High output cardiac failure

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.

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

2. The circulation is a The circulation is a
consumer-led economy!consumer-led economy!
Just like electricity, it isJust like electricity, it is
the consumer not thethe consumer not the
producer that determinesproducer that determines
current flow.current flow.
It is the tissues not the heartIt is the tissues not the heart
that determine cardiac output.that determine cardiac output.

3. Ohms Law and The CirculationOhms Law and The Circulation

4. BP = CO x SVRBP = CO x SVR
Any in CO SVRAny in CO SVR
Any in SVR COAny in SVR CO
So BP tends to remain stableSo BP tends to remain stable

5. The tissues control blood flow locally by vasodilation.The tissues control blood flow locally by vasodilation.
This is in response primarily to This is in response primarily to ↓↓PaOPaO
22 and and ↑↑PaCOPaCO
22,,
but also occurs in response to acidosis and thermal load.but also occurs in response to acidosis and thermal load.
As the microcirculation vasodilates, so the systemic vascular As the microcirculation vasodilates, so the systemic vascular
resistance of the circulation falls, SVRresistance of the circulation falls, SVR↓↓

6. The stroke volume The stroke volume automaticallyautomatically increases as the afterload increases as the afterload
reduction makes ejection easier.reduction makes ejection easier.
If SVRIf SVR↓↓ ↓↓ then BP will fall and sympathetic responses willthen BP will fall and sympathetic responses will
increase heart rate and stroke volume producing an increased increase heart rate and stroke volume producing an increased
cardiac output.cardiac output.
The increased CO is caused by the The increased CO is caused by the tissue needstissue needs,,
not by some higher “control centre”.not by some higher “control centre”.

7. Cardiac OutputCardiac Output L/min L/min
SVR SVR
d/s/cm- d/s/cm-
55
As As SVRSVR falls, falls,
COCO rises and rises and
BPBP remains remains
stable.stable.

8. Initially, the fall in SVR can be compensated by an increased Initially, the fall in SVR can be compensated by an increased
Cardiac Output which maintains BP, the Cardiac Output which maintains BP, the compensated phasecompensated phase, ,
but this process cannot go on forever! Eventually, the heart but this process cannot go on forever! Eventually, the heart
cannot increase CO further and BP will fall. This is the cannot increase CO further and BP will fall. This is the
decompensated phasedecompensated phase..
The point at which this occurs depends on the The point at which this occurs depends on the cardiac reservecardiac reserve,,
and depends on and depends on preloadpreload availability and on availability and on inotropyinotropy..

9. Increasing CO in response to tissue need is normal.Increasing CO in response to tissue need is normal.
Most common causes of this at rest are anaemia, Most common causes of this at rest are anaemia,
pregnancy, thyrotoxicosis, pyrexia and childhood!pregnancy, thyrotoxicosis, pyrexia and childhood!
So when does a high CO become “High Output Failure”?So when does a high CO become “High Output Failure”?
When BP cannot be maintained against a low SVR, When BP cannot be maintained against a low SVR,
or when oxygen delivery cannot be maintained.or when oxygen delivery cannot be maintained.
The diagnostic triad is high CO, low BP, very low SVR.The diagnostic triad is high CO, low BP, very low SVR.

10. BP 74/38BP 74/38
Normal ValuesNormal Values
800 - 1600800 - 1600
84 Kg male, 47 years, Septicaemia.84 Kg male, 47 years, Septicaemia.
80 - 11080 - 110
6.2 – 7.16.2 – 7.1
2.8 – 3.62.8 – 3.6
14 - 2214 - 22

11. Aortic Minute DistanceAortic Minute Distance
== mean aortic flow velocitymean aortic flow velocity
Immediately shows if the circulation isImmediately shows if the circulation is
Hyperdynamic (>22 m/min)Hyperdynamic (>22 m/min)
Normodynamic (14 – 22 m/min)Normodynamic (14 – 22 m/min)
Hypodynamic (<14 m/min)Hypodynamic (<14 m/min)

12. Cardiac Output = 17 l/min (CI = 9.1 l/min/mCardiac Output = 17 l/min (CI = 9.1 l/min/m
22
))
How can this possibly be heart failure?How can this possibly be heart failure?
1. Failure to maintain BP (74/38)1. Failure to maintain BP (74/38)
2. What is the 2. What is the inotropyinotropy level here? level here?
Smith-Madigan Inotropy Index = 0.77 W/mSmith-Madigan Inotropy Index = 0.77 W/m
22

(normal = 1.6 – 2.2)(normal = 1.6 – 2.2)
This shows severe myocardial depression, but with such a This shows severe myocardial depression, but with such a
low afterload the underlying heart failure is not obvious!!low afterload the underlying heart failure is not obvious!!

13. Total Inotropy = PE + KETotal Inotropy = PE + KE
( = blood ( = blood pressurepressure + blood + blood flowflow))
Inotropy = BPm x SV x 10Inotropy = BPm x SV x 10
-3 -3
++

1 x SV x 101 x SV x 10
-6-6
x x ρρ x V x V
22
7.5 x FT7.5 x FT 2 x FT2 x FT
(The Smith-Madigan Formula)(The Smith-Madigan Formula)

14. PE : KE Ratio - PKRPE : KE Ratio - PKR
PE = 0.62 W/mPE = 0.62 W/m
22
KE = 0.15 W/mKE = 0.15 W/m
22
PE:KE Ratio (PKR) = 4:1PE:KE Ratio (PKR) = 4:1
Normal ratio ~ 30:1Normal ratio ~ 30:1
A much greater fraction of cardiac work is going intoA much greater fraction of cardiac work is going into
blood flow than normal. This is typical of septicaemia.blood flow than normal. This is typical of septicaemia.

15. BP = 74BP = 74//3838
Hallmarks of SepticaemiaHallmarks of Septicaemia
HyperdynamicHyperdynamic
High Stroke VolumeHigh Stroke Volume
High Cardiac OutputHigh Cardiac Output
Low SVRLow SVR
High DOHigh DO
22
Low inotropy indexLow inotropy index
Low PKRLow PKR

16. N.B. Paediatric SepticaemiaN.B. Paediatric Septicaemia
is very different…is very different…
HypodynamicHypodynamic
SV is lowSV is low
CO/CI is lowCO/CI is low
SVR is highSVR is high

17. What does inotropy tell us?What does inotropy tell us?
To treat the low BP then we must know the inotropy index.To treat the low BP then we must know the inotropy index.
If we just use a vasopressor agent e.g. phenylephrine then If we just use a vasopressor agent e.g. phenylephrine then
there is insufficient myocardial power to cope with the there is insufficient myocardial power to cope with the
increase in afterload. The ventricle will dilate and fail.increase in afterload. The ventricle will dilate and fail.

18. What does inotropy tell us?What does inotropy tell us?
SMII of 0.77 W/mSMII of 0.77 W/m
22
is typical of LVF patients. is typical of LVF patients.
It means that the heart is on a flat Starling curve and It means that the heart is on a flat Starling curve and
will not respond to volume expansion alone.will not respond to volume expansion alone.
We must increase the inotropy of the heart We must increase the inotropy of the heart before before we we
can use volume expansion.can use volume expansion.

19. ““Flat” Starling Curves and Inotropy IndexFlat” Starling Curves and Inotropy Index
+SV+SV +inotropy+inotropy
Left ventricular end diastolic volumeLeft ventricular end diastolic volume
StrokeStroke
VolumeVolume

20. What does inotropy tell us?What does inotropy tell us?
Left ventricular end diastolic volume = PreloadLeft ventricular end diastolic volume = Preload
Can be calculated from SMII and Stroke VolumeCan be calculated from SMII and Stroke Volume
Determines need for fluid expansionDetermines need for fluid expansion
LVEDV = (2.8/SMII) x SV + 0.05 (2.8 – SMII)LVEDV = (2.8/SMII) x SV + 0.05 (2.8 – SMII)
44
x 1.1 x 1.1
(Smith-Madigan LVEDV formula)(Smith-Madigan LVEDV formula)

21. SMII = 1.1 W/mSMII = 1.1 W/m
22
What is the LVEDV? What is the LVEDV?
StrokeStroke
VolumeVolume
Left ventricular end diastolic volumeLeft ventricular end diastolic volume
LVEDVLVEDV
SVSV

22. What does inotropy tell us?What does inotropy tell us?
To raise BP we must use a vasoconstrictor withTo raise BP we must use a vasoconstrictor with
positive inotropic propertiespositive inotropic properties
e.g. Noradrenaline (Norepinephrine)e.g. Noradrenaline (Norepinephrine)
Dopamine, Metaraminol etc.Dopamine, Metaraminol etc.

23. Tissue MarkersTissue Markers
What role do these play in pathogenesis?What role do these play in pathogenesis?
IL1?IL1? IL6?IL6? Thromboxane?Thromboxane?
TNF? TNF? NO?NO? Prostacycline?Prostacycline?
PAF?PAF? White cell proteases?White cell proteases?
Etc……Etc……

24. Tissue MarkersTissue Markers
Millions of dollars have been Millions of dollars have been
spent developing antagonists of spent developing antagonists of
tissue markers. Clinical trials tissue markers. Clinical trials
have failed to show any outcome have failed to show any outcome
benefits for their use.benefits for their use.

25. I believe that tissue markers are simply I believe that tissue markers are simply
tombstones indicating cellular damage & death.tombstones indicating cellular damage & death.

26. LactateLactate
Lactate is a product of anaerobic respiration Lactate is a product of anaerobic respiration
in the tissues – it indicates tissue hypoxia.in the tissues – it indicates tissue hypoxia.
As such, it can be used to guide therapy.As such, it can be used to guide therapy.

27. Aerobic respiration in tissues.Aerobic respiration in tissues.
All the tissues of the body need oxygen for optimal function. All the tissues of the body need oxygen for optimal function.
Therefore Therefore ANYANY indicator of normal function can be useful as indicator of normal function can be useful as
a guide to therapy.a guide to therapy.
The organs most sensitive to oxygen lack are the brain, The organs most sensitive to oxygen lack are the brain,
kidneys, heart and liver.kidneys, heart and liver.
Cerebral function, urine output and concentration, inotropy and Cerebral function, urine output and concentration, inotropy and
LFT’s all show abnormalities with intracellular hypoxia.LFT’s all show abnormalities with intracellular hypoxia.

28. Gastric Mucosal pHGastric Mucosal pH
HH
++
production in the gastric mucosa is highly production in the gastric mucosa is highly
sensitive to tissue hypoxia.sensitive to tissue hypoxia.
A rising pH in the gastric mucosa suggests A rising pH in the gastric mucosa suggests
decreased visceral perfusion and/or hypoxia. decreased visceral perfusion and/or hypoxia.
Can be used as a marker of gut perfusion.Can be used as a marker of gut perfusion.

29. DODO
22 v VO v VO
22
OxygenOxygen
DeliveryDelivery
OxygenOxygen
UsageUsage

30. Oxygen Delivery - DOOxygen Delivery - DO
22
DODO
22 = 1.34 x Hb x SaO = 1.34 x Hb x SaO
22/100 x CO/100 x CO

31. TissuesTissues
Oxygen Usage - VOOxygen Usage - VO
22
Arterial bloodArterial blood Venous bloodVenous blood
OO
22 content = content =
1.34 x Hb x SaO1.34 x Hb x SaO
22/100 x CO/100 x CO
= ~ 1,000ml/min= ~ 1,000ml/min
OO
22 content = content =
1.34 x Hb x ScvO1.34 x Hb x ScvO
22/100 x CO/100 x CO
= ~ 750ml/min= ~ 750ml/min
VOVO
22 = = A[O2] – V[OA[O2] – V[O
22]] = 1000 – 750 = = 1000 – 750 = 250ml/min250ml/min

32. Cytotoxic HypoxiaCytotoxic Hypoxia
If VOIf VO
22 is low (< 4ml/kg/min) despite adequate is low (< 4ml/kg/min) despite adequate
DODO
22 (> 12ml/kg/min) then cytotoxic hypoxia is (> 12ml/kg/min) then cytotoxic hypoxia is
present.present.
ScvOScvO
22 will be =>80% (normal ~75%) will be =>80% (normal ~75%)
(CVP sample is close enough to PA sample to use clinically)(CVP sample is close enough to PA sample to use clinically)

33. How do we treat High Output How do we treat High Output
Cardiac Failure / Septicaemia?Cardiac Failure / Septicaemia?

34. Measure haemodynamics as soon as possible. Measure haemodynamics as soon as possible.
Early septicaemia is a time bomb – Early septicaemia is a time bomb –
minutes matter and the clock is ticking.minutes matter and the clock is ticking.

35. Balancing oxygen need with oxygen deliveryBalancing oxygen need with oxygen delivery
1) Measure DO1) Measure DO
22
2) If possible, measure VO2) If possible, measure VO
22
3) Or use Lactate / pH as a surrogate of VO3) Or use Lactate / pH as a surrogate of VO
22
4) Is DO4) Is DO
22 adequate? – if not, adequate? – if not, ↑↑DODO
22
5) Is VO5) Is VO
22 adequate? – if not, adequate? – if not, ↓↓VOVO
22

36. Increasing DO2Increasing DO2
1)1) ↑ ↑SaOSaO
22 if possible. Give 100% O if possible. Give 100% O
22
2) 2) ↑↑CO if low. Keep CO =>90ml/kg/minCO if low. Keep CO =>90ml/kg/min
3) 3) ↑↑Hb if anaemia present (=>120g/L)Hb if anaemia present (=>120g/L)
4) 4) ↑BP if MAP < 80mmHg

37. Decrease VODecrease VO
22
1) Reduce pyrexia – Paracetamol iv1) Reduce pyrexia – Paracetamol iv
2) Reduce anxiety / cerebral O2) Reduce anxiety / cerebral O
22 usage – Sedate usage – Sedate
3) Reduce muscle O3) Reduce muscle O
22 usage – Paralyse usage – Paralyse
4) Consider cooling patient4) Consider cooling patient

38. 5) Use high F5) Use high F
IIOO
22 – 100% if necessary – 100% if necessary
6) Broad spectrum antibiotics – e.g. Timentin6) Broad spectrum antibiotics – e.g. Timentin
7) Calculate LVEDV – if LVEDV < 75ml/m7) Calculate LVEDV – if LVEDV < 75ml/m
22
ANDAND
SMII > 1.2 W/mSMII > 1.2 W/m
22
then volume will be required. then volume will be required.
8) If SMII < 1.2 W/m8) If SMII < 1.2 W/m
22
start inotropes start inotropes

39. Use of InotropesUse of Inotropes
If SVR If SVR ↓↓ ↓↓ then start noradrenaline at 200ng/kg/minthen start noradrenaline at 200ng/kg/min
Re-measure SMII regularly aiming at SMII > 1.4Re-measure SMII regularly aiming at SMII > 1.4
Re-calculate LVEDV aiming at 75ml/mRe-calculate LVEDV aiming at 75ml/m
22
Do not allow SVR > 750 – if noradrenaline Do not allow SVR > 750 – if noradrenaline →↑↑→↑↑SVR SVR
then then balance inotropes.balance inotropes.

40. Balancing InotropesBalancing Inotropes
Aim for SMII >1.4 W/mAim for SMII >1.4 W/m
22
If excessive vasoconstriction with a single agent then If excessive vasoconstriction with a single agent then
add in a vasodilating inotrope e.g. dobutamine.add in a vasodilating inotrope e.g. dobutamine.
Aim for MAP =>80mmHg and SVR = 700 – 750,Aim for MAP =>80mmHg and SVR = 700 – 750,
CO => 90ml/Kg/min, DOCO => 90ml/Kg/min, DO
22 > 12ml/kg/min. > 12ml/kg/min.

41. BP 74/38BP 74/38
SMII = 0.77, LVEDV = 89 ml/mSMII = 0.77, LVEDV = 89 ml/m
22
, DO, DO
22 = 2,609 ml/min = 2,609 ml/min
VOVO
22 = 387 ml/min (4.5ml/kg/min). = 387 ml/min (4.5ml/kg/min).
Action.Action.
Start Noradrenaline atStart Noradrenaline at
200 ng/kg/min200 ng/kg/min

42. BP 114/62BP 114/62
SVR high, CO low, DOSVR high, CO low, DO
22↓ to ↓ to 652ml/min, SMII = 1.13652ml/min, SMII = 1.13

Action.Action.
Add dobutamine at Add dobutamine at
8 mcg/kg/min8 mcg/kg/min

43. BP 122/66BP 122/66
DODO
22 = 1,018ml/min, SMII = 1.48 W/m = 1,018ml/min, SMII = 1.48 W/m
22
..
Action.Action.
↑↑Dobutamine 10mcg/kg/minDobutamine 10mcg/kg/min
↓↓NA to 150ng/Kg/min.NA to 150ng/Kg/min.
CO = 6.1, SMII = 1.56CO = 6.1, SMII = 1.56
DODO
22 = 1162, SVR = 744, = 1162, SVR = 744,
BP = 124/62, LVEDV = 79mlmBP = 124/62, LVEDV = 79mlm
22
VOVO
22 = 4.9 ml/kg/min = 4.9 ml/kg/min
Urine ++Urine ++
☺☺

44. Has the haemodynamic Has the haemodynamic
approach to septicaemia / approach to septicaemia /
HOCF improved outcomes?HOCF improved outcomes?

45. Haemodynamic strategy – June 2005Haemodynamic strategy – June 2005
MortalityMortality
20
16
12
8
4

46. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A,
Knoblich B, Peterson E, Tomlanovich M.Knoblich B, Peterson E, Tomlanovich M.
Early goal-directed therapy in the treatment Early goal-directed therapy in the treatment
of severe sepsis and septic shock.of severe sepsis and septic shock.
N Engl J Med (2001 Nov 8) 345(19):1368-77 N Engl J Med (2001 Nov 8) 345(19):1368-77
Reduced mortality by 34%Reduced mortality by 34%

47. They They triedtried to optimise haemodynamics in to optimise haemodynamics in
6 hours! (many took longer)6 hours! (many took longer)
We We normallynormally optimise haemodynamics in optimise haemodynamics in
under 90 minutes!under 90 minutes!

48. Optimising haemodynamics in Optimising haemodynamics in
septicaemia / HOCF saves lives!septicaemia / HOCF saves lives!
Optimising haemodynamics Optimising haemodynamics earlyearly
saves even more lives!saves even more lives!

49. Thank you!Thank you!