Shock.

DEFINITION Shock is a dramatic syndrome in which the circulatory supply of oxygen does not meet the metabolic demands of vital organs and tissues. There are five major types of shock observed: hypovolemic, septic, cardiogenic, distributive, and obstructive (see Table 1). PATHOPHYSIOLOGY An initial insult triggers shock disrupting blood flow to end organs leading to inadequate tissue perfusion. The body's compensatory mechanisms are initiated to maintain perfusion to vital organs leading to compensated shock. If treatment is not introduced during this period of compensated shock, the patient develops decompensated shock causing tissue damage that in turn leads to multi-system organ dysfunction and death (See Figure 1). The compensatory mechanisms are neuro-hormonal and include changes in heart rate, stroke volume, vascular smooth muscle tone, and fluid retention by the kidneys, etc. Through these mechanisms, the patient shunts blood flow away form non-vital tissues such as the periphery and gut to vital organs which include the brain, the heart, and the kidneys. If through these various mechanisms adequate perfusion to the heart and other vital organs cannot be maintained, the patient develops hypotension and decompensated shock. All forms of shock effect either preload, afterload (systemic vascular resistance – SVR), myocardial contractility or some combination of all three components leading to poor tissue perfusion. It is common for more than one of these processes to occur simultaneously. Preload decrease • External fluid losses: vomiting / diarrhea, bleeding, burns • Internal losses: excessive capillary leakage leading to significant third spacing. Afterload (SVR) • Abnormally decreased can lead to profound hypotension: sepsis – warm shock, anaphylaxis, spinal cord injury, toxins, etc. • Significantly increased as a compensatory mechanism: cardiogenic shock – which may amplify the primary problem, sepsis – cold shock Depressed myocardial contractility • Primary insult as seen in cardiomyopathies, arrhythmias, or immediately after cardiac surgery • Secondarily suppressed as noted in SIRS, pancreatitis, or septic shock. Once shock is initiated, it is important to recognize that mediators of tissue damage are activated and may cause progression from compensated shock to