Contents
|
A & P Back
to Basics |
Page 2 |
|
Principles of
Haemodynamic Monitoring |
Page 7 |
|
Shock |
Page 11 |
|
Pulmonary
Artery Flotation Catheters - Swans |
Page17 |
|
Principles of
Inotropes |
Page 24 |
|
PiCCO |
Page 37 |
Introduction
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.
Back To Basics
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.
w
Those increasing contractility are called positive e.g. dobutamine and
adrenaline
w
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:-
w
ANAPHALACTIC
w
HYPOVOLAEMIC
w
NEUROGENIC
w
CARDIOGENIC
w
SEPTIC (Distributive)
Hypovolaemic Shock.
Caused by a reduction
in circulating volume. The body can cope
with a loss of 10 to 15 %.
Causes:
-
w
HAEMORRHAGE
w
DEHYDRATION
w
BURNS
w
ASCITES, PERITONITIS
w
EXCESSIVE DIURESIS
Clinical
Features
w
HYPOTENSION
w
TACHYCARDIA
w
SWEATING COLD AND
CLAMMY
w
OLIGURIA
w
REDUCED L.O.C.
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TACHYPNOEA
w
CYANOSIS
w
HYPOTHERMIA
w
DYSRYTHMIA
w
THIRST
w
N & V
Hypotension:
- Reduced venous return ®
reduced SV ®
reduced CO ®
Hypotension.
Tachycardia: -
Reduced BP reduced stimulation of the carotid baroreceptors
®increased
sympathetic activity of the cardiovascular centre in the brain ®
increase in HR.
Sweating
Cold and Clammy: -
sympathetic stimulation leads to peripheral vaso
constriction (stimulation of alpha receptors) also causes stimulation of sweat
glands.
Oliguria:
-Vasoconstriction ®
reduced renal blood flow therefore reduced filtration and reduced urine output.
Renin is released (Quick reminder of the renin angiotensin pathway-)
Renin
- enzyme that splits angiotensinogen into angiotensin I Angiotensin I is
converted into Angiotensin II under the influence of
A.C.E. Angiotensin II causes the secretion of aldosterone from the adrenal gland allowing Na and water to
be retained to increase circulating volume, further reducing urine output.
In response to stimulation of osmo and volume receptors A.D.H. is released this allows
more water to be retained by increasing the permeability of the distal tubules.
Results in an increase in circulating volume and therefore BP
Reduced
L.O.C: - Confusion caused by cerebral hypoxia.
Tachypnea: -
Reduced oxygen to the cells ®
anaerobic metabolism ®
increase in lactic acid production ®
lactic acidosis. Central chemoreceptors sense the
increase in hydrogen ions therefore stimulates the respiratory centre in the
brain to increase the respiratory rate in order to “blow off” excess
hydrogen H+ HCO3 «
H2CO3 «
H2O + CO2
Reduced oxygen level in the blood also
stimulates the resp. Centre to increase rate.
Cyanosis:
- Reduced peripheral oxygen. Increased
amounts of reduced haemoglobin of more than 5g/dl = blue.
Hypothermia:
-
Anaerobic metabolism does not create much heat
therefore leading to reduction of core body temperature.
Dysrhythmia Kidneys
retain potassium to excrete hydrogen. Hyperkalaemia
causes Dysrhythmia. Reduced coronary artery blood flow leads to ischaemia. Lactic
acid is also cardiotoxic.
Thirst:-It
is thought that osmoreceptors and A.D.H. production
stimulates the “thirst “ centre in the brain.
N&V:
- Due to reduced blood flow to the G.I.T.
Causing ¯
G.I.T. Activity this could also lead to stress ulceration. Acidosis also makes
one feel nauseous.
This list is not exhaustible and some of
the reasons may be debatable.
In our ITU we tend to see three of the
main causes of shock that require invasive haemodynamic monitoring, so we will
look at these in a little more detail.
Management
of hypovolaemic shock: -
Oxygenation
-
Main problem is that of hypoxaemia therefore 100%
oxygen is needed and early I.P.P.V. should be considered. Although I.P.P.V. May
worsen hypotension due to the increase in intrathoracic
pressure causing a reduced venous return.
Fluids
- circulating volume, replace lost
fluids, good I.V. access is needed use of colloids and Blood. Stop further loss
of fluid e.g. Go to theatre if A.A.A.
Monitoring
-
Arterial line, C.V.P. E.C.G. Urine output, pulse oxymeter
blood gases, monitor L.O.C.
Once fluid level is optimum may need
inotropes.
Treat underlying cause.
Complications:
-
i.
Renal failure: - acute
tubular necrosis (A.T.N.)
ii.
A.R.D.S.
iii.
Heart failure / dysrhythmias due to ¯
cardiac output
iv.
G.I.T. Ischaemia -
stress ulceration
v.
Liver failure ¯
detoxification and ¯
clotting
vi.
D.I.C.
Cardiogenic Shock: - End
stage of heart failure, Shock due to dysfunction of the heart and pump failure.
Causes:
-
v
M.I.
v
Tamponade
v
Myopathy
v
Arrhythmia
v
Following cardiac surgery
e.g. Heart transplant
v
Chest trauma
v
Mitral
and Aortic regurgitation
v
Infection
Treatment:
- prognosis is very poor. Mortality of 80 - 90%. Try to treat the underlying cause to
prevent shock from occurring.
Swan
Ganz Catheter: - To monitor the effect of inotropes
and fluid therapy. Use of nitrates to ¯ afterload and
hopefully increase cardiac output. Less resistance in the aorta allows
for a bigger to S.V. to occur.
Intra
Aortic Balloon Pump (I.A.B.P.): -
Inflates at the start of diastole and forces blood into the coronary artery
system. During systole it deflates and the sudden drop in pressure reduces
afterload and allows for a larger stroke volume.
Surgery:
- to remove the underlying cause e.g. Emergency C.A.B.G. Aneurysm repair etc.
SEPTIC SHOCK. (Distributive Shock)
In a previously fit and well person
“septic” shock has a mortality rate of 50%, which is even higher if there is a
significant existing morbidity
Clinical
features: - Septic shock occurs in two distinct but
overlapping phases.
Warm
Shock (hyperdynamic): -
This is the first stage of septic shock and is characterised by a high cardiac
output and a low vascular resistance. Vasodilation
causes a relatively reduced circulating volume together with an increased
capillary permeability, results in a rapid hypotension despite a high cardiac
output. Fever and chills may develop as an immune system response and urine
output may fall. However if compensating mechanisms are present then it may be
difficult to first see the potential danger, as the patient looks well perfused. An increase in circulating catecholamines
causing blood pressure to be normalised.
Cold
Shock (hypodynamic): -
This is a late presentation and often irreversible phase of septic shock. It is
characterised by vasoconstriction, hypotension, hypoperfusion
decreased venous return and decreased cardiac output. The symptoms may include:
-
w
A rapid thready pulse
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Cold clammy skin
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Subnormal or elevated
temperature
w
Depressed level of
consciousness
Eventually patients with cold shock
develop multiple system failure e.g. A.R.D.S., D.I.C., liver and kidney
failure.
A comprehensive description of the pathophysiology of septic shock is beyond the scope of this
guide - as there is still debate, discussion and research being done in this
complex field.
What we can say is that the events that
lead from sepsis to full blown septic shock are probably initiated by the
presence of a large number of bacteria, which have not been controlled by the
immune response.
The problems are caused by endotoxins
that are released when the bacteria are destroyed and the cell membranes are
broken down
Endotoxins
stimulate the release of various vaso active
substances: - including histamine and prostaglandin. These potent vasodilators
cause a decrease in peripheral vascular resistance and an increase in capillary
permeability, allowing fluid to enter the interstitial spaces from the
intravascular spaces resulting in volume depletion and relative hypovolaemia.
Management:
-
1.
Identify and treat the
underlying cause. The patient may need U.S.S., C.T., B.A.L. Blood cultures,
surgery or a line change. In an ideal world antibiotics should not be started
until sensitivity is obtained. Practically cultures are sent than blind
antibiotics are commenced
2.
Oxygen therapy usually
I.P.P.V. A.R.D.S. is a common
complication of this condition patients have a high oxygen requirement and
there are bilateral lung field infiltrates on the chest X Ray that look like
pulmonary oedema however a normal P.A.W.P. indicates a non cardiogenic
cause
3.
Invasive monitoring
using a Swan Ganz catheter.
4.
Replace circulating
volume using colloids other clotting factors and blood may be needed.
5.
Inotropes to increase
vascular resistance and blood pressure. These can be titrated according to
cardiac output measurements.
6.
Support of failed
renal system with H.D./H.F.
7.
Psychological care of
the patient and family. The patient may be very anxious if he is not already
sedated and families need a lot of reassurance and explanation of current
treatment and progress or deterioration.
8.
Good life
insurance!!!!!!
A
Bit of History
The
pulmonary artery flotation catheter.
During the late
60’s and early 70’s Drs H.J.C. Swan and William Ganz developed a balloon tipped
flotation catheter. The function of the catheter was to be able to continuously
measure at the bedside certain intracardiac pressures. Before this the patient
would have to have been transferred to a cardiac catheterisation lab; and then
only intermittent measurements would be obtained.
By floating a flexible catheter into the pulmonary
artery and using a balloon to occlude it then indirect measurements can made of
the pressure in the left ventricle.
Since the
initial design there have been many modifications so that now we are able to
continuously measure cardiac output and venous oxygen saturation, as well as
infuse drugs and measure right-sided heart pressure.
Incidentally
the first Swan Ganz catheter to be inserted in this country was done in a
What
is a Wedge?
Pulmonary
Artery Wedge Pressure:- When the tip of the Swan is properly
positioned in the PA, a wedge pressure can be obtained. By inflating the
balloon the tip will “float” into a smaller branch of the PA and occlude
forward flow. When this occurs there is an unrestricted vascular chamber from
the pulmonary artery through the pulmonary vascular system, the pulmonary vein,
the left atrium, the open mitral valve and the left ventricle. therefore the theory is, the pressure in front of the
occluded catheter tip is the same as the pressure in the left ventricle during
diastole (because this is the time when all of the valves are open and the
heart is filling with blood)
Nursing responsibilities during insertion
of a Swan Ganz Catheter.
1. Ensure the comfort of the patient
2. Make sure the transducer is flushed and
re zeroed and ready to read P.A.
3. Observe the monitor for signs of dysrhythmias
4. Observe the waveforms as the catheter
passes through the different chambers of the heart
Nursing Care: -
Nursing care of
the patient with a “Swan” is complex; the nurse must be able to interpret the
data obtained as well as being able to alert medical staff of potential or
actual complications.
1. Prevention of infection is paramount
2. The position of the tip may change
forward migration will be indicated by a wedge trace with a deflated balloon spontaneous wedging, this may cause
pulmonary infarction. Notify a doctor to reposition the catheter.
3. Over inflation of the balloon may cause
the PA to rupture, prolonged inflation may result in pulmonary infarction and
insertion of air into a ruptured balloon could cause an air embolus.
4. Inflation of the balloon should be done
slowly while observing the pressure tracing on the monitor. When the pressure
changes from PA to Wedge no more air should be inserted. There should be a
slight resistance felt, if there is no resistance and a wedge trace can not be
obtained then a balloon rupture should be suspected. The syringe should be
therefore labeled as ruptured and medical staff informed.
5. After wedging the catheter always make sure the monitor returns to a PA trace.
The clinical
information obtained from invasive pressure monitoring is truly beneficial in
the care of the critically ill patient. The role of the nurse in the prevention
and detection of complications is pivotal.
Nursing
management of these patients does not begin and end with writing numbers on a
chart the psychological care of the patient and their families is very
important, they will ask questions want to know what you are doing and what all
of the numbers mean .So you need to confident in your ability to explain to
them what, why and when !!!! In a way they will
understand.
CHARACTERISTIC
INTRACARDIAC PRESSURE WAVEFORMS DURING THE INSERTION OF A SWAN GANZ CATHETER.
|
Site |
Pressure (mmHg) |
|
Right
atrium Mean |
0-7 |
|
Right
Ventricle Systolic End
diastolic |
15-25 0-8 |
|
Pulmonary
artery Systolic Diastolic Mean |
15-25 8-15 10-20 |
|
Pulmonary
Artery Wedge Mean |
6-12 |
These are “
Remember to add
5 mmHg plus PEEP for ventilated patients.
Troubleshooting
guide !!!
|
Problem |
Possible cause
|
Nursing
actions |
Rationale |
|
Damped pressure trace: Shows as low
amplitude tracing (low systolic/high diastolic pressure) |
Clot occluding
catheter Catheter
kinked touching the vessel wall, or malpositioned Air in the
system Blood on the
transducer Equipment
fault/error |
Check patency
by aspirating: continue until blood flows back easily then flush. If no blood
can be aspirated do NOT flush. Ask the
patient to cough deflate the balloon and gently flush, may need medical staff
to reposition. Check X ray Check flush
bag and obtuarators for bubbles Flush the
system check the pressure bag Check taps are
open correctly and that settings on the monitor are correct |
Risk of
pulmonary emboli. All clots should be cleared. Risk is minimized by use of a
constant flushing system and. An occluded catheter should be removed. Coughing and
flushing may help displace the catheter Air will
distort readings Blood on the
transducer will distort readings Methodical
checking can be very revealing! |
|
Wedge pressure unobtainable |
Monitoring problem Balloon
over/under inflated Balloon
rupture Catheter
displaced Monitor may be
still set on Zero |
Contact
technician Deflate
balloon and reinflate No resistance
to inflation. Do NOT inject Inform medical
staff to reposition Check settings |
Over inflation
may cause vessel damage or balloon rupture. Risk of air embolus Risk of air
embolus Catheter may
require repositioning or replacing |
|
Sudden changes in pressures or
configuration |
Patient in
pain or agitated. Transducer not
at correct level. Catheter
displaced spontaneous wedging |
Ensure
adequate sedation or analgesia reassure patient to ally anxiety Re Zero Inform medical
staff to reposition |
Pressures may
rise in response to pain Should be done
regularly Risk of
pulmonary infarction |
|
|
(Diagram taken from “Invasive
Haemodynamic Monitoring: Physiological Principles and Clinical Applications” –
Baxter)
Why!?
Most I.T.U. patients will probably have a P.A. catheter inserted at
some point during their stay. The main reason being
cardiovascular instability due to shock of one kind or another.
We have established our “basics” now we
will look at how the P.A. Catheter can help make accurate diagnoses and enable
the titration of vaso active drugs.
Cardiac Output Measurement Using The Thermodilution Method.
In the early
1950’s, Fegler first described measuring cardiac output using the
thermodilution method. It was not until the early 1970’s that Drs Swan and Ganz
demonstrated reliability of this technique with a special temperature sensing
pulmonary artery catheter. Since that time the thermodilution method has become
the standard for clinical practice.
The
thermodilution method uses a known amount of solution (10 mls of 5% dextrose)
at a known temperature (room air), which is then rapidly injected into the C.V.P. Lumen of the Swan.
This cooler solution mixes with and cools the blood, and the temperature is
measured downstream by a thermistor bead embedded in the tip of the catheter.
The resultant change in temperature is then plotted on a time-temperature
curve.
A normal curve
will characteristically show a sharp upstroke from the rapid injection followed
by a smooth downslope back to the baseline. The area under the curve is
inversely proportional to the cardiac output. The computer in the monitor uses
an equation to make the exact calculation. Usually several measurements are
made and an average result taken.
There are
conditions where the thermodilution method may produce unreliable results for
example those that have a back flow of blood on the right side; tricuspid or
pulmonary valve regurgitation and ventricular or atrial septal defects.
Direct Measurements: -
v
Heart
Rate
v
Blood
Pressure
v
Pulmonary
Artery Pressure
v
Central
Venous Pressure
v
Cardiac
Output
Derived Parameters: -
v
Mean
Arterial Pressure
v
Cardiac
Index
v
Stroke
Volume
v
Systemic
Vascular Resistance
v
Pulmonary
Vascular Resistance
v
Stroke
Work Index
|
Cardiac Index Cardiac Output |
205 – 4.2 L/min/m2 4 – 8 L/min |
|
Heart Rate |
70 – 120 beats/min |
|
Mean Arterial Pressure |
70 – 90 mmHg |
|
Mean pulmonary artery pressure |
< 30 mmHg |
|
Right Atrial pressure (CVP) |
12 – 20 mmHg |
|
Pulmonary artery wedge pressure |
12 – 20 mmHg |
|
Systemic vascular resistance (SVR) |
900 – 1600 dyne/sec/cm5 |
|
Pulmonary vascular resistance (PVR) |
20 – 120 dyne/sec/cm5 |
|
SvO2 |
70 – 75% |
Inotropes.
General Principles: -
i.
Defence
of blood pressure in critically ill patients forms the
basis of haemodynamic resuscitation and organ perfusion.
ii. Hypovolaemia is the most common cause of hypotension
and low cardiac output in critically ill patients and must be assiduously
monitored and corrected.
iii. The main indication for inotropes is to
increase myocardial contractility for a given preload or afterload.
Unresponsive to fluid replacement therapy.
iv. MAP and CO should be interpreted within
the context of the pre morbid state.
v. The use of inotropes in anything other
than tiny doses requires invasive monitoring with an arterial line and a PA
catheter.
vi. Inotropes primarily increase cardiac
output and MAP however all of these agents have variable effects on heart rate
and vascular resistance, which are neither predictable nor constant.
vii. No single drug or combination has been
proved to be superior to another.
Mechanism
of different Inotropes.
Digitalis
Glycosides: - Inhibits Na+ and K= pump and causes
impaired transport of Na+
and K+ out of the cardiac cell.
This leads to a rise in intracellular Na+
Na+ is exchanged for Ca++
Increases intracellular Ca++ leads to
Increased
contractility.
Catecholamines:-( dopamine, noradrenaline, and
adrenaline) Stimulate sympathetic receptors
(Different doses of these drugs affect
receptors in different ways however in low doses b effects dominate) Stimulation of b1 receptors results in Increased contractility.
Phosphodiesterase inhibitors:-( e.g.
Enoximone) Phosphodiesterase is an enzyme that converts active cAMP into
inactive cAMP. By inhibiting this reaction there is an Increase in
intracellular active cAMP, which allows for a greater influx of Ca++ . As we know increased intracellular Ca++ causes Increased contractility.
b1 effects: - Increase contractility
(inotropy)
Increase
heart rate (chronotropy)
b2 effects: - Increase inotropy
Vasodilation
Bronchodilation
a1 effects: - Increase inotropy
a2 effects Increase
inotropy
Vasoconstriction
Agent |
Infusion dose |
Uses |
|
Adrenaline b effects @ low doses a effects @
high doses |
6 mg in 100mls
of 5% dextrose ml/hr =
mcg/min |
Resuscitation Severe sepsis Cardiogenic shock Acute asthma Anaphylaxis Maintenance of
cerebral perfusion pressure Medical pacing |
|
Noradrenaline a effects
at high doses |
6mg in 100ml
of 5% dextrose ml/hr =
mcg/min |
Vasodilated
states e.g. septic shock |
|
Dopamine a & b effects |
400mg in 100
mls of 0.9% Na+Cl or 5% dextrose ml/hr =
mcg/kg/min |
No
advantage over Adrenaline or noradrenaline “Renal dose” is no longer
advocated |
|
Dobutamine b effects
mild a 2 effects |
1
gram in 250 mls 0.9% Na+Cl or 5% dextrose |
Primarily a
vaso dilator with weak Inotropic action. Traditionally used in cardiogenic
shock in low output high afterload states |
|
Enoximone |
100
mg diluted up to 50 mls with saline = 2 mg/ml |
Cardiogenic
shock due to Pump failure and high afterload |
Cardiac Output Measurement Using Thermodilution
Evaluation of Cardiac Performance
The hearts ability to function as a pump can be
evaluated through the use of a Swan Ganz catheter. During end diastole, under
most conditions, ventricular pre load is indirectly reflected by their
respective atria. Left ventricular pre load can be evaluated by observing the
PADP (pulmonary artery diastolic pressure), or more accurately the PAOP, as
while the catheter is wedged, left heart pressures are reflected.
As left ventricular function deteriorates, end
diastolic pressure (pre load) increases. This increase is reflected back to the
atria where for the left heart the PAOP will also be recorded higher. Cardiac
output will decline as a result, and clinically the patient will exhibit signs
of poor organ perfusion.
It was thought that by obtaining the CVP the left
heart function could be assessed. At that time the only readily available
monitoring means was the CVP catheter. Since the utilization of the PA catheter
this concept has been dispelled.
By using the RA port on the PA catheter the RV preload
can be assessed. Increased RV preload as a result of severe lung disease or RV
dysfunction will be reflected in an elevated RA pressure. There are certain
pulmonary and right-sided heart diseases where only the right-sided pressures
will be abnormal. In these conditions a CVP catheter is inadequate for
assessing left ventricular function.
Both the right and left ventricular function can be
assessed by using a PA catheter. The information obtained from the PAOP
reflects the left heart function while the RA lumen reflects right heart
function. Under conditions of severe left heart failure and resultant right
heart failure both values will be elevated.
Thermodilution Method
In the 1950’s Fegler first
described measuring cardiac output by the Thermodilution method. It was not
until the early that Drs. Swan and Ganz demonstrated reliability and
reproducibility of this method with a special temperature sensing pulmonary
artery catheter. Since that time, the Thermodilution method of obtaining
cardiac output has become a standard for clinical practice.
The Thermodilution method applies indicator dilution
principles, using temperature change as the indicator. A known amount of solution
at a known temperature is injected rapidly into the right atrial lumen of the
catheter. This cooler solution mixes with and cools the surrounding blood, and
the temperature is measured downstream in the pulmonary artery by a thermistor
embedded in the catheter. The resultant change in temperature is then plotted
on a time-temperature curve.
A normal curve characteristically shows a sharp
upstroke from rapid injection of the injectate. This is followed by a smooth
curve and slightly prolonged downslope back to the baseline. Since this curve
is representing a change from warmer temperature to cooler and then back to
warmer temperature, the actual curve is in a negative direction. For continuity
for most graphs the curve is produced in an upright fashion. The area under the
curve is inversely proportional to the cardiac output.
When cardiac output is low, more time is required for
the temperature to return to baseline, producing a larger area under the curve.
With high cardiac out put the cooler injectate is carried faster through the
heart, and the temperature returns to baseline faster. This produces a smaller
area under the curve.
A modified Stuart- Hamilton equation is used to
calculate cardiac output taking into consideration the change in temperature as
the indicator, modification include the measured temperature of the injectate
and the patients blood temperature along with the specific gravity of the
solution injected.
CO = V x (TB – TI) x (SI x CI)
x 60 x CT x K
A (SB x CB) 1
Where:
V = Volume
of injectate in mls.
By paper speed (mm/sec)
K = calibration
constant in mm/°C
TB. TI = temperature of blood and injectate
SB, SI = specific
gravity of blood and injectate
CB, CI = specific
heat of blood and injectate
(SI x CI) = 1.08
when 5% dextrose is used
(SB x CB)
60 = 60 sec/min
CT = correction factor for injectate
warming
Don’t worry you
do not need to know or even understand this equation as the computer in the
monitor calculates it for you (thank God for technology!)
The thermistor
port of the catheter is attached to the monitor. Calculations are performed
internally with the results displayed on the screen. You can see from the
equation why 5% dextrose must be used, however it is possible to use another
solution as long as the computer has been told which fluid you are using in
order to adjust the value for the specific gravity. For ease and to reduce
errors custom and practice dictates that 5% dextrose is used.
Most monitors
display the actual cardiac output time - temperature curve. By observing the
Thermodilution curve assessment of injection technique and artificial
influences can be noted.
The temperature
of the injectate is room temp. The computer is registering a change (signal) in
temperature from the patient’s base line (noise). In some conditions, a
variation in temperature can occur with respirations,
this decreases the “signal-to-noise” ratio and produce an abnormally low
cardiac output. Other conditions where an increased signal to noise ratio may
be beneficial is in the febrile patient, low cardiac output states, and
patients with wide respiratory variations.
We use either the
closed system or the continuous cardiac output monitor Conditions where Thermodilution may produce
unreliable results are those that have a backward flow of blood on the right
side; tricuspid or pulmonic valve regurgitation, and ventricular or atrial
septal defects.
The Swan-Ganz
Thermodilution catheter is a powerful tool for the clinician in assessment and
management of the critically ill patient. Use of the catheter by itself is not
an intervention. Instead it is a diagnostic adjunct that if utilized and the
data interpreted properly leads to appropriate therapeutic interventions.
Significance of Hemodynamic Measurements
The determinants
of cardiac performance are heart rate (HR), preload, afterload and
contractility, but by indirect calculations other performance factors can be
assessed.
Direct Measurement
·
Heart
rate One of the more easily obtainable
values for assessing haemodynamic status is the heart rate. As a component of
cardiac output, the heart rate plays an integral part as to the diastolic
filling time and therefore end diastolic volume. It can be palpated or obtained
via an ECG.
·
Systolic
and Diastolic Blood Pressures. Blood pressure is the measured
tension within the blood vessels during ventricular systole and resting
diastole. This measurement can be obtained indirectly with a sphygmomanometer
or more accurately with an arterial catheter.
·
Pulmonary
Artery Pressure. With the use of the Swan-Ganz catheter P.A. systolic
and diastolic can be obtained, as can wedge pressure values.
·
Right
Atrial Pressure. Right ventricular filling pressures can be obtained
using the R.A. port can provide information about right ventricular function.
·
Waveform
Analysis. Measurement of the “a” and “v” wave of the RA and PAW
tracings can provide valuable information as to filling pressures and disease
states.
·
Cardiac
Output. Through the use of Thermodilution an accurate
determination of cardiac performance can be made.
Derived Parameters
From the direct
measurements obtained, derived parameters can be calculated to further assess
cardiac performance and normalize values obtained for body size (indexing)
·
Mean
Arterial Pressure. This is the
average pressure throughout the vascular system during systole and diastole.
The maintenance of a minimal pressure is necessary for coronary artery and
tissue perfusion. This value can be measured using the following formula:
MAP = SBP + (DBP X 2)
3
Normal
MAP = 70 –105 mmHg
·
Cardiac
Indexing. The normal range for cardiac output is wide 4-8 litres
per min. Since the value assesses the function of the ventricle, normalizing
the value to body size can offer more precise information. To index a
haemodynamic value, the patient’s body surface area (BSA) is obtained from a
nonogram using the patient’s height and weight. Any value that is to be indexed
can then be divided by the BSA.
CI = CO
BSA
Normal
cardiac index = 2.5 to 4 l/min/m²
·
Stroke
Volume. This is the amount of blood pumped out of the
ventricle with one contraction. Since stoke volume is part of the cardiac
output equation the value can be derived mathematically,
SV = CO X 1000 ml/L
HR
Normal
Stroke volume is 60 to 100 ml/beat
·
Stroke
volume index. As with cardiac output Stroke Volume can also be
indexed by dividing CI by HR.
Normal SVI = 33 to 47 ml/beat/m²
By calculating the SV or SVI, some
indication of the state of contractility can be evaluated.
·
Vascular
Resistance. Another variable of ventricular function is vascular
resistance. Resistance is the relationship of pressure to flow. As blood flows
through the vascular system there is resistance. This value is the clinical
representation of afterload; the amount of resistance the ventricle must overcome
to eject blood volume.
·
Systemic
Vascular Resistance. (SVR) measures the afterload or resistance for the
left ventricle. Since resistance relates to pressure to flow, pressure is
arrived at by measuring the gradient between the beginning of the circuit (MAP)
and the end (CVP). This value is then divided by the flow or cardiac output. A
rounded conversion factor of 80 is used to adjust the value into units of
force;
Dyne-sec-cm5
SVR = (MAP – CVP) X 80
Learning Outcomes for performing
Thermodilution
The nurse should be aware of normal A
& P of the heart and lungs and the flow of blood through these organs.
The nurse shall demonstrate knowledge of PAWP PA &
CVP interpretations on ventilated and spontaneously breathing patients.
The nurse should understand the significance of the
haemodynamic profile and be able to titrate inotropes
according to the results as directed by the doctors.
The nurse should be familiar with the set up of the
monitor and be able to input relevant data i.e. height and weight of the
patient
Performing Cardiac Output Studies using Thermodilution
·
Check the PA trace to make sure the Swan is in correct
position.
·
Check that nothing else is running on the CVP lumen
·
Preferably no fast IV’s should be running as this can
affect the baseline temp
·
Need exactly 10 ml of 5% Dextrose (the
calculation takes into account the specific gravity of this solution)
·
Inject as rapidly as possible, timed with end
expiration
·
Check no leaks while injecting
·
Watch the shape of the curve
·
Repeat injections (usually 3 or 4) when the monitor is
“ready”
·
Awareness of errors – Hypothermic patient, incorrect
volume injected (leaks), rapid infusions of other fluids, shunts or valvular
heart disease, very low cardiac outputs.
Introduction
Patient
Monitoring
Term
used for the automatic visual display of measurements such as blood pressure,
respiration, pulse and temperature.(Churchill
Livingstone, 1989)
On
the whole it is the ITU nurse who monitors the patients 24/7
They
have to observe, communicate analyse and interpret
data in order to care effectively for the patient (Field 1997) and it has never
been easier with all of the equipment now available to us.
The
introduction of the Swan Ganz catheter in the 70’s
has helped improve our knowledge of cardiovascular function(Boldt
et al, 1995) we can now monitor cardiac output continuously using heated
electrodes, so results in therapy and can be observed in real time and
adjustments made.
Can
the use of CCO be justified from a clinical point of view? A multi centre trial
failed to show increased survival in disease matched ITU patients receiving a
PA catheter versus those who did not (Gresham Bayne, 1997) So
What are the alternatives?
Pulmonary
Artery Catheters are still the “Gold Standard” in the assessment of cardiac
output (Hoeft, 1995). However the interpretation of
Pulmonary Artery Occlusion Pressure (PAOP) or Wedge pressure can be difficult
due to many artifacts in measurement. (Paul et al, 1987)
Factors
like Intrathoracic pressure, myocardial contractility
may affect the results of PAOP estimation.
Lichtwarck-Aschoff et al (1992)
were able to show that a much better indicator of circulating blood volume and
cardiac pre load is to
measure the intrathoracic blood volume
(ITBV) or the intrathoracic blood volume index
(ITBVI) and extra vascular lung water (EVLW) content of the lungs.
These
measurements can be obtained through arterial pulse contour cardiac output and trans pulmonary thermodilution (Sakka et al, 1999)
This
method uses a standard central line with a temperature sensor on the distal
.lumen and a thermo dilution sensor arterial catheter, placed in either the
femoral or brachial artery. This is a much less invasive method and reduces the
risk associated with the insertion of a PA catheter. e.g.,
ventricular dysrhthmias, endocardidtis,
valvular damage, embolism, cardiac rupture, cardiac tamponade, pulmonary artery rupture, thrombosis, embolism,
hemorrhage and infarction (Thelan et al 1998).
Although
the thermodilution curve is longer and flatter than
in traditional PA thermodilution it is not influenced
by respiratory cycle. The algorithm used computes left ventricular stroke
volume by measuring the area under the systolic part of the waveform from the
end of diastole to the end of the ejection phase.
and dividing the area by the aortic
impedance (Godje at al 1999). This calculation
provides a measure of stroke volume.
Changes
in ITBV have been shown to correlate well with changes in cardiac output and
may be a more appropriate monitoring parameter for cardiac preload (Sakka et al 1999)
Another
interesting aspect of PiCCO is the ability to measure
extra vascular lung water (EVLW) a measurement Paul et al (1997) suggested may
be an alternative approach determining pulmonary and a guide to fluid
resuscitation in shock. Godenheim et al (1985) suggests that the restricting
excessive intravasclular fluid volume expansion in
patients with ARDS the patients out come may be improved. Robin et al (1985)
note that resolution of pulmonary odema may be more
rapid when EVLW is used as a therapeutic guide especially if the cause is due
to cardiac failure.
New
methods of haemodynamic monitoring that are less
invasive can only be a positive step forward. Utilizing all available
information will help us deliver the best possible care for our patients.
WHAT IS PiCCO?
PiCCO technology is based on a haemodynamic monitoring method, which is a combination of transpulmonary thermodilution and
arterial pulse contour analysis. By “transpulmonary”,
this means the injection of cold fluid which traverses the lungs after being
injected through a CVP line, and that the thermodilution
curve is being measured in a systemic artery.
Generally, we use the CVP lumen of a quad line and ideally a femoral
artery and gaining readings of cardiac output, cardiac index, stroke volume,
cardiac function index, extravascular lung water and intrathoracic blood volume, totally eliminates the need for
a right heart (pulmonary artery) catheter.
EQUIPMENT
FOR USE OF PiCCO
PiCCO Plus Monitor
PiCCO transducer cable (white)
PiCCO cable (grey)
PiCCO transducer pack (inline sensor found in
transducer pack should be
attached to CVP port of quad line and PiCCO grey cable)
1
Litre pressure bag and 1 Litre
saline
PiCCO line 20 cm standard length
for femoral artery, smaller lines for brachial and axillary
arteries, ask medics before opening pack!
Sterile
line insertion trolley
2
x 20ml cold saline (kept in drug fridge)
INDICATIONS FOR USE OF PiCCO
Patients
in whom cardiovascular monitoring and circulatory volume status monitoring is
necessary eg.
Shock
ARDS
Acute
cardiac insufficiency
Major
cardiac, orthopaedic and abdominal surgery
Acute
multitrauma / severe burns
Transplant
surgery
PERFORMING
A PiCCO THERMODILUTION MEASUREMENT
The
PiCCO Plus monitor requires calibration and
re-zeroing every 12 hours, so doing this at the beginning of each shift will familiarise you with the monitor, and the patient’s
cardiovascular and fluid status.
A
calibration simply means performing a set of thermodilution
measurements by injecting cold saline past the inline sensor on the CVP line.
You
may perform as many intermittent measurements as necessary to check the
patient’s cardiovascular and volume status, and also after changes to, or
initiation of, new treatments.
PLEASE
REFER TO STAGE 5 ON THE QUICK SET-UP GUIDE ON THE FOLLOWING PAGE to perform a
measurement.
SETTING UP OF PiCCO AND
INPUT SCREEN
RE-ZEROING THE PiCCO
The
PiCCO transducer needs to be re-zeroed before
attaching to the patient and approximately every 12 hours thereafter.
Open
transducer to air. Press enter key, then AP key then ‘O’key. When the numbers go to zero, close to air and press
enter. AP correction should be left at 0
cm if transducer is at usual mid-heart level.
Press enter again, then select waveform page to monitor blood pressure.
PATIENT INPUT SCREEN
When
PiCCO is first inserted, you need to key in certain
patient details:
Height
in cm
Weight
in kg
Injectate volume 20 ml (should be preset by PiCCO)
Injectate temperature < 8oC (should
be preset by PiCCO)
CVP (This is
acceptable for changes up to 5, but it is advisable to re-input CVP if it
changes, and check when receiving patient or performing measurements)
PiCCO Plus will display “invalid/faulty
catheter” under ‘catheter type’, ignore this as PiCCO
will automatically read the catheter type and input it when the cable is
attached to the patient.
(Our
catheter types are usually PV2015L20 for a 20 cm line).
WHAT DO THE PARAMETERS MEAN ??
!!
PULSE
CONTOUR CARDIAC OUTPUT / INDEX
CI
= 3.0 – 5.0 l/min/m2
Cardiac
output is the amount of blood ejected by the left ventricle in one minute. The PiCCO measures this using the heart rate and the area under
the aortic flow curve on the arterial blood pressure trace.
The
displayed cardiac output/index is the mean value of the last 12 seconds. Continuous pulse contour cardiac output
measurement as done by the PiCCO monitor is a
reliable and reproducible alternative to continuous cardiac output measurement
using a heated PA catheter.
INTRA-THORACIC
BLOOD VOLUME
ITBVi = 850 – 1000
ml/m2
<850
= underfilled
> 1000 = adequate – overfilled
ITBV
consists of the GEDV (global end diastolic volume), the volume of blood within
the heart plus the pulmonary blood volume.
Three volumes are found within the thorax, the intrathoracic
blood volume, the intrathoracic gas volume and the extravascular lung water.
Due to limited expansion of the thorax, the three volumes interact and
change proportionally to each other.
ITBV is a volumetric measurement of cardiac preload (ventricular
end-diastolic pressure), and in mechanically ventilated patients is a sensitive
indicator of the circulatory blood volume.
EXTRAVASCULAR
LUNG WATER
EVLWi = 3.0 – 7.0
ml/kg
>7.0
ml/kg indicates pulmonary oedema
The
water content in the lungs increases in left heart failure, pneumonia, sepsis,
burns etc, and measurement of EVLW relates specifically to pulmonary oedema eg . in ARDS, which is not only the
increased permeability to water, but also to proteins. Prognosis based on EVLW has indicated a
higher risk of mortality with EVLW of greater than 14 ml/kg.
CARDIAC
FUNCTION INDEX
CFI
= 4.5 – 6.5 l/min
<
4.5 indicates poor myocardial contractility
CFI
reflects myocardial contractile function.
It is measured independently of cardiac preload and reflects the inotropic state of the heart. Positive inotropic
stimulation increases the curve, therefore the reading.
STROKE
VOLUME VARIATION
<
10% =
well-filled/overloaded
10
– 15% = normal
>
15% =
dehydrated/underfilled
Stroke
volume is the amount of blood ejected from the ventricle with each contraction.
The
SVV is measured as the mean difference between the highest and lowest stroke
volume over the last 30 seconds. Stroke
volume will change on inspiration (increases with venous return) and on
expiration (against venous return).
Positive pressure ventilation impedes venous return, therefore there may
be a larger variation in stroke volume in mechanically ventilated patients who
are dehydrated, as the heart cannot compensate for the differences in stroke
volume on inspiration and expiration if the blood volume is not available ie. the patient is dry, and the
blood is not available for refill into the ventricles on preload (ventricular
end diastole).
This
is only accurately measured in ventilated patients.
If the patient is tachyarrhythmic
eg. atrial
fibrillation, SVV will be inaccurate as ventricular refill will be irregular,
therefore stroke volume is not measured properly.
CONTINUOUSLY MONITORED AND DISPLAYED
Arterial
Blood Pressure
Heart
Rate
Blood/Body
Temperature - BT
Continuous
Pulse Contour Cardiac Output/Index – CO/CI
Stroke
Volume - SV
Stroke
Volume Variation - SVV
Systemic
Vascular Resistance - SVR
OBTAINED BY THERMODILUTION MEASUREMENT
Transpulmonary Cardiac Output - CO
Intrathoracic Blood Volume -
ITBV
Extravascular Lung Water -
EVLW
Cardiac
Function Index - CFI
(Global
End Diastolic Volume *) - GEDV
(Global
Ejection Fraction *) - GEF
*
The PiCCO Plus monitor in our ITU is set to display
ITBV and CFI, instead of GEDV and GEF when a thermodilution
measurement is done, however these can be displayed by selecting them via the
configuration key – CFG – if they are requested specifically by the medical
staff.
REFERENCES
Boldt J, Heesen
M, Muller M, Hemplemann G (1995) Continous monitrting of
critically ill patients with a newly pulmonary arterial catheter. A cost analysis.
Anaesthetist:June 44:6 p423 -
428
Churchill Livingstone (1989) Nurses’
Dictionary 16th ed.
Field
D (1997) Cardiovascular Assessment Nursing
Times. August 27, Vol 93 No 35, p45 – 47
Godje O, Hoke K, Lichtwarck-Aschoff M , Lamm P, Reichart B: (1999)
Less invasive continuous cardiac output determination by femoral artery thermodilution calibrated pulse contour analysis, a
comparison to conventional pulmonary arterial cardiac output. Critical
Care Medicine: 27 (11): 2407 – 2412, 1999
Goldenheim P D and Kazemi
H (1984) Cardiopulmonary monitoring of critically ill
patients (parts 1 and 2).
Vital
Signs – are we monitoring the right parameter?
Nursing
Management
28 (5): p 74 – 76
Hoeft A (1995) Transpulmonary
Indicator Dilution: an alternative approach to haemodynamic
monitoring. Year Book of Intensive Care and Emergency Medicine Springer
– Verlag
Lichtwarck-Aschoff M, Zeravik J and Pfeiffer U J (1992)
Intrathoracic blood volume
accurately reflects circulatory status in critically ill patients with
mechanical ventilation.
Intensive
Care Medicine 18: p 142 – 147
Marx,
G., T. Cope, L. McCrossan, S. Swaraj,
C. Cowan, S.M. Mostafa, R. Wenstone,
M. Leuwer.
Assessing fluid responsiveness by stroke volume variation in
mechanically ventilated patients with severe sepsis.
Eur J Anaesthesiol
2004; 21:132-138.
Robin G D (1985) The cult of the Swan Ganz catheter. Overuse and abuse of
pulmonary flow catheter. Anaesthetist
International Medicine : 103, p445 -
449
Sakka S G, Bredle D L, Reinhart K and Meier-Hellmann A (1999)
Comparison of pulmonary artery and arterial thermodilution cardiac output in critically ill patients.
Intensive
Care Medicine 25: 843 –846, 1999
Thelan L A, Urden L D, Lough M E and Stacey K M (1998) Critical Care Nursing
: Diagnosis management 3rd edition Moseby
London