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The failure of adequate perfusion and oxygenation to the body, or shock, is a disease entity that is a significant contributor of morbidity and mortality. This sinister illness can be very difficult to diagnose and adequately treat. Transient states of shock, defined as a systolic blood pressure (SBP) less than 100 mm Hg, have been reported to be present in up to 19% of emergency department (ED) patients, however, persistent shock is present in around 1–3% of all ED patients. While it is relatively uncommon, it suffers from an overall mortality rate as high as 20%. Death comes from multiorgan failure (MOF) that is commonly instigated by systemic hypoperfusion. The common denominator of all forms of shock is cellular hypoxia, which can be caused by either decreased oxygen delivery to the organs or from the inability of the tissues to utilize oxygen. The most common forms of shock are caused by decreased oxygen delivery and can be due to decreased oxygen in the blood, decreased quantity of blood in circulation, inability for the cells to adequately utilize oxygen, or an inadequate increase in oxygen content in response to a stress. The two main factors that contribute to tissue perfusion are systemic vascular resistance (SVR) and the cardiac output (CO). CO is determined by both the heart rate (HR) and the stroke volume (SV). An alteration in any of those variables can instigate a state of shock. Early in the disease progression the body is able to compensate if one of those variables is compromised. For example, a healthy patient with low SVR will increase the cardiac output to help maintain systemic perfusion. However, these compensatory mechanisms are finite and the different states of shock often involve more than one system (eg, septic shock can produce relative hypovolemia and myocardial dysfunction).


The identification of shock can be difficult, especially in the early phases. We often depend on the vital signs, but these can be misleading. Traditionally, a state of shock should be suspected with a persistent SBP less than 90 mm Hg even after adequate fluid administration. While this may be a good screening and identification tool, one must keep in mind that no individual vital sign derangement can adequately predict shock. A patient who has hypertension at baseline may have a significant and damaging decrease in SBP without dipping below 90 mm Hg. Also, patients in the early phases of shock are usually able to increase their adrenergic tone due to the upregulation of intrinsic catecholamines, which raises the blood pressure. The presence of tachycardia can also be used to identify a patient in shock; however, there are situations where a patient may be in a shock state and be unable to increase their heart rate, such as the shock state causing myocardial depression, and patients on calcium channel blockers (CCB) or β-blockers (BBs). Calculating a shock index ...

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