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INTRODUCTION

  • Shock involves a group of syndromes that cause acute, generalized circulatory failure associated with inadequate tissue and organ perfusion. Shock is characterized by systolic blood pressure (SBP) <90 mm Hg (or reduction of at least 40 mm Hg from baseline) or mean arterial blood pressure (MAP) <70 mm Hg with tachycardia and organ perfusion abnormalities.

  • Classes of shock based on etiologic mechanisms include (1) hypovolemic, (2) cardiogenic, (3) obstructive, and (4) vasodilatory/distributive. Patients may have components of more than one shock syndrome upon presentation.

PATHOPHYSIOLOGY

  • Circulatory shock develops when the cardiovascular system is unable to deliver an adequate oxygen supply to meet tissue demands, resulting in cellular dysfunction, a shift in cellular metabolism to anaerobic pathways, and elevated blood lactate concentrations.

  • Hypovolemic shock is caused by inadequate venous return because of internal or external loss of intravascular fluids (eg, trauma, surgery, hemorrhage), resulting in insufficient cardiac preload and decreased stroke volume.

  • Cardiogenic shock results from loss of pump function because of decreased cardiac contractility (eg, acute myocardial infarction [AMI]), acute valvular abnormality, or arrhythmia (eg, ventricular tachycardia).

  • Obstructive shock results from extracardiac obstruction to blood flow into or out of the heart, such as tension pneumothorax, cardiac tamponade, or pulmonary embolism.

  • Vasodilatory/distributive shock is characterized by loss of vascular tone; this involves tissue hypoperfusion due to decreased systemic vascular resistance (or hypoperfusion despite normal or elevated cardiac output). Distributive shock is a subset of vasodilatory shock characterized by maldistribution of blood flow in organ microcirculation. Most cases of vasodilatory shock result in distributive shock. Almost all cases of septic shock result in vasodilatory/distributive shock.

  • The body responds to an abrupt decrease in tissue perfusion with subsequent restoration of perfusion, leading to a systemic inflammatory response syndrome (SIRS) with release of numerous mediators that interact to cause further injury. This “ischemia-reperfusion injury” results in edematous obstruction of capillaries, oxygen free-radical damage of cell membranes, activation of cellular (eg, white blood cells, platelets) and humoral (eg, procoagulants, anticoagulants, complement, kinins) components, release of other inflammatory mediators, and formation of microthrombi.

  • As part of the stress response, anti-inflammatory pathways are also activated to counterbalance the proinflammatory effects on tissues. Vagal nerve-mediated release of acetylcholine leads to suppression of proinflammatory cytokines by macrophages. The renin–angiotensin–aldosterone and hypothalamic–pituitary–adrenocortical systems are activated, with release of angiotensin II, vasopressin, and cortisol to maintain blood pressure (BP) via vasoconstriction and renal sodium and water retention. Cortisol and catecholamine release from the adrenal glands also inhibits proinflammatory cytokine production.

CLINICAL PRESENTATION

  • Patients may report dizziness, lightheadedness, confusion, and low urine production.

  • Symptoms related to the underlying shock etiology will be present (eg, cough, fever, malaise with pneumonia; chest pain with AMI).

  • Vital signs may reveal tachycardia (eg, >120 bpm), tachypnea (eg, >30 breaths/min), hypotension (eg, SBP <90 mm Hg), and low or normal body temperature (eg, 36°C–37°C [96.8°F–98.6°F]) in the absence of infection. Temperature ...

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