2 - Qatar Critical Care Conference Proceedings
  • ISSN: 0253-8253
  • EISSN: 2227-0426


Shock is a state of ‘acute circulatory failure’, the key feature of which is an inability for tissues and cells to get enough oxygen to meet their needs, ultimately resulting in cell death1. Shock can be classified as hypovolemic, cardiogenic, obstructive or distributive although many patients will have several types of shock simultaneously1. Although it is important to identify and treat the underlying cause of shock (e.g., antibiotics and source removal for septic shock; thrombolysis or embolectomy for massive pulmonary embolism causing obstructive shock1, hemodynamic support must be started immediately in all cases to provide a minimum perfusion pressure and prevent development or worsening of organ dysfunction. In this context, both “flow” “pressure” are important components. Indeed, the arterial pressure is determined by blood flow and vascular tone, i.e., blood pressure = cardiac output x systemic vascular resistance. The essential aspects of shock resuscitation can be remembered using the simple VIP mnemonic: ventilate (ensure adequate oxygenation), infuse (provide adequate fluid resuscitation), and pump (administer vasoactive agents). Fluid administration should be guided by repeated fluid challenges so that patients receive enough fluid but not too much, as excess fluid can have multiple harmful effects. If hypotension is severe, vasopressors should be started early, at the same time as fluids, to increase systemic vascular resistance and thus arterial pressure. Prolonged periods of hypotension are associated with worse outcomes2. Importantly, although an initial mean arterial pressure (MAP) target of 65 mmHg may be a useful aim, this will not be optimal for all and target values should be adapted according to the individual patient, taking into account various factors including age and history of chronic hypertension. Indeed, if the MAP target is too low, resultant hypoperfusion may lead to cellular death and organ dysfunction, but a target that is too high may be associated with edema and excessive vasoconstriction as a result of higher amounts of fluid and vasoactive agents3, which may also impair organ function. Patients with circulatory shock must therefore be carefully monitored, including regular assessment of cardiac output, and treatment and targets adapted accordingly. Monitoring organ perfusion at the bedside is difficult without specific tools to assess the microcirculation. As such, we must generally rely on three “windows” that can indicate inadequate perfusion, i.e., impaired cutaneous perfusion, impaired renal function, and impaired mental status1. Plasma lactate levels can also be useful, with changes over time providing some indication of adequacy of tissue oxygenation. Although these changes are too slow to help acutely guide therapy, the trend can provide valuable information about patient status over time. If flow remains inadequate and there is no, or only a poor, response to fluids, an inotropic agent may be considered. Dobutamine is the inotrope of choice. In this context, measurement of mixed (SvO) or central venous (ScvO) oxygen saturation can help as it provides an indication of the balance between oxygen delivery and consumption, with low values ( < 70%) suggesting that increasing oxygen delivery could be beneficial4.


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  • Article Type: Conference Abstract
Keyword(s): fluidshock and vasopressor
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