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 . 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  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.  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  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.  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.