1. Dr Caroline Daly Cardiologist, SJH
Echo in the ITU
Dr Caroline Daly
Cardiologist, SJH

2. Scope of uses of ECHO in ICU
Following cardiac surgery
Diagnosis
Monitoring

3. Advantages Cheap Portable Widely available
Non invasive, no toxic contrast, no radiation

4. 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

5. Key Questions in ITU Systolic function and RWMA
tamponade and pericardial effusion
hypovolemia and volume responsiveness
acute cor pulmonale
hypoxemia
complication of AMI
chest trauma
assessment of shock

6. Disadvantages of TTE in ITU
Poor ECHO images in:
Obese
COAD/hyperinflated chest
Chest wall deformity
Oedema
Post cardiac surgery –wounds, pain, drains

7. TOE 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%)

8. 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

9. FATE - interpretation Look for obvious pathology
Masses, vegetations, intra thoracic foreign bodies
Assess morphology/dimensions
Assess myocardial function
Assess valves
Image pleura on both side
Relate the information to the clinical context

10. Normal FATE view Subcostal 4 chamber Apical 4 chamber
Parasternal long axis
Parasternal LV short axis
Pleural scanning

11. Extended FATE Normal FATE + Subcostal vena cava Apical 2 chamber
Apical long axis
Apical 5 chamber
Parasternal short axis mitral plane
Parasternal aorta short axis

12. FATE Hypovolemia Myocardial dysfunction Pericardial effusion
Pulmonary embolism
Papillary muscle rupture
VSD in AMI
Severe valve dysfunction
Pleural effusion/ pneumothorax

13. Key morphological parameters
LV shape / chamber dimension / thickness
RV shape / chamber dimension / thickness
Atrial dimension
IV septum position

14. 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

15. 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)

16. Pre-existing cardiac disease?
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

17. 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

18. Severe Hypovolaemia IVC diameter IVC respiratory variation
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

19. Volume Overload Dilated, fixed IVC Pitfalls cardiac tamponade
constrictive pericarditis

20. 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

21. 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

22. 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

23. RV function RVEDA / LVEDA > 0.6 moderate dysfunction
> 1 severe dysfunction
Paradoxical septal movement

24. Mitral Valve Excessive leaflet mobility Restrictive leaflet mobility
myxomatous valve disease,
torn chordae,
prolapse,
Flail
myocardial infarction, torn papillary muscle
Restrictive leaflet mobility
rheumatic disease
calcific disease
dilated cardiomyopathy
acute ischemic disease

28. 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”

29. 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

30. FEEL
high quality CPR with minimal interruptions to reduce the no-flow intervals
FEEL < 10 sec

31. RV Small and hyperkinetic RV: tamponade
Dilated and hypokinetic RV: RV failure
LV dysfunction
RV AMI
Acute pulmonary embolism

32. LV Severe LV hypokinesia LV hyperkinesia LV AMI, Sepsis related
Myocarditis
DCM
LV hyperkinesia
Acute valvular dysfunction (AR, MR),
HOCM,
diastolic dysfunction

33. 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

34. Advanced Critical Care Echo
Evaluating LV systolic function
Evaluating RV function
Monitoring Cardiac Output
Fluid Responsiveness
IVC and LV
Diastolic function
RV function
Tamponade

35. Cardiac Output Cardiac output = Stroke volume x Heart Rate
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)

36. CO by TOE in liver transplantation
Curr Cardiol Rev August; 7(3): 184–196.

37. Continuous monitoring of CO (TOE)
Meta-analysis of comparison of 2 available ultrasonographic devices- CO evaluation from pulsed-wave 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 to 2.00 l/min.
Is good to track changes

38. Haemodynamics in ITU

40. 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

41. 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.

42. 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

43. Diastolic Dysfunction
Important cause of cardiogenic pulmonary oedema and failure to wean even with reasonable systolic function.
IHD
Hypertension AS
Cardiomyopathy
Sepsis (sepsis induced cardiomyopathy)
Inotropes (adrenaline). PDE inhibitors (lusitropes) preserve diastolic function better.

44. 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.

45. 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.

46. 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

47. 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.
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.

48. 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.

49. 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.

50. Tamponade physiology

58. Ultrasound in cardiac arrest due to pneumothorax.
Typically, cardiac chambers are small and hyperkinetic (a), inferior vena cava is dilated (b)