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Haemodynamic monitoring
Non-invasive monitoring
ECG
- logical to use a specific lead to view an area known to result in ischaemic
changes on the 12 lead ECG but for routine use, use of the CM5 lead gives
>80% detection of LV ischaemia (monitors anterior and lateral left
ventricle) and causes few problems with the diagnosis of a dysrhythmia. Attach
RA lead to manubrium, LA to V5 position and LL to usual position. Set monitor
to lead I.
- MCL1 (modified chest lead)is useful in patients with rhythm disturbances as
atrial activity and conduction defects are easily seen. Attach LA lead to left
subclavian position, LL to V1 and RA as ground; set monitor to lead III.
Blood pressure
- most automated devices use an oscillotonometric technique and as a result
the most accurate pressure is the mean arterial pressure.
- tend to overestimate at low pressure and underestimate high pressure but the
95% confidence limits are +/- 15 mmHg over the normotensive range
- give erroneous results in patients in AF or with other arrhythmias
- cuff width most important determinant of the accuracy of the pressure
reading. Should be 40% of mid-circumference of limb (the length should be
twice the width). Cuffs which are too narrow tend to overestimate BP while
those which are too wide tend to underestimate
- complications include: ulnar nerve injury (usually associated with cuff
being placed too low on upper arm), oedema of the limb, petechiae and
bruising, friction blisters, failure to cycle and drip failure.
Urine output
- although strictly speaking this is a monitor of renal perfusion only, urine
output is often used as a guide to adequacy of cardiac output as the kidney
receives 25% of cardiac output. When renal perfusion is adequate urine output
will exceed 0.5 ml/kg/h.
- use of diuretics such as frusemide and dopamine abolishes its usefulness as
a haemodynamic monitor.
Thoracic electrical bioimpedence
- non-invasive method of estimating cardiac output continuously
- considerable doubt as to whether it does so accurately. A very recent study
of a new system found that the mean relative error of the system compared to
thermodilution cardiac output measurement was only 16.6%, however this was
associated with a large standard deviation of 12.9%, indicating that in some
patients it is grossly inaccurate.
- recent data suggests that at least one device is adversely affected by the
increase in lung water seen in critically ill patients
Oesophageal Doppler monitor
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Transoesophageal echocardiography
- can be used to estimate end-diastolic volume and cardiac output
- accurate but has a number of disadvantages
- expensive equipment
- specialist training required
- short term use only
- risk of dislodgement of ETT, NGT
- risk of oesophageal injury
Arterial pressure monitoring
- invasive measurement may result in an overestimate of systolic pressure due
to systolic overshoot. Result of the physical properties of the system and can
be eliminated by increasing the damping of the system (eg by using smaller
gauge tubing) thus reducing the resonant frequency of the system. However
increasing the damping reduces the sensitivity of the system. To prevent
systolic overshoot the system should have a resonant frequency of > 30 Hz
for heart rates up to 180/min and > 20 Hz for rates up to 120/min while
retaining sufficient sensitivity. A method of determining the resonant
frequency and damping coefficient of the system is given in table
1. Mean arterial pressure is accurately monitored even if the
system does not meet the criteria above. The tubing connecting the arterial
cannula to the transducer should be non-compliant and < 1 m in length
- arterial pressure trace can also be used to give an indication of adequacy
of preload. In mechanically ventilated patients the effect of positive
intrathoracic pressure during inspiration is to increase left ventricular
output and systolic arterial pressure early in inspiration, followed a few
heart-beats later by a fall. This variation in arterial pressure is
exaggerated in the presence of reduced preload and a significant correlation
has been demonstrated between the systolic arterial pressure variations and
end diastolic area estimated with transoesophageal echocardiography.
- Systolic pressure variation can be quantified by establishing a baseline
during a period of apnoea and then measuring the maximum subsequent upward (d
up) and downward (d
down) variation (figure 1).
- d down:
- normal: 5-6 mmHg
- in one study shown to provide be a better predictor of responsiveness to
fluid loading than PAOP and LV end-diastolic area
- due to a a transient fall in venous return
- directly affected by magnitude of tidal volume and can be greatly
exaggerated in presence of air trapping or fall in chest wall compliance
- d up:
- normal: 2-4 mmHg
- occurs in early inspiration
- due to augmentation of stroke volume due to increase in L sided preload. In
patient with impaired LV contractility may also reflect afterload reducing
effect of positive intrathoracic pressure
- Systolic pressure variation cannot be interpreted in presence of irregular
arrhythmias and can only be used in controlled ventilation
Figure 1.
- complications associated with invasive arterial pressure monitoring are
listed in table
2.
The morbidity associated with arterial cannulation is less
than that associated with 5 or more arterial punctures.
Central Venous Pressure (CVP)
- can be monitored using catheters inserted via the internal jugular,
subclavian and femoral veins.
- correct placement should be confirmed by observation of a change in pressure
in different phases of respiration, free aspiration of blood through the
catheter and radiological confirmation of the position of the tip of the
catheter in the superior vena cava (internal jugular and subclavian catheters)
- femoral vein pressure can be used reliably as a guide to central venous
pressure in ventilated patients who do not have excessively high
intra-abdominal pressure
- used as a guide to right ventricular filling. However, right ventricular
preload is determined by end-diastolic volume not pressure and therefore,
without knowledge of the ventricular compliance, an isolated CVP reading is of
limited value. Compliance not only varies from patient to patient but varies
with time in the same patient. Thus dynamic changes in CVP are more useful
than absolute values. If the CVP rises > 7 mmHg in response to a fluid
challenge (eg 50-200 ml of colloid over 10 mins) then the patient is probably
maximally filled and any further filling will result in development of
pulmonary oedema. If, however, the CVP returns to within 3 mmHg of its
original value within 10 mins then the risk of pulmonary oedema is only
moderate; nevertheless no further filling is required. If the CVP rises less
than 3 mmHg the patient is probably underfilled.
- in most patients LV filling will be adequate if RV filling is adequate but
in those patients with impaired RV function (eg some patients with inferior
myocardihal infarction, patients with severe sepsis) or lung disease leading to
pulmonary hypertension this may not be the case. In addition left sided
pressures may be abnormally high despite normal right sided pressures in
patients with left ventricular dysfunction
- analysis of waveform may yield further information (table
3). a wave is due to atrial contraction and follows p
wave of ECG. c wave results from tricuspid valve closure. x
descent is due to combination of atrial relaxation and downward displacement of
AV junction during early part of ventricular systole. v wave corresponds
to flow of blood into atrium against a closed tricuspid valve. y descent
due to rapid flow of blood from atrium into ventricle in early ventricular
diastole
- complications are listed in table
4.
- although the pulmonary artery catheter has become a standard part of
haemodynamic monitoring in critically ill patients there is no conclusive
evidence that its use leads to decreased mortality and it may
instead increase mortality.
- waveforms seen as the catheter passes through the heart and pulmonary artery
to the wedged position are illustrated in figure 2
- normal pressures are given in table
5.
Pulmonary artery occlusion pressure (PAOP)
- approximates to LA pressure (LAP), which approximates to left ventricular
end-diastolic pressure (LVEDP). The relationship between LVEDP and left
ventricular end-diastolic volume is illustrated in figure
3.
- in a number of conditions PAOP may not reflect LVEDP. These
conditions are listed in table 6.
- chest radiographs are not reliable means of detecting the fact that the
catheter tip is outside zone III because of the effect of lung disease on West’s
zones. However the following characteristics suggest the tip is outside zone
III: a smooth-looking PAOP tracing, PADP < PAOP, increase in PAOP > 50%
of change in alveolar pressure and a decrease in PAOP > 50% of the
reduction in PEEP.
- should be easy to aspirate blood from the tip of the PA catheter with the
catheter "wedged" and the blood should be arterialized.
- in patients with a markedly reduced vascular bed "wedging" the
balloon may reduce venous return sufficiently to to result in an underestimate
of both LAP and LVEDP.
- LVEDV is determined by LV compliance and the transmural pressure. The
transmural pressure can be obtained by subtracting the pressure surrounding
the heart (approximately equal to the intrapleural pressure) from the LVEDP.
Intrapleural pressure is closest to zero at end expiration and thus LVEDP most
closely approximates to transmural pressure at end expiration.
- analysis of the waveform may give some indication of cardiac pathology. Both
constrictive pericarditis and pericardial tamponade cause the same
abnormalities in the PAOP trace as in the CVP trace but the changes are seen
more clearly in the CVP trace. Mitral regurgitation may cause a large v wave
in the PAOP trace, which may cause it to be confused with the PA waveform. The
two can be distinguished by examining the timing of the waves relative to the
T wave of the ECG. The peak of the PA systolic wave occurs within the T wave
of the ECG while the v wave occurs after the T wave. Large v waves may also be
present in association with mitral stenosis, congestive heart failure or
ventricular septal defect.
Pulmonary artery diastolic pressure (PADP)
- PADP is closely related to PAWP except when the patient has pulmonary
hypertension or is tachycardic. When the heart rate is > 120 beats/min
there is insufficient time during diastole for venous run-off so PADP is
spuriously high.
Thermodilution cardiac output measurement
- injection of cold injectate into the right atrium causes a fall in
temperature monitored in the pulmonary artery.
- fall in temperature will be greater the lower the degree of dilution of the
injectate.
- the lower the cardiac output the lower the degree of dilution as the
injectate is injected.
- fall in temperature also depends on the temperature and the volume of the
injectate. The relationship of these factors to the cardiac output is given by
the Stewart-Hamilton equation:
where Q = cardiac output, V = volume injected, TB = blood temperature, TI =
injectate temperature, K1 and K2 = computational constants, and TB(t)dt
= change in blood temperature as a function of time.
- the colder the injectate the greater the signal-to-noise ratio and the
better the accuracy and precision. However in most clinical situations 10 ml
of injectate at room temperature provides an acceptable measurement.
- smaller volume of injectate can be used in situations where volume
overload is a concern without significantly affecting the results.
- careful filling of syringes is necessary to avoid error due to variable
injectate volumes.
- respiration affects cardiac output as well as pulmonary artery blood
temperature so, ideally, measurements should be made in the same phase of
respiration. However it is difficult to synchronize injection with
respiration and in practice an average of 3 evenly spaced measurements with
variation of <10% between measurements gives an accurate estimation of
cardiac output
- causes of inaccuracy in measurements are listed in table
7. The cardiac index is the cardiac output divided by the
body surface area. The latter is obtained from nomograms using the patient’s
height and weight.
Derived values
- formulae used to calculate these values and their normal ranges are given
in table
8.
- systemic vascular resistance is used as a guide to left ventricular
afterload and left ventricular stroke work as a measure of contractility.
Note that a change in preload can increase left ventricular stroke work
without an increase in contractility and therefore preload must remain
constant in order for stroke work to be used as a direct estimate of
contractility. An alternative is to plot stroke work against an estimate of
preload (eg PAOP) and compare that with a normal range; a shift to the left
and up is interpreted as an improvement in ventricular function while a
shift to the right and down is thought to reflect deterioration.
- note that oxygen delivery is actually a measure of oxygen leaving the left
ventricle and not oxygen delivery to tissue.
- pulmonary vascular resistance calculated according to the formula given
may not be the most sensitive indicator of intrinsic pulmonary vascular
disease because it is highly dependent on the cardiac index and therefore to
a large extent reflects ventricular function. The PAEDP-PAOP gradient may be
a better indicator.
- has been used as a measure of adequacy of tissue perfusion.
- varies directly with cardiac ouput, Hb and arterial saturation and
inversely with metabolic rate.
- normal is approximately 75% but falls when oxygen delivery falls or tissue
oxygen demand increases. When it falls as low as 30% oxygen delivery is
insufficient to meet tissue oxygen demand and there is an increased
potential for anaerobic metabolism and lactic acidosis.
- situations with increased mixed venous oxygen saturations are more
difficult to interpret; sepsis, A-V fistulae, cirrhosis, left-to-right
cardiac shunts, cyanide poisoning, hypothermia and unintentional PA catheter
wedging have all been reported as being associated with increased values.
Increased values of Sv'O2 in sepsis may reflect a failure of
cells to take up and utilise oxygen.
- the relatively common occurrence of sepsis and of more than one medical
problem in a patient means that Sv'O2 cannot be used in isolation
to monitor adequacy of tissue perfusion. A normal value may simply reflect a
combination of low cardiac output and sepsis.
- can be measured either continuously using a fibre-optic Swan-Ganz catheter
or by taking blood samples from the distal lumen of the Swan-Ganz catheter
and measuring the saturation in a co-oximeter. At the low PvO2 in
mixed venous blood the calculated saturations produced by blood gas machines
are not accurate.
Right ventricular ejection fraction pulmonary artery catheter
- utilises a PA catheter with a rapid response thermistor and an injection
port that is designed to ensure uniform mixing of the iced injectate in the
right atrium.
- mean residual fraction (MRF) is calculated over time by dividing the
temperature change by the R-R interval. The ejection fraction (RVEF) = 1 -
MRF.
- EDV can then be calculated from the stroke volume (CO/HR) divided by RVEF.
- reasonable estimates of RVEF can be obtained provided that there is no
valve regurgitation or arrhythmias.
Continuous thermodilution cardiac output
This uses infusion of heat from a filament in the right atrium rather than
an injection of cold saline and stochastic system identification to enhance
the signal-to-noise ratio. The monitor gives the average cardiac output over
the previous 3-6 minutes updated every 30 seconds. Results appear to agree
well with those obtained by bolus thermodilution.
Pulmonary capillary pressure (PCP)
- major determinant in the formation of pulmonary oedema.
- in patients with normal lungs it can be calculated from the the sum of PAOP
and 40% of the difference between MPAP and PAOP. Based on the assumption that
the ratio of pulmonary venous resistance to the total pulmonary vascular
resistance is 0.4. In patients with lung disease or injury this may not be the
case.
- when the pulmonary artery is occluded the pressure distal to the balloon
falls from pulmonary artery pressure to PAOP. The fall is characterised by
first a fast and then a slow phase. The fast phase results from the cessation
of pulmonary artery blood flow distal to the occlusion while the second phase
results from the release of blood stored in the pulmonary capacitance vessels.
The level to which the pressure falls purely as a result of cessation of
pulmonary artery flow is PCP. Thus PCP can be calculated by extrapolating the
slow phase back to the time of occlusion. This, however, requires knowledge of
the precise time of occlusion. By using a double-port pulmonary artery
catheter which has a pulmonary artery port both at the tip of the catheter and
1 cm proximal to the balloon it is possible to determine the precise time of
occlusion from the time at which the two pulmonary artery pressure curves
abruptly diverge
Complications
- listed in table
9.
- in one study of 6245 catheter insertions use of the pulmonary artery
catheter was associated with death in 1 case, pulmonary infarction in 4,
intrapulmonary haemorrhage in 4, permanent right bundle branch block in 3,
complete heart block in 1 and ventricular ectopics requiring treatment in 193
- if catheter appears to be knotted on CXR remember that it may not be
actually knotted. Pull out other catheters in reverse order in which they were
inserted and then repeat CXR. If there is a true knot: pull catheter back
until it is at end of sheath. Pull hard and knot will usually enter sheath.
Then remove whole apparatus. If there is no sheath pull back as far as
possible then cut down to vein under local anaesthesia. If the catheter still
cannot be removed (only 0.5% of knots) refer to vascular
surgeons/interventional radiologists/cardiologists.
- risk factors for major morbidity (with PA rupture being the most important)
include pulmonary hypertension, anticoagulation, catheter in position for
>3 days.
Cardiac output using the Fick method
- Application of the Fick principle to oxygen uptake in the lungs can be used
to measure cardiac output.
- This method has traditionally been considered to be
the "gold standard" of cardiac output measurement. However the
preconditions for accurate measurement of cardiac output using the oxygen Fick
method are not met in most ICU patients.
- Use of modified carbon dioxide Fick
methods result in greater agreement with thermodilution cardiac output
measurement. Not
widely applied and relies on controlled ventilation and steady state CO2
metabolism
PiCCO
- less invasive than a pulmonary artery catheter and utilizes any available
central venous line and a product specific thermodilution catheter placed in
an artery (e.g. femoral or axillary). Various catheter sizes are available
allowing the technique to be used in paediatric patients
- works by a combination of pulse contour analysis and intermittent
transpulmonary thermodilution. Following three cold saline bolus injections
via the CVP line detected by the thermodilution catheter the device software
can integrate this information with the arterial waveform to give a
continuous display of cardiac output (response time 12sec). CO obtained
using the PiCCO correlate well with those obtained using a PAC. Additional
information includes BP, heart rate, stroke volume, systemic vascular
resistance, stroke volume variation (SVV) and pulse pressure variation (PPV).
SSV and PPV can be used to estimate volume responsiveness in mechanically
ventilated patients as described in the arterial pressure monitoring
section.
- the transpulmonary thermodilution also allows calculation of a number of
parameters with potential clinical application including global
end-diastolic volume (GEDV) and intrathoracic blood volume (ITBV) that
reflect cardiac preload, and extra vascular lung water (EVLW) that may
correlate with degree of acute lung injury.
- complications include those of arterial and central venous cannulation.
Regional blood flow
Jugular bulb oxygen saturation (SjO2)
- proposed as a method of identifying those patients in whom cerebral
metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) are
mismatched
- has become widely used as a clinical monitor in neurosurgical intensive care
units
- use is based on the Fick principle, according to which cerebral
arterial-mixed venous oxygen difference (AVDO2) is related to CMRO2
and CBF in the following way:
AVDO2 = CMRO2/CBF
Assuming that arterial saturation, haemoglobin concentration and the affinity
of haemoglobin for oxygen remain constant, the ratio of CMRO2:CBF
is proportional to the cerebral mixed venous oxygen saturation. SjO2
is assumed to be equal to cerebral mixed venous oxygen saturation.
- two major limitations:
- reflects adequacy of global cerebral oxygen delivery and gives no
indication of adequacy of regional cerebral oxygen delivery. Thus a
normal SjO2 is compatible with critical ischaemia in some parts of
the brain with simultaneous luxury perfusion in others.
- results become difficult to interpret when increased oxygen extraction can no
longer compensate for reductions in oxygen delivery. In this situation CMRO2
falls and thus the SjO2 remains unchanged despite a fall in
cerebral oxygen delivery.
Further reading
Gomersall CD, Oh TE. Haemodynamic monitoring. In Oh TE (ed), Intensive Care
Manual, 4th ed. Oxford: Butterworth Heinemann, 1997, pp 831-8
Perel, A. Assessing fluid responsiveness by the systolic pressure variation
in mechanically ventilated patients. Systolic pressure variation as a guide to
fluid therapy in patients with sepsis-induced hypotension. Anesthesiology 89(6),
1998.
© Charles Gomersall July 1999, Charles Gomersall & Sarah Ramsay December
2002
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