Hemodynamics - Putting the puzzle together

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.

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….

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?

Oxygen Delivery – DO2 X
Blood Pressure

X
Hb SpO2 Cardiac Output SVR

Stroke Volume Heart Rate

Preload Inotropy Afterload

To live we have to have…
Blood pressure…
and blood flow!

Blood Pressure

Blood pressure
doesn’t tell us
anything about
the heart’s ability
to deliver
oxygen!

Her blood pressure is normal.

Anybody NOT want to know her C.O. and DO2?!!
(By permission of Dr Joe Brierley, GOSH, London.)

Haemodynamics used to be
a highly invasive science…

Insertion of PA Catheter was

Difficult (especially in children)
Dangerous
Time consuming
Expensive
Of doubtful value!

All the data provided by PAC
(and more) can be obtained non-invasively…

Oxygen Delivery – DO2
Blood Pressure

Hb SpO2 Cardiac Output SVR



The Ultrasonic Cardiac Output Monitor
- USCOM

Suprasternal CW Doppler

Parasternal CW Doppler

What other data do we get?
Vpk = Peak Ejection Velocity

CO / CI = Cardiac Output / Index

Why Cardiac Index v Cardiac Output?

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…

MD = Minute Distance = Aortic Velocity

SV = Stroke volume
Ejection Time + SV = Inotropy

SVR = Systemic Vascular Resistance

Central Venous Oxygen Saturation

Afterload
Depends on:
Degree of vasoconstriction / dilation
Density & viscosity of blood
Flow rate of blood / surface tension forces
Elasticity of arteries
Stroke volume
……

These are all the same factors
that determine mean aortic root
pressure…
So afterload is exactly the same as mean
aortic root pressure.
MAP = diastolic + ⅓ (systolic – diastolic)
But can we use radial artery pressure?

Integrated Pressure
P2

ΔP

P1
Δt
t P2
Mean Pressure = ∫ P1 P.dt
= Pressure time integral = Pti

time

Pti-Aortic and Pti-Radial are close enough
in clinical practice to make no significant
difference to haemodynamic calculations.
(error typically <5%)

Oxygen Delivery – DO2
Blood Pressure

(Hb) SpO2 Cardiac Output SVR



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

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, ……

Why is inotropy so important?

BP = SVR x HR x SV : SV x HR = CO.


Fluid loading Blood Pressure

Power of the heart

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.

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!!

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 can we measure PE & KE?
Is the measurement reliable?
How long does it take?
Can we monitor Rx with it?

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 = MAP x SV
Flow Time
ΔP = Mean Arterial Pressure - CVP
SV and Flow Time are measured directly using
CW Doppler.

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.

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)

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.

Inotropy Index
But 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

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

Cardiogenic Shock
74 year old man with STEMI
BP 84/44, pulse 114, SpO2 84% on 10L/min O2
Pulmonary Oedema +++
No urine output
PaO2 64mmHg, PaCO2 28mmHg
Lactate 8.4

>2.4

60-75

8 12 14 Dobutamine mcg/kg/min
0.62 0.97 1.13 1.38 SMII W/m2

<90

800-1200

Preload
JVP / 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.

Pulmonary artery catheter
What 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, pulmonary
vascular patency, vasoconstriction, shunts,
arrythmias, mitral valve problems….etc.

PAC
Attempts to measure left ventricular end
diastolic pressure - LVEDP

Left ventricular preload is strictly the left
ventricular end diastolic volume – LVEDV

Ventricular end diastolic pressure only acts
as an acceptable surrogate if we know the
ventricular compliance.

Can basic physiology help us?
Inotropy

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.

OK, this is all very clever stuff but
does it make any difference to
patient outcomes?

Haemodynamic strategy – June 2005

20

16

12

8 Mortality

4

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!...

Hemodynamics - Putting the puzzle together

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