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Non-invasive haemodynamic monitoring by Echocardiography

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A lecture highlighting the role of Echocardiography as a major hemodynamic monitoring tool in the Intensive Care settings and the assessment of loading conditions.

Published in: Health & Medicine

Non-invasive haemodynamic monitoring by Echocardiography

  1. 1. Non-invasive Hemodynamic Monitoring by Echocardiography and Assessment of Loading Conditions Senior Clinical Fellow Adult Intensive Care Royal Brompton Hospital, London, UK hatem.soliman@gmail.com @hatemsoliman ECHO Network Workshop, Royal Papworth Hospital, Cambridge. October 12th, 2018 Dr. Hatem Soliman Aboumarie MBBS, MRCP, MSc (ICM), PGDip (Cardio), EDICM, ASCeXAM
  2. 2. Outline Volume status and Central venous pressure Pulmonary artery hemodynamics Left sided filling pressures Cardiac output and shock states
  3. 3. Volume Status
  4. 4. Volume Status Static parameters: IVC & LVEDA Dynamic parameters for the assessment of fluid responsiveness Systemic venous flow: Vena cavae, jugular and hepatic veins Tricuspid valve inflow and tissue Doppler imaging
  5. 5. LVEDA Left parasternal short-axis view, mid-papillary level Normal: 9.5–22 cm2; very low (<5.5 cm2/m2 BSA)  Hypovolemia Suboptimal image quality (especially endocardial definition and off-axis position) Pitfall Leung JM, Levine EH. Anesthesiology 1994 Nov;81(5)1102-1109. Static parameters
  6. 6. Measuring the IVC 0.5– 3 cm from the caval–atrial junction in the subcostal view
  7. 7. IVC vs. RAP GuidelinesStatic parameters ASE Guidelines
  8. 8.  cardiac index  RV afterload Courtesy of Prof. Xavier Monnet Mechanical breath  Biphasic response Early  LV SV (due to squeezing pulmonary blood volume) Few beats later  LV SV (due reduced RV SV)
  9. 9. Respiratory Variations
  10. 10. Heart-lung interactions IVC/SVC Collapsibility (Spontaneous Breathing) IVC/SVC Dispensability (Mechanical Ventilation) CO/SV/aortic velocity variability (Mechanical Ventilation) C. Charron, V. Caille et al, Current Opinion in Critical Care, vol. 12, no. 3, pp. 249–254, 2006. Volume responsiveness  SV by 15% or more after a fluid challenge
  11. 11. Collapsibility Index CI = (Dmax − Dmin )/Dmax x 100% DI = (Dmax − Dmin )/Dmin x 100% In Mechanically Ventilated patients Distensibility Index In the spontaneously breathing patient
  12. 12. Barbier C, et al Intensive Care Med. 2004 Sep;30(9):1740-1746. IVC Distensibility Index Fluid responsive
  13. 13. SVC Collapsibility Index = (Dmax - Dmin)/Dmax x 100 SVC collapsibility index of >36%  Fluid responsive. Vieillard-Baron A. et al 2004. Intensive Care Medicine 30 1734–1739. The most reliable index of fluid responsiveness
  14. 14. Movement in and out of plane  will exaggerate IVC collapsibility Beware of hepatic vein confluence Do not mistakenly interrogate the aorta Falsely  : RV failure, tamponade, pulmonary embolism, TR, pulmonary hypertension, ECMO cannulae Falsely  : Increased intra-abdominal pressure, status asthmaticus IVC Pitfalls
  15. 15. A pre-bolus threshold of 12% discriminates between responders and non-responders. Aortic Blood Velocity Respiratory Variation Teboul JL et al. Chest 2001, 119:867–873
  16. 16. Pitfalls Beware of RV failure Cor pulmonale Severe ARDS Severe pulmonary hypertension Cardiac translation  ↗ AoV variability High PEEP  ↗ AoV variability Invalid if open chest
  17. 17. Passive Leg Raise (PLR) Gives 300-500 mL auto-transfusion Only dynamic test validated in spontaneously breathing patients. Be careful Abdominal compartment syndrome Unstable pelvic/low lumbar fracture 12%PLR-induced changes in VTIAo Lamia B, et al. Intensive Care Med. 2007;33:1125-1132. Maizel J, et al. Intensive Care Med. 2007;33:1133-1138.
  18. 18. Volume Status Static parameters: IVC & LVEDA Dynamic parameters for the assessment of fluid responsiveness Systemic venous flow: Vena cavae, jugular and hepatic veins Tricuspid valve inflow and tissue Doppler imaging
  19. 19. Systemic venous flow Pitfalls Severe TR  alters systolic venous flow pattern AF, Post-cardiac surgery  reduces hepatic vein systolic flow regardless of RAP Vs > Vd  Normal CVP/RAP Vs < Vd  Elevated CVP/RAP (>8 mm Hg) Ghio S, Recusani F et al. Echocardiography 2001;18:469–77. Vena cavae, jugular, hepatic veins
  20. 20. Tricuspid valve inflow E/e’ > 6  CVP/RAP > 10 mm Hg Pitfalls Adequate in mech. ventilated patients  IVC might not be applicable May not be accurate in patients who have undergone cardiac surgery Nageh MF, et al . Am. J. Cardiol. 1999;84:1448–1451, A8.
  21. 21. Pulmonary Artery Hemodynamics
  22. 22. Pulmonary Artery Hemodynamics Systolic PA Pressure Diastolic PA Pressure Mean PA Pressure Pulmonary Vascular Resistance
  23. 23. Systolic PA Pressure Well validated TR peak systolic gradient + RAP = SPAP In absence of pulmonic stenosis
  24. 24. Pearls Use multiple imaging planes Color Doppler signals should be used for optimal alignment with the regurgitant jet. Injection of agitated saline  enhance the Doppler flow velocity tracing and give a better signal  reducing the false-negative results.
  25. 25. Pitfalls Variations in angle of interrogation Underestimation of RAP Severe TR Poor TR signal Underestimation Overestimation overestimation of the RAP overestimation of the TR peak velocity Mistakenly using the TV closing spike for the tricuspid peak velocity.
  26. 26. Diastolic PA Pressure PR end-diastolic gradient + RAP = DPAP
  27. 27. Mean PA Pressure Mean TR gradient + RAP (easiest) Peak PR gradient + RAP DPAP + 1/3 (SPAP-DPAP)
  28. 28. Pulmonary Vascular Resistance Abbas AE, et al. J Am Coll Cardiol 2003;41:1021–7. PVR (WU) = (TR velocity/RVOT VTI) x 10 + 0.16 (Abbas Formula) (3.9/10.2) x 10 + 0.16 = 3.98 WU Significant pulmonary HTN = PVR > 3 WU
  29. 29. Left sided filling pressures
  30. 30. Left-sided filling pressures Mitral inflow parameters Pulmonary venous flow Left atrial dimensions
  31. 31. 50% of patients with acute heart failure have preserved ejection fraction TDI analysis of the mitral annulus allows for rapid estimation of left atrial pressure Left-sided filling pressures
  32. 32. E/A ratio >2 and E wave deceleration time <120 ms predict a LAP >20 mmHg Lateral e′ <10 and medial e’<7 cm/s are highly suggestive of diastolic dysfunction and elevated left atrial pressures Average E/e′ of >14 elevated left atrial pressure Pearl Cut-off of E/e′ In Mechanically Ventilated patients 12 Left-sided filling pressures
  33. 33. Nagueh Formula PCWP = 1.24 x (E/e') + 1.9 e' = (e'lateral + e'septal) / 2 www.csecho.ca/cardiomath Nagueh SF et al. J Am Coll Cardiol 1997;30:1527-1533 www.csecho.ca/cardiomath Left-sided filling pressures
  34. 34. Pitfall E/e′ ratio is not accurate in normal subjects, patients with heavy annular calcification, mitral valve and pericardial disease. Nagueh S. et al EHJ-CVI (2016) 17, 1321–1360
  35. 35. Left-sided filling pressures Mitral inflow Mitral annulus Pulmonary venous flow Left atrial size
  36. 36. Lung US for B-lines
  37. 37. Cardiac Output
  38. 38. CO = HR X Stroke Volume Cardiac output SV = LVOT CSA x LVOT VTI
  39. 39. (LVOT area x LVOT VTI) VTI = Velocity Time Integral LVOT Area = 3.14 x (1⁄2 LVOT diameter)2 Stroke Volume
  40. 40. Pearls The LVOT VTI a surrogate for the stroke volume Normal value >20 cm Record the measured LVOT area in the pt. records Average of 5-10 beats in AF
  41. 41. SV variations are exaggerated with: Pitfalls Hypovolaemia Larger Tidal Volumes Cardiac tamponade Presumes LVOT is circular. It isn’t! Non-alignment of Doppler beam: VTI will be underestimated Error in LVOT diameter will be squared
  42. 42. Cardiogenic DistributiveHypovolaemic Obstructive Shock
  43. 43. Dilated right chambers Decreased cardiac output RV/LV area ratio >0.6; gross dilatation is seen with a ratio >1.0 Acute PE Changes in right ventricular contraction Elevated pulmonary artery pressures Intra‐ cavity emboli Normal Hyperdynamic Hypodynamic
  44. 44. Acute PE PAcT of 70– 90 ms indicates a pulmonary artery systolic pressure of >70 mmHg Mid‐systolic notch also indicates severe pulmonary hypertension D‐ shaped LV
  45. 45. RA systolic collapse for longer than one-third of the cardiac cycle Cardiac Tamponade RV diastolic collapse Echo Findings RA then RVOT then whole RV then LA then LV. Dilated IVC
  46. 46. Exaggerated respiratory variations of the mitral and tricuspid inflow (Pulsus Paradoxus) Cardiac Tamponade Echo Findings
  47. 47. The opposite of respiratory variations if positive pressure ventilation Cardiac Tamponade Pitfalls The speed of accumulation rather than the amount pVA-ECMO  Not an Echo diagnosis unless flows are compromised
  48. 48. Typical with basal septal hypertrophy Dynamic LVOT Obstruction Close approximation of lateral wall and septum Echo Findings Systolic anterior motion of the anterior mitral leaflet. Dagger-shaped Doppler pattern of LVOT flow
  49. 49. Pitfall Tachycardia, hypovolemia, and inotropes makes critically ill more prone to it Dynamic LVOT Obstruction
  50. 50. Monitoring of the pt on pVA-ECMO Underlying LV dysfunction  afterload due to retrograde VA ECMO flow Insufficient unloading of LV Pulmonary congestion, edema, hemorrhage.Blood stagnation in LV
  51. 51. LV unloading Before septostomy After septostomy
  52. 52. Weaning and Recovery LVEF > 35-40% LVED diameter < 55mm Aortic velocity time integral (VTI) >10 cm Aortic Valve opening pattern Absence of LV dilatation Intensive Care Med (2015) 41:902-905.
  53. 53. Echo-guided ventilator weaning algorithm
  54. 54. 6-hour Bundle April, 2015, www.survivingsepsis.org
  55. 55. Integrated Approach
  56. 56. Echo is the single most useful non-invasive hemodynamic tool PCWP evaluation is possible by Echocardiography LVOT VTI is a useful surrogate for LV Stroke Volume 1 2 3 take-home messages5 Integrated approach is the key to proper management4 Proper training, accreditation and quality control is pramount.5
  57. 57. The Anatomy Lesson of Dr. Nicolaes Tulp. 1632. Rembrandt
  58. 58. Non-invasive Hemodynamic Monitoring by Echocardiography and Assessment of Loading Conditions Senior Clinical Fellow Adult Intensive Care Royal Brompton Hospital, London, UK hatem.soliman@gmail.com @hatemsoliman ECHO Network Workshop, Royal Papworth Hospital, Cambridge. October 12th, 2018 Dr. Hatem Soliman Aboumarie MBBS, MRCP, MSc (ICM), PGDip (Cardio), EDICM, ASCeXAM

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