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pressure and flow.
Thus, if peripheral vasodilators are used it is very helpful to document that as
pressure is lowered, stroke volume and cardiac output increase appropriately. How
much pressure should be reduced is dependent on the clinical response of the
patient. Peripheral resistance is often very high in these patients because of the low
cardiac output and exaggerated sympathetic response resulting in intense periph-
eral vasoconstriction. As the vascular bed dilates, blood pressure falls, cardiac
output increases, and peripheral perfusion improves with improvement in urine
flow and correction of metabolic disturbance, usually lactic acidosis. Clearly the
pressure that is associated with optimal clinical response should be the target.
It should also be remembered that patients who present acutely with left ven-
tricular failure and high peripheral resistance are often inappropriately treated
with diuretics which leads to occult hypovolemia [7]. Peripheral vasodilators are
usually given and dilating both the venous and arterial beds the hypovolemia
becomes obvious with a sudden severe fall in cardiac output and mean arterial
pressure. Apart from the obvious effect on peripheral perfusion, the fall in diastolic
arterial pressure can have profound effects on myocardial perfusion exacerbating
any underlying ischemic potential. These rapid changes in the physiological status
of the patient further confirm the importance of adequate invasive monitoring in
such clinical situations.
Blood Pressure and Prognosis in Acute Hypovolemia and Sepsis
Blood pressure has been and is still used as a therapeutic target in the manage-
ment of acute hypovolemia in the emergency room, particularly in patients with
Arterial Pressure: A Personal View 91
trauma. Based mainly on anecdotal experience, a systolic pressure of 100 mmHg is
the usual target, together with a heart rate not in excess of 120 beats/minute. This
is mainly achieved by fluid resuscitation, initially with crystalloid and then blood
and colloid depending on the clinical situation.
However, this protocol is not without considerable controversy [8, 9], particu-
larly in the management of penetrating trauma such as gunshot and stab wounds.
It is argued that systolic pressure should be maintained between 70 and 80 mmHg
by restricting fluid resuscitation to a minimum. The protagonists of this protocol
argue that this minimizes the delay in getting the patient to the operating room and
more importantly reduces the risk of thrombus that may have formed at the site of
the vascular injury from being `blown off\u2019 by inappropriate systolic pressure.
Although the concept of the `golden hour\u2019 in which resuscitation should be
optimized is widely accepted, there is unfortunately little scientific evidence justi-
fying a systolic pressure of 100 mmHg as a means of achieving this goal. Indeed
studies [8] have demonstrated no correlation between pressure and simultaneously
measured oxygen delivery. This protocol is usually undertaken by emergency
room physicians.
In contrast, patients with septic shock are more likely to be managed within the
ICU where the blood pressure target is usually a mean pressure of 65 to 70 mmHg.
It is not at all clear why this difference has emerged although it may be related to
the fact that measurements of cardiac output are much more likely to be made in
the ICU environment. This almost certainly leads to better control of the circulation
particularly when markers of perfusion such as lactate, base deficit, and mixed
venous oxygen saturation are also monitored.
Although there are several studies demonstrating the prognostic values of base
deficit and lactate [10, 11], in trauma patients blood pressure is still considered the
most important physiological variable whilst flow is rarely measured in the emer-
gency room. This is perhaps understandable because of the practical difficulties in
making such measurements in the acute situation. It is of particular interest,
therefore, that Rivers et al. [12] used central venous saturation as a surrogate for
cardiac output in severely septic patients admitted to an emergency room and
showed that the group where central venous saturation was maintained at 75% had
a significantly lower mortality than the control group where saturation was main-
tained at around 68%. The mean blood pressure was significantly higher in the
treatment group at 6 hours as a result of more aggressive fluid resuscitation.
However, there was a subgroup of 63 patients (Rivers, unpublished data, per-
sonal communication) who had raised lactate levels and low central venous satu-
rations where the mean arterial blood pressure was greater than 100 mmHg. These
were younger and otherwise fitter patients with less comorbidity. The patients
assigned to the control group had a 60-day mortality of almost 70%. In very marked
contrast, the patients in the treatment group had a 60-day mortality of only 24%.
This is an extraordinary difference in outcome even though it is a relatively small
number of patients. Indeed the mortality in these control patients was 13% higher
than that of the control group from the whole study. How can these differences be
explained?
The patients in this study were clearly severely hypovolemic as reflected by the
very low central venous saturations of less than 50% on admission to the emergency
92 D. Bennett
room. As these patients in the subgroup were younger than those in the main body
of the study, their cardiovascular reflexes were more likely to be intact resulting in
profound arteriolar constriction to maintain mean blood pressure above 100
mmHg. As the authors point out, it is well known that mean blood pressure is well
maintained as blood is lost by a proportional increase in systemic vascular resis-
tance until about 18% of the total blood volume has been lost, even though cardiac
output will have fallen significantly. It is only then, as peripheral resistance reaches
a plateau, that the continuing loss of blood volume is associated with a steep fall in
both cardiac output and mean arterial pressure.
These results are similar to the findings in normal subjects [13] where hypovo-
lemia has been produced by prolonged passive 50° head up tilt. This led to a 9%
rise in mean arterial pressure, a 37% fall in cardiac output, a rise in peripheral
resistance of 41%, and rise in heart rate of 48%. After 30 minutes, the subjects
became pre-syncopal and mean arterial pressure fell to 20% below baseline value
Fi.g. 1 Two different arterial pressure profiles during Valsalva maneuvers in 2 normal individuals,
both in supine position. A: \u201ctypical\u201d response. B: \u201csquare\u201d response usually associated with large
intrathoracic volumes. a, phase I; b, early phase II; c, late phase II; d, phase III; e, phase IV. [32]
Arterial Pressure: A Personal View 93
and heart rate exactly to base line. Simultaneously measured central venous satu-
ration fell linearly from 75 to 60% during this period. These findings suggest that
in the very acute situation with rapid changes in vascular volume, blood pressure
probably is not the optimal physiological variable to be monitored and indeed in
some circumstances relying on blood pressure alone may result in an increase in
mortality. Rivers (unpublished data, personal communication) has suggested that
in his study, the subgroup of patients with mean BP above 100 mmHg in the control
group received less aggressive volume resuscitation thus prolonging tissue hypop-
erfusion and hypoxia.
Studies in ICU patients, where the focus has been the maintenance of blood
pressure, have not been particularly fruitful. Most intensivists accept that pressure
needs to be kept at a level which allows adequate tissue perfusion particularly of
the kidneys and heart and that alpha agonists are the most widely used agents to
achieve this. More recently there has been increased interest in studying the role
of vasopressin [14\u201316] and its analogs in patients with hypotension due to sepsis.