|
A & P Back
to Basics |
Page 2 |
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Principles of
Haemodynamic Monitoring |
Page 7 |
|
Shock |
Page 11 |
|
Pulmonary
Artery Flotation Catheters - Swans |
Page17 |
|
Principles of
Inotropes |
Page 24 |
|
PiCCO |
Page 37 |
I Hope you find this booklet valuable and are able to
use it for your own reference or when teaching others.
More information is accessible through my website at:
http://www.rocket.pwp.blueyonder.co.uk/
Please feel free to contact me through the “E Mail”
link on the website or directly on the ITU on Ext 2400 if you have any problems
or queries.
Cardiac output is the rate which the heart pumps blood,
often defined as: The volume of blood pumped out of the left ventricle into the
aorta in one minute.” This is calculated by multiplying the Stroke volume (the
volume of blood pumped out with each contraction) by the heart rate.
Therefore Cardiac output (CO) = Stroke
volume (SV) x heart rate (HR)
For example an adult at rest has a heart
rate of about 72 beats/min and a stroke volume of 70mls therefore CO = 72 x 70
= 5 litres per minute.
At rest normal cardiac output is about 5
litres per minute.
This can increase to 25
litres/min during exercise or 35 litres for an athlete. When an
increased cardiac output is needed to supply other organs e.g. the gut during
digestion or muscles during exercise it is achieved by increasing the heart
rate or the stroke volume.
The mechanisms by
which the HR & SV can be altered.
A. Control of the Heart.
In the absence of nervous or hormonal
control the sinoatrial node discharges spontaneously and rhythmically @ 100
beats per minute
Factors altering the heart rate: -
1. Nervous:
Most important is the influence of the
autonomic nervous system. The heart is supplied by both the sympathetic and
parasympathetic nerves.
Sympathetic nerves to the heart originate
in the cardiovascular centre (group of neurones within the medulla) these
affect the SA node, AV node and portions of the myocardium. Stimulation causes
an increase in heart rate.
Parasympathetic nerves to the heart (vagus nerve)
also originates in the medulla. This affects SA node And AV node. Stimulation
causes decrease in the heart rate.
At rest HR is usually 60 to 80 / minute.
This is rather less than the inherent rate of the discharge of the cardiac
pacemaker (SA node) Therefore at rest the parasympathetic influence is
dominant.
Primarily the heart rate is regulated by
the slowing effects of the parasympathetic and the accelerating effects of the
sympathetic.
2. Hormonal
Adrenaline (released from the adrenal
medulla) causes increase in heart rate by stimulating the b receptors in the
cardiac muscle conduction system.
3. Stretch: -
The stretching of the left atrium wall by
increased venous return causes increase in heart rate by 10 to 15 % because
stretch receptors in the atrial wall/superior vena cava and the inferior
venacava send impulses that stimulate sympathetic output this is called the Bainbridge
Reflex.
4. Temperature.
Rise in temperature causes increase in HR
because it increases the rate of discharge from the SA node. Converse also
applies.
5. Drugs.
To increase the HR -
Isoprenaline / Adrenaline.
To reduce to HR -
Beta-blockers e.g. propanolol.
The HR is also sensitive to plasma
electrolyte concentrations and hormones other than adrenaline.
The heart rate is usually faster in
females and declines with age.
B Control of
Stroke Volume.
In the normal heart the most important
factor that controls the amount of blood pumped from a ventricle with each
heart beat (Stroke Volume) is the amount of blood in the ventricle immediately
before contraction. This is called the ventricular end diastolic volume. V.E.D.V.
The more blood in the ventricles the
greater the amount pumped -Starlings Law: The force of the muscle contraction is
proportional to the initial muscle fibre length (i.e. Stretch).
1 Venous
Return.
The force of contraction adjusts
according to the volume of blood in the ventricles this is called auto
regulation.
Blood volume: - reduced circulating
volume e.g. Due to bleeding leads to reduced venous return.
The position of the person e.g.
Trendelenburg, will increase venous return.
Intrathoracic pressures caused by
I.P.P.V. Will reduce venous return.
2. Nervous.
Sympathetic nervous stimulation increases
ventricular and atrial contractility.
Normally when the
ventricles contract they do not empty completely.
When contractility improves, the ventricles empty more completely therefore
increasing SV.
Sympathetic stimulation not only causes a
more forceful contraction but also a more rapid contraction. This is important
when an increase in HR reduces the time available for diastolic filling of the
ventricles; because if contraction can be made more rapid there will be a
larger fraction of the cardiac cycle available for filling, and coronary blood
flow during diastole.
Drugs affecting
contractility.
Inotropic
drugs.
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Those increasing contractility are called positive e.g. dobutamine and
adrenaline
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Those decreasing contractility are called negative inotropes e.g. b blockers.
3
Hormonal Regulation: - Circulating
catecholamines, adrenaline& noradrenaline produce changes in myocardial
contraction (and hence in S.V.)
4
Arterial Blood Pressure: - An increase in the
resistance to the ejection of blood from the ventricles can reduce the S.V.
This is caused by the ability of the large arteries to expand and contract.
This is called Afterload. Arterial blood pressure gives an indication of the
degree of
afterload.If
the B.P. is high and the force of contraction is constant then the ventricles
will not empty as much and S.V. will be reduced.
In
a normal heart changes in blood pressure do not affect the overall cardiac
output as the heart can self adjust.
Drugs
that can reduce afterload are nitrates like Isoket.
Summary: - A normal functioning heart will pump out all of
the blood that is returned to it from the veins. Therefore venous return is the
prime factor in determining cardiac output, and vice versa.
Basic principles of fluids, pressure,
flow & resistance.
All
fluids when in a confined space exert a pressure.
Hydrostatic
pressure refers to the force that a fluids exerts
against the walls of it’s container.
The
pressure that blood exerts in the vascular system is called: -
Blood
Pressure
BP
Is the result of blood flow and vascular resistance.
Blood
Flow: - The circulation is a closed system
therefore total flow leaving the heart must equal the total flow returning to
the heart - This blood flow equals cardiac output.
Blood
pressure = cardiac output X total peripheral resistance
B.P.
Can be maintained or altered by manipulation of cardiac output and or total
peripheral resistance.
Systolic
pressure: - is determined by the amount of blood
being forced into the aorta or arteries with each ventricular contraction i.e.
The S.V. and the force of the contraction. Increase in either will raise
systolic pressure and vice versa. Also increase in afterload caused by vascular
disease will also raise systolic pressure. In old age the vascular tree is more
rigid so systolic hypertension is common.
Diastolic
pressure: - This reflects peripheral resistance.
If
there is vasoconstriction the diastolic will rise.
If
there is vasodilation the diastolic will fall.
Drugs
to vasodilate e.g. hydralazine will ¯
diastolic pressure.
If
the heart rate falls then the diastolic will fall as there is an increased time
for the blood to flow out of the arteries (& vice versa)
The
difference between the systolic and diastolic is called the Pulse Pressure.
Mean
Arterial Pressure:-
This represents the pressure driving blood through the systemic circulation.
This is estimated by adding 1/3 of the pulse pressure to the diastolic
pressure.
If
BP = 120/70mmHg Then Pulse pressure =
50 mmHg
1/3
of 50 = 17
Add
17 to the diastolic of 70 = 87
Therefore
M.A.P. = 87mmHg.
Glossary
Afterload
= The resistance of the ejection of blood offered by
the systemic circulation
Cardiac
Output = The amount of blood ejected by the left
ventricle in one minute
Contractility
= The ability
of myocardial cells to contract (shorten) in response to an electrical impulse.
Oxygen
consumption = The amount of oxygen used by the tissues in one minute.
Oxygen
delivery = The amount of oxygen delivered to the
tissues in one minute.
Preload
= Ventricular end diastolic pressure
Pulmonary
capillary wedge pressure =
Reflects left ventricular end diastolic pressure
Stroke
volume = Volume of blood ejected per ventricular contraction.
Systemic
vascular resistance = MAP
- CVP X 80
CO
Principles of
haemodynamic monitoring
Haemodynamic monitoring refers to the
monitoring of blood flow and pressure within the cardiovascular system.
Indirect monitoring usually suggests a non invasive method of assessment i.e. a
manual BP recording with a sphygmomanometer. Direct or invasive monitoring
involves cannulating the patient and allows the continuous and ongoing
assessment of critical pressures associated with cardiovascular function. In
short Direct monitoring provides the most accurate
physiological data in the I.C.U.
For monitoring purposes in the ICU three
components are needed:-
1. A catheter or cannula of some kind
2. A transducer- to provide the
conversion of the pressure into an observable waveform
3. A monitor- to display and store the
data
All pressure monitoring systems need to
be connected to an IV solution to it to stop the line and catheter from
becoming occluded. The fluid in the line is pressurised to 300mmhg by the use
of a pressure bag; this is to prevent back flow of blood up the line and into
the solution itself.
Nursing management of
pressure lines
Each ICU has it’s
own protocol for the care of IV pressure lines though nurses must be able to
recognise fundamental issues related to their management. These are mainly
issues of infection control bleeding and embolic complications.
Safety and emergency
procedures - pressure lines
1. Don’t become complacent ....arterial
lines and Swan-Ganz catheters are common place in most ICU’s and nurses are
very familiar with their uses etc. However ...these lines carry potential fatal
consequences for the patient if they are not managed correctly
2. Always ensure that you can see the
line- a patient in the ICU who is critically ill may have 10 or more infusions
going at once!...they can easily become knotted and twisted and confusingly
spaghetti-like! If the line is an arterial one inserted into a radial artery or
dorsalis pedis (foot) You must be able to see the line at all times. Should the
line be hidden under the sheets the patient could have become inadvertently
disconnected and be slowly (or if their BP is good)....quickly ...exhanguinating!!
3. Observe all sites for signs of
infection
4. Assess the patients overall general
condition ...not just the data on the chart
5. NEVER EVER ALLOW INJECTIONS TO BE
GIVEN INTO ARTERIAL LINES. In the ICU we like to think we give safe and
effective INTRAVENOUS injections not INTRAARTERIAL ones....(
Which can cause immediate arterial sclerosis and ischaemia leading to the
patient requiring amputation )
Make doubly sure that your injection
ports on an arterial line are blanked off with a small blank cap....not an
injection bung!!
6. Secure all lines firmly to the patient
and inform the patient of it’s purpose and function.
Wherever practical mark the lines
“ARTERIAL”
7. No air please!!!.....not even a tiny
bit!
The haemodynamic
profile.
A haemodynamic profile can be extremely
useful in building up a picture of the patients overall cardiovascular
function. The reason for the degree of dysfunction are many, though it is
reasonable to say that a patient requiring continuous haemodynamic monitoring
will have one or more of the following conditions:
Cardiac
failure
Pulmonary
oedema
Respiratory
failure
Major
trauma
Sepsis
Profoundly
shocked
Why do we need
haemodynamic monitoring?
To
determine the effectiveness of cardiovascular function
As
an evaluation of treatment (particularly inotropes)
As
an assessment of their volaemic state (i.e. burns and
trauma)
A typical haemodynamic
profile.
Systemic
arterial pressure i.e. systolic and diastolic
Mean
arterial pressure usually 80 - 90 mmHg
Central
venous pressure (or right atrial pressure)
4 - 10 mmHg (12 – 15
mmHg IPPV)
Pulmonary
artery pressure
15 - 25 mmHg systolic
8 - 10 mmHg diastolic
Pulmonary
artery wedge pressure
6 - 12 mmHg (10 – 17 mmHG IPPV)
Cardiac
output
4 - 8 litres/minute
Cardiac
index
2.5 -4.2 l/min/m2
Systemic
vascular resistance (or SVR)
900 - 1600
dynes/sec/cm5
Pulmonary
vascular resistance
20 - 120 dynes/sec/cm5
Stroke
volume
60 - 100 ml
Calculation of
haemodynamic parameters.
Mean arterial pressure
Diastolic
X 2 + Systolic
3
Systemic vascular
resistance
(Mean
arterial pressure - CVP) X80
Cardiac
output
Pulmonary vascular
resistance
(Mean
PA pressure - Wedge X80
Cardiac
Output
Shock
!!!
DEFINITION:
- Inadequate
delivery of oxygen to the tissues.
“ A
syndrome characterised by a reduction in blood flow and inadequate perfusion,
leading to tissue hypoxia and failure of cell function”
There are five types of shock:-
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ANAPHALACTIC
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HYPOVOLAEMIC
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NEUROGENIC
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CARDIOGENIC
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SEPTIC (Distributive)
Hypovolaemic Shock.
Caused by a reduction
in circulating volume. The body can cope
with a loss of 10 to 15 %.
Causes:
-
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HAEMORRHAGE
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DEHYDRATION
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BURNS
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ASCITES, PERITONITIS
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EXCESSIVE DIURESIS
Clinical
Features