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High output cardiac failure

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Optimising haemodynamics in septicaemia / HOCF saves lives! Optimising haemodynamics early saves even more lives!

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

Published in: Health & Medicine, Technology

High output cardiac failure

  1. 1. High Output Cardiac Failure 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. The circulation is a consumer-led economy! Just like electricity, it is the consumer not the producer that determines current flow. It is the tissues not the heartthat determine cardiac output.
  3. 3. Ohms Law and The Circulation
  4. 4. BP = CO x SVR Any in CO SVR Any in SVR COSo BP tends to remain stable
  5. 5. The tissues control blood flow locally by vasodilation. This is in response primarily to ↓PaO2 and ↑PaCO2, but also occurs in response to acidosis and thermal load.As the microcirculation vasodilates, so the systemic vascular resistance of the circulation falls, SVR↓
  6. 6. The stroke volume automatically increases as the afterload reduction makes ejection easier. If SVR↓↓ then BP will fall and sympathetic responses willincrease heart rate and stroke volume producing an increased cardiac output. The increased CO is caused by the tissue needs, not by some higher “control centre”.
  7. 7. As SVR falls, CO rises and BP remains stable.SVR d/s/cm-5 Cardiac Output L/min
  8. 8. Initially, the fall in SVR can be compensated by an increasedCardiac Output which maintains BP, the compensated phase, but this process cannot go on forever! Eventually, the heart cannot increase CO further and BP will fall. This is the decompensated phase.The point at which this occurs depends on the cardiac reserve, and depends on preload availability and on inotropy.
  9. 9. Increasing CO in response to tissue need is normal. Most common causes of this at rest are anaemia, pregnancy, thyrotoxicosis, pyrexia and childhood!So when does a high CO become “High Output Failure”? When BP cannot be maintained against a low SVR, or when oxygen delivery cannot be maintained.The diagnostic triad is high CO, low BP, very low SVR.
  10. 10. 84 Kg male, 47 years, Septicaemia. BP 74/38 Normal Values 80 - 110 14 - 22 6.2 – 7.1 2.8 – 3.6 800 - 1600
  11. 11. Aortic Minute Distance = mean aortic flow velocityImmediately shows if the circulation is Hyperdynamic (>22 m/min) Normodynamic (14 – 22 m/min) Hypodynamic (<14 m/min)
  12. 12. Cardiac Output = 17 l/min (CI = 9.1 l/min/m2) How can this possibly be heart failure? 1. Failure to maintain BP (74/38) 2. What is the inotropy level here? Smith-Madigan Inotropy Index = 0.77 W/m2 (normal = 1.6 – 2.2)This shows severe myocardial depression, but with such a low afterload the underlying heart failure is not obvious!!
  13. 13. 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)
  14. 14. PE : KE Ratio - PKR PE = 0.62 W/m2 KE = 0.15 W/m2 PE:KE Ratio (PKR) = 4:1 Normal ratio ~ 30:1A much greater fraction of cardiac work is going intoblood flow than normal. This is typical of septicaemia.
  15. 15. Hallmarks of SepticaemiaBP = 74/38 Hyperdynamic High Stroke Volume High Cardiac Output Low SVR High DO2 Low inotropy index Low PKR
  16. 16. N.B. Paediatric Septicaemia is very different… Hypodynamic SV is low CO/CI is low SVR is high
  17. 17. What does inotropy tell us?To treat the low BP then we must know the inotropy index.If we just use a vasopressor agent e.g. phenylephrine then there is insufficient myocardial power to cope with the increase in afterload. The ventricle will dilate and fail.
  18. 18. What does inotropy tell us? SMII of 0.77 W/m2 is typical of LVF patients.It means that the heart is on a flat Starling curve and will not respond to volume expansion alone.We must increase the inotropy of the heart before we can use volume expansion.
  19. 19. “Flat” Starling Curves and Inotropy IndexStrokeVolume +SV +inotropy Left ventricular end diastolic volume
  20. 20. What does inotropy tell us?Left ventricular end diastolic volume = PreloadCan be calculated from SMII and Stroke Volume Determines need for fluid expansionLVEDV = (2.8/SMII) x SV + 0.05 (2.8 – SMII)4 x 1.1 (Smith-Madigan LVEDV formula)
  21. 21. SMII = 1.1 W/m2 What is the LVEDV?StrokeVolume SV LVEDV Left ventricular end diastolic volume
  22. 22. What does inotropy tell us?To raise BP we must use a vasoconstrictor with positive inotropic properties e.g. Noradrenaline (Norepinephrine) Dopamine, Metaraminol etc.
  23. 23. Tissue MarkersWhat role do these play in pathogenesis? IL1? IL6? Thromboxane? TNF? NO? Prostacycline? PAF? White cell proteases? Etc……
  24. 24. Tissue Markers Millions of dollars have been spent developing antagonists of tissue markers. Clinical trials have failed to show any outcome benefits for their use.
  25. 25. I believe that tissue markers are simplytombstones indicating cellular damage & death.
  26. 26. LactateLactate is a product of anaerobic respiration in the tissues – it indicates tissue hypoxia. As such, it can be used to guide therapy.
  27. 27. Aerobic respiration in tissues. All the tissues of the body need oxygen for optimal function. Therefore ANY indicator of normal function can be useful as a guide to therapy. The organs most sensitive to oxygen lack are the brain, kidneys, heart and liver.Cerebral function, urine output and concentration, inotropy and LFT’s all show abnormalities with intracellular hypoxia.
  28. 28. Gastric Mucosal pHH+ production in the gastric mucosa is highly sensitive to tissue hypoxia.A rising pH in the gastric mucosa suggestsdecreased visceral perfusion and/or hypoxia. Can be used as a marker of gut perfusion.
  29. 29. DO2 v VO2Oxygen OxygenDelivery Usage
  30. 30. Oxygen Delivery - DO2DO2 = 1.34 x Hb x SaO2/100 x CO
  31. 31. Oxygen Usage - VO2 Arterial blood Venous blood Tissues O2 content = O2 content =1.34 x Hb x SaO2/100 x CO 1.34 x Hb x ScvO2/100 x CO = ~ 1,000ml/min = ~ 750ml/min VO2 = A[O2] – V[O2] = 1000 – 750 = 250ml/min
  32. 32. Cytotoxic Hypoxia If VO2 is low (< 4ml/kg/min) despite adequate DO2 (> 12ml/kg/min) then cytotoxic hypoxia is present. ScvO2 will be =>80% (normal ~75%)(CVP sample is close enough to PA sample to use clinically)
  33. 33. How do we treat High OutputCardiac Failure / Septicaemia?
  34. 34. Measure haemodynamics as soon as possible. Early septicaemia is a time bomb – minutes matter and the clock is ticking.
  35. 35. Balancing oxygen need with oxygen delivery 1) Measure DO2 2) If possible, measure VO2 3) Or use Lactate / pH as a surrogate of VO2 4) Is DO2 adequate? – if not, ↑DO2 5) Is VO2 adequate? – if not, ↓VO2
  36. 36. Increasing DO2 1) ↑SaO2 if possible. Give 100% O22) ↑CO if low. Keep CO =>90ml/kg/min3) ↑Hb if anaemia present (=>120g/L) 4) ↑BP if MAP < 80mmHg
  37. 37. Decrease VO2 1) Reduce pyrexia – Paracetamol iv2) Reduce anxiety / cerebral O2 usage – Sedate 3) Reduce muscle O2 usage – Paralyse 4) Consider cooling patient
  38. 38. 5) Use high FIO2 – 100% if necessary 6) Broad spectrum antibiotics – e.g. Timentin7) Calculate LVEDV – if LVEDV < 75ml/m2 AND SMII > 1.2 W/m2 then volume will be required. 8) If SMII < 1.2 W/m2 start inotropes
  39. 39. Use of InotropesIf SVR ↓↓ then start noradrenaline at 200ng/kg/min Re-measure SMII regularly aiming at SMII > 1.4 Re-calculate LVEDV aiming at 75ml/m2Do not allow SVR > 750 – if noradrenaline →↑↑SVR then balance inotropes.
  40. 40. Balancing Inotropes Aim for SMII >1.4 W/m2If excessive vasoconstriction with a single agent then add in a vasodilating inotrope e.g. dobutamine. Aim for MAP =>80mmHg and SVR = 700 – 750, CO => 90ml/Kg/min, DO2 > 12ml/kg/min.
  41. 41. SMII = 0.77, LVEDV = 89 ml/m2, DO2 = 2,609 ml/min VO2 = 387 ml/min (4.5ml/kg/min). Action. BP 74/38 Start Noradrenaline at 200 ng/kg/min
  42. 42. SVR high, CO low, DO2↓ to 652ml/min, SMII = 1.13 BP 114/62 Action. Add dobutamine at 8 mcg/kg/min
  43. 43. DO2 = 1,018ml/min, SMII = 1.48 W/m2. Action. ↑Dobutamine 10mcg/kg/minBP 122/66 ↓NA to 150ng/Kg/min. CO = 6.1, SMII = 1.56 DO2 = 1162, SVR = 744, BP = 124/62, LVEDV = 79mlm2 VO2 = 4.9 ml/kg/min Urine ++ ☺
  44. 44. Has the haemodynamic approach to septicaemia /HOCF improved outcomes?
  45. 45. Haemodynamic strategy – June 2005201612 8 Mortality 4
  46. 46. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M.Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med (2001 Nov 8) 345(19):1368-77 Reduced mortality by 34%
  47. 47. They tried to optimise haemodynamics in 6 hours! (many took longer)We normally optimise haemodynamics in under 90 minutes!
  48. 48. Optimising haemodynamics insepticaemia / HOCF saves lives!Optimising haemodynamics early saves even more lives!
  49. 49. Thank you!

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