There is a common failure to understand that the hypovolaemia in patients with severe sepsis requires successive fluid challenges rather than a simple fluid infusion. Large fluid deficits can result from diarrhoea or third space losses in peritonitis, but vasodilatation and capillary leak also lead to dramatic intravascular volume depletion. Fluid challenges should be titrated to the clinical endpoints of blood pressure, heart rate, urine output, and other markers of perfusion. In persistent hypotension with hypoperfusion, it is essential that the attending doctor stays with the patient until acceptable parameters have been reached or the patient is transferred to the ICU for further monitoring and treatment with vasoactive drugs.
Invasive or more sophisticated monitoring than simple pulse, blood pressure, and urine output should be instituted early in severe sepsis. Early goal-directed therapy has been shown to improve outcome. Severe sepsis is a complex ICU disease. Close attention must be paid during the administration of fluids as signs of pulmonary oedema and bilateral infiltrates on the chest x ray film can appear without obvious fluid overload if ARDS is present (see later). PA catheters are often used in severe sepsis precisely because it can be difficult to evaluate the degree of hypovolaemia, the presence of cardiac dysfunction, and thus the aetiology of any pulmonary oedema.
Unlike other causes of shock, the cardiac output is often maintained or even increased in severe sepsis. Septic shock results from alterations in the distribution of blood flow. There is loss of control of the microvasculature with the abnormal distribution of cardiac output. Reduced oxygen and nutrient delivery to the tissues causes organ dysfunction. The goal of therapy is therefore to restore tissue perfusion through the use of fluids and vasoactive drugs.
Systemic vascular resistance (SVR) can be measured by invasive and non-invasive means and is of great value in titrating vasoactive drugs in severe sepsis, when the SVR is usually low. SVR may be thought of as the resistance against which the heart pumps. It is calculated using a PA catheter as follows:
MAP - CVP in mmHg x 80 (correction factor)
CO in litres per minute
The normal range is 1000-1500 dyn.s cm-5. SVR is mainly determined by the diameter of arterioles, which is affected by intrinsic autoregulation, locally produced substances that vasodilate (for example, nitric oxide), hypoxaemia, neural factors, and circulating toxins. SVR increases with normal ageing in Western populations. SVR x body surface area in kg m-2 gives the systemic vascular resistance index (SVRI), which is often used in clinical practice.
Ideally, blood pressure is measured invasively with an arterial line, as measurement of blood pressure with a cuff is often unreliable and inaccurate at low blood pressures. The level of mean arterial pressure (MAP) to aim for is not clear but most studies have shown that a MAP of < 60 mmHg is associated with compromised autoregulation in the coronary, renal, and brain circulations. MAP is not commonly used on general wards - a practical guide is that you should aim for a blood pressure that adequately perfuses the tissues and this is usually - but not always - >90 mmHg systolic. To a certain extent adequate perfusion depends on the patient's usual blood pressure, which should be identified if possible. Some patients require higher pressures for adequate perfusion.
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