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Key points Invasive arterial pressure monitoring is one of of this wave form: a steady component which is
the most frequent monitoring techniques used reflected by the mean pressure within the system
Arterial waveforms may
in critically ill patients and in anaesthetized (or the MAP); and a pulsatile component which
provide a deeper insight into
overall haemodynamic subjects in whom rapid changes in the haemo- oscillates around this mean value in a complex
status. dynamic status is anticipated during the peri- manner and determined by:2
operative period. The arterial waveforms
An understanding of the (i) SV,
obtained via an indwelling arterial cannula are
principles of (ii) vascular capacitance,
ventricular-vascular coupling transduced and displayed on a monitor providing
(iii) peripheral vascular resistance, and
is essential. a beat-to-beat estimate of the systolic, diastolic,
(iv) heart rate.
and mean arterial pressures (MAPs). However, it
Vasodilatation usually causes
is now well established that a more detailed
lower systolic/diastolic These physiological concepts, broadly referred
pressures associated with a study of the arterial waveforms and their interac-
to as ventricular-vascular coupling3 should be at
wide pulse pressure (PP) and tions with respiration, may provide a more in-
the very heart of our attempts in evaluating an ar-
delayed dicrotic notch. formative and composite assessment of the
terial waveform. For clinical purposes, it is useful
overall cardiovascular status. Understanding of
Vasoconstriction is usually to consider that systolic pressure (SP) which is the
associated with a narrow PP. the physiological determinants that influence the
maximum pressure recorded in the arterial tree
shape of an arterial pressure waveform is
Regular calibration is during ventricular ejection is primarily influenced
however an absolute prerequisite if we are to
essential when pulse by SV and vascular capacitance—a measure of
successfully utilize the simple arterial wave-
contour analysis is used to how stiff or distensible the arteries are. When vas-
measure cardiac output. forms to evaluate global haemodynamic status
cular capacitance is constant, an increase in SV
in our patients.
will result in an increase in SP, and for a given
SV, a change in vascular capacitance will have a
corresponding effect on SP. The ability to main-
Ventricular-vascular coupling: tain pressure within the arterial tree during dia-
physiological determinants of stole (when the ventricle is not contracting and the
the shape of an arterial aortic valves have closed) depends on the ability
waveform of the proximal arteries to recoil and continue to
The arterial waveform is produced through the squeeze the blood forwards against the resistance
dynamic interactions between the volume of offered by the peripheral vascular beds. These
Mahesh Nirmalan MD FRCA PhD blood ejected by the heart during each beat, the factors explain why elderly subjects have a higher
FFICM
speed with which this volume is ejected by the SP (reduced vascular compliance associated with
Reader and Honorary Consultant in
Intensive Care Medicine heart, the ability of the vascular tree to distend arteriosclerosis) and a lower diastolic pressure (in-
Manchester Royal Infirmary and and accommodate this ejected volume, the rate ability of the stiff arteries to recoil and maintain
University of Manchester at which the ejected volume of blood is able to the pressure within the compartment) and why a
Oxford Road
Manchester M13 9WL flow away from the central arterial compartment neonate tends to have a lower SP (because of a
UK into the peripheral tissues. Figure 1 shows the very compliant or distensible arterial tree) and a
Tel: þ44 (0)161 276 4712 aortic pressure and aortic flow recorded in an higher diastolic pressure (because of the compli-
E-mail: m.nirmalan@manchester.ac.uk
(for correspondence) animal model showing very clearly the time lag ant vessels being able to recoil well and sustain
that exists between the flow peak and the pres- the pressure better within the arterial compartment
Paul M Dark FRCS PhD FFICM
sure peak indicating that the pressure peak is the when cardiac ejection has ceased).
Reader and Honorary Consultant in
Intensive Care Medicine
result of a dynamic interaction between the Figure 2 illustrates some of the principles
Salford Royal Hospitals and University of stroke volume (SV) and the vascular wall.1 inherent in ventricular-vascular coupling dur-
Manchester When evaluating an arterial waveform it is im- ing an acute change in arterial capacitance asso-
Manchester
UK portant to recognize two very broad components ciated with the application of an aortic cross
doi:10.1093/bjaceaccp/mkt078 Advance Access publication 10 February, 2014
285 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 14 Number 6 2014
& The Author [2014]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.
For Permissions, please email: journals.permissions@oup.com
Arterial pressure wave form analysis
90
0.4
85
Aortic pressure
0.3
Pressure (mm Hg)
80
Velocity (m s–1)
75 0.2
70
Aortic flow 0.1
Fig 2 Brachial arterial pressure tracings in a patient undergoing abdominal
65 aortic aneurysm repair, before (blue) and after (red) the application of the
0 aortic cross clamp. Note that, the application of the aortic cross-clamp
60 results in an acute reduction in vascular compliance. This is reflected by an
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 acute increase in the SP and an acute reduction in the diastolic pressure.
Time (s)
286 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 14 Number 6 2014
Arterial pressure wave form analysis
Fig 4 Arterial pressure in a patient with severe sepsis. Note the effects of
vasodilatation on the position of the dicrotic notch. The solid arrow indicates
where one would expect to see the notch (approximately one-third the way
down the descending limb) and the dashed arrow shows where the notch
was actually seen. The considerable delay in the timing of the dicrotic notch
makes the secondary dicrotic wave appear almost as a separate and distinct
wave. All the distinct properties of vasodilatation, reduced SP, reduced DP,
widened PP, and a delayed dicrotic notch, are evident in this example.
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 14 Number 6 2014 287
Arterial pressure wave form analysis
Fig 6 Arterial pressure recording in an animal model of severe hypovolaemic shock. (A) Notice the effect of IPPV on arterial pressure during normovolaemic
(blue) and hypovolaemic (red) conditions. (B) Observe the following effects of severe hypovolaemia: marked oscillation on systolic and diastolic pressure with
respiration and very prominent beat-to-beat changes in PP and the area under the systolic portion of the arterial trace (Psys).
mentioned manifestations of hypovolaemia on the arterial pres- then be used to convert subsequent PP and Asys to estimates of SV
sure tracings: Lakhal and colleagues5 6 have demonstrated that and therefore CO. This approach of making an indirect estimate of
in ARDS patients mechanically ventilated with low tidal CO using parameters that are derived from a high-fidelity arterial
volumes and high ventilatory frequencies, PP variation may in trace (usually the PP and Asys) is commonly referred to as ‘Pulse
fact be a poor indicator of both circulating volume status and contour analysis’ (PCA). It, however, has to be borne in mind that
volume responsiveness. the estimates of CO obtained through PCA remains valid only as
long as the mathematical relationships established between the dif-
Figure 6 clearly shows the effects of IPPV on arterial pressure under
ferent parameters remains accurate. In other words, should either
normovolaemic and hypovolaemic conditions. Focus on the follow-
vascular capacitance or peripheral vascular resistance change
ing points:
because of the onset of new sepsis, use of vasopressors, administra-
(i) The normal fluctuations in the arterial pressure waveforms tion of regional blocks, etc. The estimates of CO obtained through
associated with IPPV and the transient increase in pressure during PCA also becomes inaccurate unless recalibration is undertaken
inspiration followed by a reduction during the expiratory phases. under the new set of circumstances. Vascular capacitance and per-
(ii) Note the beat-to-beat variations in PP and the ‘exaggerated swing’ ipheral vascular resistance are very variable in anaesthetized/critic-
in the presence of hypovolaemia. ally unwell subjects and therefore monitoring devices that claim to
undertake PCA without adequate provision for regular/periodic cali-
bration can be potentially misleading and should not be accepted for
Pulse contour analysis and the indirect clinical use in high-risk patients.9
estimation of cardiac output Two commonly used systems that utilize PCA for the estimation
of CO are the PiCCO (PULSION Medical Systems, Munich,
As explained in the previous section, the size of the pulsatile compo-
Germany) and the LiDCO (LiDCO Group Plc, London, UK) systems.
nent of the arterial pressure waveform (either PP or the area under
Both systems utilize transpulmonary indicator dilution techniques to
the systolic portion of the waveform Asys) are intimately linked to
provide periodic calibration of the arterial trace before PCA is used to
SV, vascular capacitance, and the systemic vascular resistance (the
derive CO. Whereas the former is based on transpulmonary thermal
role of the heart rate is in fact relatively minor in this context).
dilution, the latter depends on transpulmonary lithium dilution to
Under steady states and relatively stable conditions, when the vascu-
achieve this calibration. The relative merits and validity of these systems
lar capacitance and the systemic vascular resistance are relatively
in the clinical arena have been reviewed extensively before.10
constant, SV becomes the main determinant of both PP and Asys (see
Fig. 7). Under such conditions, if it is in fact feasible to measure
cardiac output (CO) directly using an independent method (such as
Pressure wave reflections
pulmonary artery thermal dilution or transpulmonary thermal dilu-
tion),7 8 it then becomes possible to establish the mathematical rela- In addition to the primary SP peak and the dicrotic wave, several
tionship between PP, Asys, and the independently measured SV. This other smaller secondary waves are frequently evident in an arterial
relationship—once established through this calibration step—can pressure trace (Fig. 8). Such secondary waves are usually produced
288 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 14 Number 6 2014
Arterial pressure wave form analysis
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 14 Number 6 2014 289
Arterial pressure wave form analysis
8. Nirmalan M, Willard TM, Edwards DJ, Little RA, Dark PM. Estimation of 10. Hadian M, Kim HK, Severyn DA, Pinsky MR. Cross-comparison of
errors in determining intrathoracic blood volume using the single transpul- cardiac output trending accuracy of LiDCO, PiCCO, FloTrac and pulmon-
monary thermal dilution technique in hypovolemic shock. Anesthesiology ary artery catheters. Crit Care 2010; 14: R212
2005; 103: 805–12
9. Sakka SG, Kozieras J, Thuemer O, van HN. Measurement of cardiac
output: a comparison between transpulmonary thermodilution and uncali- Please see multiple choice questions 25– 28.
brated pulse contour analysis. Br J Anaesth 2007; 99: 337– 42
290 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 14 Number 6 2014