARDS, pneumonia, thoracic trauma and
hepatic cirrhosis.
 Diagnosis depends on a positive agitated
saline contrast study

Weaning from mechanical
ventilation
 Discontinuation of positive-pressure ventilation
increases LV afterload and preload, and significantly
increases the rate–pressure product.
 In patients with cardiac disease; mismatch of the
dynamic changes leads: increased work, leading to
rising LAP, pulmonary edema, and/or RV dysfunction.
 A baseline echocardiogram should be performed at the
start of the weaning trial, and evidence of inotropy,
lusitropy, chronotropy (negative/positive), preload and
afterload mismatch should be actively sought.
 Evidence of increasing LAP, myocardial ischaemia,
decrease in LV/RV global function and/or worsening
atrioventricular valvular regurgitation suggests a cardiac
contribution to failure to wean.

Sepsis syndromes
 Echocardiography plays a key role in the
management of the septic ICU patient by guiding
haemodynamic management and excluding
cardiac causes for sepsis.
 Sepsis-related LV dysfunction is well recognised,
with global and regional wall motion abnormalities
 RV dysfunction develops either in isolation or
associated with LV dysfunction.
 Echocardiography may reveal a cardiac source of
sepsis related to either native/prosthetic valve
infection or indwelling catheters/implanted
devices.

 The diagnosis of endocarditis is made on the
basis of a well-established set of diagnostic
criteria, of which echocardiography is one of the
major factors.
 Three echocardiographic findings are important
 Mobile echo-dense mass(es) attached to
valvular/mural endocardium/implanted material
 Fistulae/abscess formation, and/or new
disruption/dehiscence of a prosthetic valve.
 TOE has a higher sensitivity and specificity, and is
mandated where prosthetic valve endocarditis is
suspected, to identify major complications and
guide surgical planning.

Chest trauma:
 Good comprehensive study should be
performed to diagnose/exclude:
 pericardial/pleural collections
 Aortic and mitral valve disruption
 Aortic disruption
 VSR
 Coronary artery disruption (ischaemia and/or
fistulae)
 myocardial contusion.

Use of echocardiography in icu

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