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Hemodynamics - Putting the puzzle together

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Haemodynamic data can be acquired in many ways. However we obtain the raw data we still have a big problem…
What do all these figures mean? How can we put it all together to help our patients?

Associate Professor Brendan E. Smith.
School of Biomedical Science, Charles Sturt University,
Specialist in Anaesthesia and Intensive Care, Bathurst Base Hospital, Bathurst, NSW, Australia

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Hemodynamics - Putting the puzzle together

  1. 1. Haemodynamics- putting the puzzle together. HR SVR Hb SV DO2 CVP CO SpO2 BP Associate Professor Brendan E. Smith. School of Biomedical Science, Charles Sturt University, Specialist in Anaesthesia and Intensive Care, Bathurst Base Hospital, Bathurst, NSW, Australia.
  2. 2. Data Acquisition.Haemodynamic data can be acquired in many ways Trans-Thoracic Echocardiography Trans-Oesphageal Echocardiography USCOM Doppler examination Impedence Plethysmography Pulmonary Artery Catheter PiCCO Etc etc…. Each has it’s own benefits and drawbacks, BUT….
  3. 3. However we obtain the raw data we still have a big problem… What do all these figures mean?How can we put it all together to help our patients?
  4. 4. Oxygen Delivery – DO2 X Blood Pressure X Hb SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  5. 5. To live we have to have… Blood pressure… and blood flow!
  6. 6. Blood PressureBlood pressuredoesn’t tell usanything aboutthe heart’s abilityto deliveroxygen!
  7. 7. Her blood pressure is normal.Anybody NOT want to know her C.O. and DO2?!! (By permission of Dr Joe Brierley, GOSH, London.)
  8. 8. Haemodynamics used to bea highly invasive science…
  9. 9. Insertion of PA Catheter wasDifficult (especially in children)DangerousTime consumingExpensiveOf doubtful value!
  10. 10. All the data provided by PAC(and more) can be obtained non-invasively…
  11. 11. Oxygen Delivery – DO2 Blood PressureHb SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  12. 12. The Ultrasonic Cardiac Output Monitor - USCOM
  13. 13. Suprasternal CW Doppler Parasternal CW Doppler
  14. 14. What other data do we get? Vpk = Peak Ejection Velocity
  15. 15. CO / CI = Cardiac Output / Index
  16. 16. Why Cardiac Index v Cardiac Output?
  17. 17. The same applies to Stroke Volume, SVR and many other parameters in haemodynamics so we use Stroke Volume Index - SVI SVR index – SVRI DO2 Index – DO2I VO2 Index – VO2I Etc…
  18. 18. MD = Minute Distance = Aortic Velocity
  19. 19. SV = Stroke volumeEjection Time + SV = Inotropy
  20. 20. SVR = Systemic Vascular Resistance
  21. 21. Oxygen Delivery – DO2 Blood Pressure Hb SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  22. 22. Pulse Oximeters
  23. 23. Pulse Oximetry + Hb
  24. 24. Central Venous Oxygen Saturation
  25. 25. Oxygen Delivery – DO2 Blood Pressure Hb SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  26. 26. AfterloadDepends on:Degree of vasoconstriction / dilationDensity & viscosity of bloodFlow rate of blood / surface tension forcesElasticity of arteriesStroke volume……
  27. 27. These are all the same factorsthat determine mean aortic rootpressure…So afterload is exactly the same as meanaortic root pressure.MAP = diastolic + ⅓ (systolic – diastolic)But can we use radial artery pressure?
  28. 28. Integrated PressureP2 ΔPP1 Δt t P2 Mean Pressure = ∫ P1 P.dt = Pressure time integral = Pti time
  29. 29. Pti-A Pti-R
  30. 30. Pti-Aortic and Pti-Radial are close enough in clinical practice to make no significantdifference to haemodynamic calculations. (error typically <5%)
  31. 31. Oxygen Delivery – DO2 Blood Pressure(Hb) SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  32. 32. Inotropy. Inotropy (myocardial contractility) as a concept is well known to all clinicians but not as a discrete quantity.Depressed inotropy is an important feature of many ICU presentations – 1o Cardiac Conditions – AMI, LVF, Cardiomyopathy
  33. 33. 2o Myocardial Depression –Septicaemia, Pancreatitis, Pneumonia, DKA, Burns,Hypoxia, Crush Injury, Hypovolaemia, Anaemia,Thyroid Disorders, Hyper + Hypothermia,Poisoning, Evenomation,Iatrogenic e.g. Antihypertensives, chemotherapy,Electrolyte Disorders, Sedation, Steroids, ……
  34. 34. Why is inotropy so important?BP = SVR x HR x SV : SV x HR = CO. Preload Inotropy Afterload Fluid loading Blood Pressure Power of the heart
  35. 35. How do we assess inotropy?- We use surrogates of global cardiac function- BP, HR, urine output, skin perfusion, capillary refill, skin temperature, bowel sounds, sweating, wind direction, mother’s seaweed…..- All of these are notoriously unreliable indicators of cardiac function even in the hands of senior clinicians.
  36. 36. When should we use inotropes? In >95% of cases this is done by clinical judgment alone! Which inotrope and how much? What are our therapeutic targets? How do we know we’ve reached them? If only we could measure inotropy!!
  37. 37. How Can We Measure Inotropy?
  38. 38. Conservation of EnergyThe energy produced by cardiac contraction must be converted to either Potential Energy (PE) in the form of blood pressure or Kinetic Energy (KE) in the form of blood flow. But can we measure PE & KE? Is the measurement reliable? How long does it take? Can we monitor Rx with it?
  39. 39. Potential EnergyPE developed by the heart appears in the form of the energy needed to raise the stroke volume up to arterial pressure in a given systolic time, the Flow Time. Work Done = ΔP x ΔV PE = MAP x SV Flow Time ΔP = Mean Arterial Pressure - CVP SV and Flow Time are measured directly using CW Doppler.
  40. 40. Potential Energy PE = BPm x SV x 10-3 7.5 x FT 7.5 and 10-3 are required to convert BP in mmHg to kPa and SV in ml to m3 to conform with SI units.The unit for PE is therefore Joules/second, or Watts.
  41. 41. Kinetic Energy The KE of any moving mass is given by – KE = ½mV2 The mass of blood ejected per Stroke Volume is - SV(ml) x 10-6 x Density of blood, ρ (1,055 kg/m3)The KE developed by the heart in a given flow time is – KE = 1 x SV x 10-6 x ρ x V2 2 x Flow Time (V is measured directly by CW Doppler)
  42. 42. Total Inotropy = PE + KE ( = blood pressure + blood flow)Inotropy = BPm x SV x 10-3 + 1 x SV x 10-6 x ρ x V2 7.5 x FT 2 x FT (The Smith-Madigan Formula)The SI unit of inotropy is therefore the Watt.
  43. 43. Inotropy IndexBut how do we judge inotropy in patients of varying size, e.g. large and small adults, children, infants? By analogy to cardiac index which is – Cardiac Index = Cardiac Output Body Surface Area Smith-Madigan Inotropy Index = Inotropy BSA The SI unit of SMII is therefore W/m2
  44. 44. Smith-Madigan Inotropy Index Normal Controls 1.6 – 2.2 W/m2 Left Ventricular Failure 0.4 – 1.1 W/m2 Septicaemic Shock 0.6 – 1.2 W/m2
  45. 45. Cardiogenic Shock74 year old man with STEMIBP 84/44, pulse 114, SpO2 84% on 10L/min O2Pulmonary Oedema +++No urine outputPaO2 64mmHg, PaCO2 28mmHgLactate 8.4
  46. 46. >2.4 60-75 8 12 14 Dobutamine mcg/kg/min0.62 0.97 1.13 1.38 SMII W/m2 <90 800-1200
  47. 47. Oxygen Delivery – DO2 Blood Pressure(Hb) SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  48. 48. PreloadJVP / CVP- Only looking at the right side of the heart.- Tells us little about left heart preload.- Tricuspid valve integrity? Stenosis and regurgitation both lead to errors.- Arrythmias lead to error.- Even right ventricular pressure tells us little about right ventricular volume.
  49. 49. Pulmonary artery catheterWhat pressure should we use?PA Diastolic Pressure (PADP)?PA Wedge Pressure (PAWP)?PA mean Pressure (PAPm)?Is the catheter in the right place?What about IPPV, PEEP, pulmonaryvascular patency, vasoconstriction, shunts,arrythmias, mitral valve problems….etc.
  50. 50. PACAttempts to measure left ventricular enddiastolic pressure - LVEDPLeft ventricular preload is strictly the leftventricular end diastolic volume – LVEDVVentricular end diastolic pressure only actsas an acceptable surrogate if we know theventricular compliance.
  51. 51. Can basic physiology help us? Inotropy
  52. 52. SV LVEDV
  53. 53. Passive Leg Raising - ↑SV
  54. 54. Stroke volume increases from 26ml to 32ml = 23%Patient still on left side of Starling Curve. Patient will respond to volume loading.Passive Leg Raising test can be repeated after fluid bolus.
  55. 55. Oxygen Delivery – DO2 Blood Pressure(Hb) SpO2 Cardiac Output SVRStroke Volume Heart Rate Preload Inotropy Afterload
  56. 56. OK, this is all very clever stuff but does it make any difference to patient outcomes?
  57. 57. Haemodynamic strategy – June 2005201612 8 Mortality 4
  58. 58. Conclusions• The haemodynamic jigsaw can be solved.• It can be done non-invasively.• It can be painless, simple and cheap.• It can be done anywhere, anytime.• Can, with practice, be very quick!...
  59. 59. Thank you!

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