High Output Cardiac Failure The tissues, not the heart, determine cardiac output by controlling local blood flow through vasodilation in response to changes in oxygen and carbon dioxide levels. As vascular resistance decreases, stroke volume increases, maintaining blood pressure. A high cardiac output becomes "high output failure" when blood pressure cannot be maintained against low systemic vascular resistance, or oxygen delivery is insufficient. The diagnostic triad is high cardiac output, low blood pressure, and very low systemic vascular resistance. Treatment focuses on balancing oxygen delivery and demand by optimizing preload, contractility, and afterload through fluid administration and inotropic support tailored to individual hemodynamic parameters.

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. 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 heart
that determine cardiac output.

3. Ohms Law and The Circulation

4. BP = CO x SVR
Any in CO SVR
Any in SVR CO
So BP tends to remain stable

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. The stroke volume automatically increases as the afterload
reduction makes ejection easier.
If SVR↓↓ then BP will fall and sympathetic responses will
increase 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. As SVR falls,
CO rises and
BP remains
stable.
SVR d/s/cm-5
Cardiac Output L/min

8. Initially, the fall in SVR can be compensated by an increased
Cardiac 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. 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. 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. Aortic Minute Distance
= mean aortic flow velocity
Immediately shows if the circulation is
Hyperdynamic (>22 m/min)
Normodynamic (14 – 22 m/min)
Hypodynamic (<14 m/min)

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. 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. PE : KE Ratio - PKR
PE = 0.62 W/m2 KE = 0.15 W/m2
PE:KE Ratio (PKR) = 4:1
Normal ratio ~ 30:1
A much greater fraction of cardiac work is going into
blood flow than normal. This is typical of septicaemia.

15. Hallmarks of Septicaemia
BP = 74/38
Hyperdynamic
High Stroke Volume
High Cardiac Output
Low SVR
High DO2
Low inotropy index
Low PKR

16. N.B. Paediatric Septicaemia
is very different…
Hypodynamic
SV is low
CO/CI is low
SVR is high

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. 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. “Flat” Starling Curves and Inotropy Index
Stroke
Volume
+SV +inotropy
Left ventricular end diastolic volume

20. What does inotropy tell us?
Left ventricular end diastolic volume = Preload
Can be calculated from SMII and Stroke Volume
Determines need for fluid expansion
LVEDV = (2.8/SMII) x SV + 0.05 (2.8 – SMII)4 x 1.1
(Smith-Madigan LVEDV formula)

21. SMII = 1.1 W/m2 What is the LVEDV?
Stroke
Volume
SV
LVEDV
Left ventricular end diastolic volume

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

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

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

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

29. DO2 v VO2
Oxygen Oxygen
Delivery Usage

30. Oxygen Delivery - DO2
DO2 = 1.34 x Hb x SaO2/100 x CO

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

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

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. Increasing DO2
1) ↑SaO2 if possible. Give 100% O2
2) ↑CO if low. Keep CO =>90ml/kg/min
3) ↑Hb if anaemia present (=>120g/L)
4) ↑BP if MAP < 80mmHg

37. Decrease VO2
1) Reduce pyrexia – Paracetamol iv
2) Reduce anxiety / cerebral O2 usage – Sedate
3) Reduce muscle O2 usage – Paralyse
4) Consider cooling patient

38. 5) Use high FIO2 – 100% if necessary
6) Broad spectrum antibiotics – e.g. Timentin
7) 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. Use of Inotropes
If SVR ↓↓ then start noradrenaline at 200ng/kg/min
Re-measure SMII regularly aiming at SMII > 1.4
Re-calculate LVEDV aiming at 75ml/m2
Do not allow SVR > 750 – if noradrenaline →↑↑SVR
then balance inotropes.

40. Balancing Inotropes
Aim for SMII >1.4 W/m2
If 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. 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. SVR high, CO low, DO2↓ to 652ml/min, SMII = 1.13
BP 114/62 Action.
Add dobutamine at
8 mcg/kg/min

43. DO2 = 1,018ml/min, SMII = 1.48 W/m2.
Action.
↑Dobutamine 10mcg/kg/min
BP 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. Has the haemodynamic
approach to septicaemia /
HOCF improved outcomes?

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

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. They tried to optimise haemodynamics in
6 hours! (many took longer)
We normally optimise haemodynamics in
under 90 minutes!

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

49. Thank you!