Stress, Inflammation, and Shock

Published on 13/02/2015 by admin

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Last modified 13/02/2015

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Chapter 2 Stress, Inflammation, and Shock

The systemic inflammatory changes that accompany cardiac surgery and cardiopulmonary bypass can sometimes result in a clinical state that resembles septic shock. It is now recognized that severe systemic inflammation is a nonspecific host response to a range of physiologic stressors, of which infection and cardiopulmonary bypass are but two examples. Additionally, there is evidence that inflammation plays an important role in other forms of shock (e.g., hemorrhagic and cardiogenic shock).

In this chapter the physiologic basis and interrelationships among stress, inflammation, and shock are reviewed, with particular emphasis on cardiac surgery patients.


Tissue injury results in the activation of nociceptors, which transduce a signal of actual or threatened tissue damage, via the sensory neurones, to the medulla of the brain. This signal is then integrated within the brain stem and results in activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, and the hypothalamic-pituitary axis. Hypothalamic corticotropin releasing hormone stimulates the release of adrenocorticotropic hormone from the anterior pituitary, which in turn stimulates the release of cortisol and other glucocorticoids from the adrenal cortex. In addition, growth hormone is released from the anterior pituitary, vasopressin from the posterior pituitary, and glucagon from the pancreas. The secretion of thyroid hormones and insulin are suppressed.1

This neuroendocrine response results in a multitude of changes throughout the body.

Heart rate and blood pressure are immediately increased. Blood flow is directed away from organs such as the gut and the skin. The kidneys retain sodium and water, and urine output is reduced. The metabolic consequences consist of increased catabolism of carbohydrates, proteins, and lipids. Hepatic glycogenolysis is facilitated by cortisol and catecholamines and, later, gluconeogenesis occurs from precursors such as lactate and amino acids. Despite increased glucose production, glucose uptake into most cells is decreased because of reduced insulin release and tissue insulin resistance, resulting in hyperglycemia. Protein catabolism is promoted primarily through the action of cortisol. An adult may lose as much as 0.5 kg of protein mass per day following major surgery. The amino acids that are released by protein catabolism, in particular alanine and glutamine, are used for hepatic gluconeogenesis and the synthesis of acute phase proteins (fibrinogen, C-reactive protein, α2-macroglobulin). Catecholamines, growth hormone, and reduced levels of insulin promote lipolysis and the breakdown of triglycerides into glycerol and free fatty acids. Thus, under conditions of metabolic stress, the myocardium continues to utilize free fatty acids as its predominant energy substrate while, despite hyperglycemia, glucose uptake is inhibited due to reduced levels of insulin. Because fatty acids are a less oxygen-efficient fuel than glucose, these effects can provoke or exacerbate myocardial ischemia.


Inflammation is primarily a protective response to tissue injury that helps destroy or quarantine harmful agents or damaged tissue. Inflammation may be localized (e.g., the region of redness, swelling, and warmth surrounding an insect bite) or systemic. Systemic inflammation occurs in a variety of clinical situations, including major surgery, cardiopulmonary bypass, burns, pancreatitis, myocardial infarction, and sepsis. The systemic inflammatory response is a continuum. At one end of the spectrum is a barely detectable, self-limited state manifested by a mild fever, leukocytosis, and an increase in inflammatory markers (e.g., C-reactive protein). This is the situation that typically occurs following major surgery or a myocardial infarction. At the other end of the spectrum is a profoundly harmful, self-reinforcing syndrome manifested by circulatory shock and multiple organ failure.2,3

The Mechanisms of the Inflammatory Response

During cardiac surgery, systemic inflammation develops in response to a number of pathophysiologic processes, including surgical trauma, hypothermia, exposure of blood to the cardiopulmonary bypass circuit, blood loss or transfusion, translocation of endotoxin from the gut to the circulation, and ischemia-reperfusion injury.

The mechanisms of inflammation and the interactions among the various components are extremely complex and only a brief description is provided here. The process is summarized in Fig. 2-1.

Contact Activation: Platelets, Coagulation, Complement

The exposure of blood to the cardiopulmonary bypass circuit causes the activation of platelets and the coagulation and complement cascades:

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