Rapid diagnosis of LVF in ED by non-invasive measurement of 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 ED presentations Brendan E. Smith and Veronica M. Madigan, School of Biomedical Science, Charles Sturt University, Bathurst, NSW, Australia. Specialist in Anaesthesia and Intensive Care, Bathurst Base Hospital, Bathurst, NSW, Australia.

1. Rapid diagnosis of LVF in ED
by non-invasive measurement
of inotropy.
Brendan E. Smith1,2 and Veronica M. Madigan1
1
School of Biomedical Science,
Charles Sturt University, Bathurst, NSW, Australia.
2
Specialist in Anaesthesia and Intensive Care,
Bathurst Base Hospital, Bathurst, NSW, Australia.

2. Introduction.
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 ED
presentations –
1o Cardiac Conditions – AMI, LVF, Cardiomyopathy
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, Steroids, ……

3. 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

4. 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, granny’s seaweed…..
- All of these are notoriously unreliable indicators
of cardiac function even in the hands of senior
clinicians.

5. 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!!

6. But how can we measure
inotropy in the ED?
First, we developed a formula based on haemodynamic theory
to calculate the maximum external energy output of the heart which
could be derived from clinical data which could be
easily acquired in the ED.
The basis of the formula is that the energy developed by the heart
during contraction due to it’s inotropy must appear
as some other form of energy in the circulation.
N.B. The heart follows the “all or nothing rule” –
when it contracts it gives it all it’s got at that moment and
that depends on its inotropy!

7. Conservation of Energy
The 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 could we measure PE & KE?
Would the measurement be reliable?
How long would it take?
Could we monitor Rx with it?

8. Potential Energy
PE 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 = ΔP x SV
Flow Time
ΔP = Mean Arterial Pressure - CVP / JVP,
SV and Flow Time are measured directly using CW Doppler.
(Uscom Ltd., Sydney, Australia)

9. 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.

10. 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 Vm2
2 x Flow Time
(Vm is measured by CW Doppler)

11. 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.

12. Inotropy Index
But how do we judge inotropy in patients of varying
size, e.g. large and small adults, children, infants?

13. Inotropy Index
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

14. Part 1 - Validation of SMII
We studied 250 normal patients undergoing preoperative
anaesthetic assessments 5 - 17 days prior to minor day
case surgery, who were normotensive and free of any
CVS disease or medication. (i.e. ASA1)
Age range - 3 to 74 years
Weight range - 13.5 to 104 kg
136 Female, 114 Male.
CW-Doppler studies carried out on the aortic valve,
via the suprasternal notch to measure SV and V.

15. Results
1. Mean Inotropy Index was 1.78 W/m2
(Range 1.35 – 2.24, SD = 0.16)
2. Inotropy index decreased almost linearly with age:-
Mean SMII for subjects < 35 years = 1.87 W/m2
(Range 1.83 – 2.27, SD = 0.08)
Mean SMII in patients > 50 years = 1.68 W/m2
(Range 1.56 – 2.25, SD = 0.14)
(p = 0.038)
3. There was no significant sex difference.
Normal SMII therefore defined as 1.6 – 2.2 W/m2
(mean +/- 2SD which encompassed 240 patients, 96%)

16. Part 2 – LVF Patients
83 ED patients diagnosed by Cardiologist as LVF
(NYHA criteria) +/- Echocardiography
Inotropy measured prior to any therapeutic
intervention.
Data collected by U/S examination,
BP & Hb estimation.
Data entered into bespoke computer program to
derive inotropy index from the S-M formula.

17. Results
1. Mean SMII was 0.73 W/m2
(0.43 – 0.97, SD 0.13)
2. Mean time to obtain SMII = 3.9 minutes
(1.5 – 7.6, SD 1.4)
3. No patient in the LVF group had an SMII
above 0.97 v the lowest SMII in the
control group = 1.35 (p < 0.001)

18. >2.4
60-75
8 12 14
0.62 0.97 1.13 1.38 (1.6 - 2.2)
<90
800-1200

19. Treatment
Diagnosis Ist SMII Treatment Final SMII
AMI 0.67 Dobutamine 1.53
Septicaemia 0.75 Fluids + Noradrenaline 1.54
Septicaemia 1.08 Fluids + Noradrenaline 1.62
Cardiomyopathy 0.72 Dobutamine 1.46
Hypovolaemia 1.21 Fluids 1.54
Hypovolaemia 1.26 Fluids 1.68
Pancreatitis 0.86 Fluids + Noradrenaline 1.58
SMII > 1.2 responded to fluids only.
SMII < 1.1 required an inotrope to restore normal haemodynamics
Recent work (n = 41) confirms SMII ~ 1.15 as cut-off point.

20. Conclusions.
• Measurement of Inotropy Index in ED is entirely feasible.
• Measurement typically takes less than 4 minutes.
• Inotropy Index in LVF is significantly lower than normal
controls (p < 0.001)
• Inotropy Index may aid diagnosis of LVF and guide
therapy with inotropic agents in ED.

24. Questions?