Transcript Scope of uses of ECHO in ICU

Echo in the ITU
Dr Caroline Daly
Cardiologist, SJH
Scope of uses of ECHO in ICU
• Following cardiac surgery
• Diagnosis
• Monitoring
Advantages
• Cheap
• Portable
• Widely available
• Non invasive, no toxic contrast, no radiation
Rationale for use of Echo in ITU
• Point-of care echocardiography in the
management of the critically ill patient
• Provides rapid assessment of cardiac function
and physiology
• Complements data available from standard
invasive hemodynamic monitoring
• Both a diagnostic and monitoring tool for
rapid bedside assessment of cardiovascular
pathophysiology in the critically ill
Key Questions in ITU
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Systolic function and RWMA
tamponade and pericardial effusion
hypovolemia and volume responsiveness
acute cor pulmonale
hypoxemia
complication of AMI
chest trauma
assessment of shock
Disadvantages of TTE in ITU
• Poor ECHO images in:
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Obese
COAD/hyperinflated chest
Chest wall deformity
Oedema
Post cardiac surgery –wounds, pain, drains
TOE
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Invasive - but minimally invasive vs other Ix
Overcomes the issues of poor image quality
Better spatial resolution & better views of posterior structures
More sensitive for detection of endocarditis - >90 % vs 68%
Complications (retrospective series n= 7200 pts in cardiac
surgery : Kallmeyer et al.)
– severe odynophagia
(0.1%)
– dental injury
(0.03%)
– endotracheal tube malpositioning
(0.03%)
– upper gastrointestinal hemorrhage (0.03%)
– oesophageal perforation
(0.01%)
Emergency Echo
• FEEL: focused echocardiography evaluation in
life support
• FATE: focused assessed transthoracic echo
Goals
• acquire standard TTE views in ACLS compliant
manner
• recognise major causes of arrest/ shock
• recognise when referral for second opinion
FATE - interpretation
• Look for obvious pathology
– Masses, vegetations, intra thoracic foreign bodies
• Assess morphology/dimensions
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Assess myocardial function
Assess valves
Image pleura on both side
Relate the information to the clinical context
Normal FATE view
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Subcostal 4 chamber
Apical 4 chamber
Parasternal long axis
Parasternal LV short axis
Pleural scanning
Extended FATE
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Normal FATE +
Subcostal vena cava
Apical 2 chamber
Apical long axis
Apical 5 chamber
Parasternal short axis mitral plane
Parasternal aorta short axis
FATE
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Hypovolemia
Myocardial dysfunction
Pericardial effusion
Pulmonary embolism
Papillary muscle rupture
VSD in AMI
Severe valve dysfunction
Pleural effusion/ pneumothorax
Key morphological parameters
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LV shape / chamber dimension / thickness
RV shape / chamber dimension / thickness
Atrial dimension
IV septum position
Pathologies to be considered
• Pericardial effusion
post cardiac surgery, post cardiac catheterization,
trauma, renal failure, infection
• Dilated RA + RV
pulmonary embolism, RV infarction, pulmonary
hypertension, volume overload
• Dilated LA + LV
ischemic heart disease, dilated cardiomyopathy,
sepsis, volume overload, aortic insufficiency
Pathologies to be considered Ctd
• LV hypertrophy
Aortic stenosis, arterial hypertension, left
ventricular outflow tract obstruction ( eg SAM
or sub-aortic membrane), hypertrophic
cardiomyopathy, myocardial deposition
(amyloid, haemochromatosis)
Pre-existing cardiac disease?
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RV dilatation = acute or chronic
LV dilatation = almost always chronic
Biventricular dilatation = chronic failure
Atrial dilatation = chronic pressure or volume
overload
• RV or LV hypertrophy = chronic pressure
overload
Severe hypovolaemia
• End systolic LV obliteration (kissing walls)
• LV end diastolic area (LVEDA) < 5.5 cm/m2 BSA
• (or < 10 cm2)
• LVEDA variation with loading
Severe Hypovolaemia
• IVC diameter
– spontaneous respiration: EED < 9 mm
– mechanical ventilation: EED < 15 mm
• IVC respiratory variation
– spontaneous respiration: > 50%
– mechanical ventilation: > 18%
• IVC variation with loading
EED = End expiratory dimension
Volume Overload
• Dilated, fixed IVC
Pitfalls
• cardiac tamponade
• constrictive pericarditis
Basic Volume Status Assessment
• Easy in severe hypovolaemia
• Easy in clear volume overload
• Difficult in less severe hypovolemia/significant
cardiac disease
• Consider pre-existing cardiac disease
• Consider respiratory status
Ventricular Function assessment
• LV global systolic function
– fractional shortening (FS)
– FS% = (LVEDD-LVESD)/LVEDD x 100%
– With RWMA is unreliable, but, simplified Teicholz
method EF % = FS % x 2
– visual ejection fraction (eyeballing)
– Simpsons (planimetry of LV cavity)
• LV regional function
• RV systolic function
Qualitative Assessment of Function
• Qualitative assessment of LV function
– tend to be underestimated in a dilated LV
– overestimated in small cavity LV
• Interpret findings in the context of drugs and
preload (volume status)
• Repeated echo assessment of LV function
• Interpret findings considering inotropic/
mechanical support
• Marked tachycardia/atrial fibrillation may
underestimate of LV systolic function
RV function
• RVEDA / LVEDA
• > 0.6 moderate dysfunction
• > 1 severe dysfunction
• Paradoxical septal movement
Mitral Valve
• Excessive leaflet mobility
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myxomatous valve disease,
torn chordae,
prolapse,
Flail
myocardial infarction, torn papillary muscle
• Restrictive leaflet mobility
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rheumatic disease
calcific disease
dilated cardiomyopathy
acute ischemic disease
Focused Echo • Focused echocardiography as an adjunct in
the peri-arrest period is likely to become a
core competency for acute medicine trainees
• World Interactive Network Focused on Critical
Ultrasound = “Winfocus” basic echo
• “Echocardiography practice, training and
accreditation in the intensive care”
http://www.cardiovascularultrasound.com/content/6/1/49
FEEL: focused echocardiography
evaluation in life support
• To assess the function of the heart and identify
treatable conditions in peri-resuscitation care
• Differentiates"true" PEA from "pseudo-PEA"
• Identify 4 treatable causes of cardiac arrest
– cardiac tamponade
– hypovolemia
– pulmonary embolism
– severe LV dysfunction
FEEL
• high quality CPR with minimal interruptions to
reduce the no-flow intervals
• FEEL < 10 sec
RV
• Small and hyperkinetic RV: tamponade
• Dilated and hypokinetic RV: RV failure
– LV dysfunction
– RV AMI
– Acute pulmonary embolism
LV
• Severe LV hypokinesia
– LV AMI,
– Sepsis related
– Myocarditis
– DCM
• LV hyperkinesia
– Acute valvular dysfunction (AR, MR),
– HOCM,
– diastolic dysfunction
Bibliography
• ICU echocardiography- should we use it in a
heartbeat? Chest 2002
• Portable echocardiography- is essential for the
treatment of acutely ill patients BMJ 2006
• Echocardiography for the intensivists Care of
the Critically Ill 2003
• Beside Ultrasonography in the ICU Chest 2005
• Echo in ICU- time for widespread use ICM
2006
Advanced Critical Care Echo
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Evaluating LV systolic function
Evaluating RV function
Monitoring Cardiac Output
Fluid Responsiveness
– IVC and LV
• Diastolic function
• RV function
• Tamponade
Cardiac Output
• Cardiac output = Stroke volume x Heart Rate
• Stroke Volume
Calculated from (i) Pulse Wave VTI and CSA of
– LVOT
– RVOT
– Mitral inflow (at annulus)
• (ii) Simpson’s (EDV - ESV = SV).
– (May be overestimated if RWMAs)
CO by TOE in liver transplantation
Curr Cardiol Rev. 2011 August; 7(3): 184–196.
Continuous monitoring of CO (TOE)
• Meta-analysis of comparison of 2 available
ultrasonographic devices- CO evaluation from pulsedwave Doppler of the descending aorta. (CardioQ and
HemoSonic 100) v thermodilution via PA
• Left ventricular stroke volume estimated by mean
systolic velocity measurement using a nomogram in the
CardioQ, and an M-mode echocardiography estimate of
aortic diameter using HemoSonic 100.
• 21 studies, 314 patients, 2400 paired measurements.
• Reasonable correlation was found between both
methods, with a mean difference of -0.69 to 2.00 l/min.
• Is good to track changes
Haemodynamics in ITU
Fluid Responsiveness
IVC
• IVC size correlated to CVP/RAP spontaneous breathing
• In controlled ventilation IVC will expand in inspiration (as
venous return is reduced) and reduce in expiration
(opposite of spont).
• Absence of respiratory variation : 90% chance will not be
fluid responsive.
>11% variation identifies responders
IVC collapsibility index
= max diameter - minimum diameter / mean diameter
x100 to get percentage
LV : fluid responsiveness
• LV
Variation in LV stroke area with respiration shown
to predict fluid responsiveness (change >16%).
• ie area of LV in PSAX papillary level in systole and
diastole and subtract systole from diastole - see
how this changes with respiration
• Impractical/time consuming without appropriate
software in machine.
LVOT : fluid responsiveness
• LVOT
Vmax or VTI variation with respiration of >12%
predicts fluid responsiveness
• (max - min / mean) x 100
VTI increase of >12% 1min after PLR predicts
fluid responsiveness
Diastolic Dysfunction
• Important cause of cardiogenic pulmonary
oedema and failure to wean even with
reasonable systolic function.
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IHD
Hypertension
AS
Cardiomyopathy
Sepsis (sepsis induced cardiomyopathy)
Inotropes (adrenaline). PDE inhibitors (lusitropes)
preserve diastolic function better.
Diastolic dysfunction
• LV compliance reduced so LVED Pressure Volume
relationship shifted up and left so:
• LV can be under-filled despite high filling pressures.
• Optimum filling range narrow (under or over filled
easily)
• Therefore a hypovolaemic LV with diastolic dysfunction
will have elevated filling pressures, may respond well
to fluid, but will easily be overloaded with pulmonary
oedema resulting.
Causes of RV dysfunction
• RV volume overload.
• RV pressure overload (ARDS, PE).
• Myocardial contusion (most anterior cardiac
chamber).
• Myocardial ischaemia.
• RCA air embolus post cardiac surgery.
• All forms of RV overload compromise LV
diastolic function.
RV Volume Overload
• RV very compliant so volume can increase with little
change in pressure.
• If severe volume increase will move over top of Starling
curve and start to fail.
• TR will also develop.
– Acute from IV fluid or renal failure.
– Chronic from ASD, VSD, severe TR or PR.
• Chronic volume overload can cause RV hypertrophy and
pressure overload.
• In pure volume overload the RV will not be hypertrophied
RV Pressure Overload
• RV very sensitive to increase in afterload and will quickly result
in dilatation and failure if acute (eg PE or ARDS).
• If chronic RV will be hypertrophied, will tolerate increased
afterload better.
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Features of pressure overload
• Dilated RV. Hypertrophied if chronic.
• Acute pressure overload (PE or ARDS) will look the same as
volume overload with septal flattening in diastole.
• If chronic from PHT(recurrent PE, L sided regurg, L heart failure,
COPD) RV will be hypertrophied and able to generate very high
pressures (>50mmHg). The septum is D shaped in systole
(paradoxical motion) going back to normal in diastole.
Tamponade
2D and M-mode.
Look for chamber collapse in diastole.
RA then RVOT then whole RV then LA then LV.
RAP will be high so IVC dilated with little or no
respiratory variation.
Tamponade
• Pulse Wave Doppler
• Assess RV and LV inflow in A4C.
• Inspiration increases flow of blood into R heart (sucks it
in) and reduced flow into L heart (pulm vessels
expand).
• This is exaggerated in tamponade (pulsus paradoxus).
• This is the opposite if positive pressure ventilation
• Measure max and min E wave velocities for each valve.
• Assess outflow of RVOT and LVOT by measuring Vmax
and/or VTI.
Tamponade physiology
Ultrasound in cardiac arrest due to pneumothorax.
Typically, cardiac chambers are small and
hyperkinetic (a), inferior vena cava is dilated (b)