Page 606 - Cardiac Nursing

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582 PA R T I V / Pathophysiology and Management of Heart Disease
results in ventilatory failure. The increased volume begins to sant factor has been identified in the serum of patients in the
pool in tissues secondary to profound venoconstriction and in- early stages of septic shock. Its presence in other forms of shock
creased capillary permeability. remains controversial.
If the myocardial ischemia is severe and prolonged enough, my-
ocardial cellular injury becomes irreversible. 190 Cytokines are sig- Irreversible Stage
naling peptides whose actions include cell growth and cell death In this stage, the compensatory mechanisms are nonfunctioning
through direct toxic effects on the heart and peripheral circulation. or no longer effective, and hypotension has reached the critical
The proinflammatory or “stress-activated” cytokines include TNF- level of adversely affecting the heart and brain (Fig. 24-17). My-
and some interleukins (i.e., IL-1 , IL-6, IL-8, IL-12). The car- ocardial hypoperfusion, resulting from hypotension and tachycar-
diac myocytes themselves are capable of synthesizing these dia, produces acidosis, which leads to further depression of
proinflammatory cytokines in response to various forms of car- myocardial function. Decreased cerebral blood flow leads to de-
diac injury. The local inflammatory response can appear within pressed neuronal function and activity and loss of the central neu-
minutes of an abnormal stress. Local inflammation of the cy- ronal compensatory mechanisms. 197
tokines and other mediators includes deleterious effects of LV The progressive general hypoxia and reduction in cardiac out-
remodeling, which include myocyte hypertrophy, alteration in fe- put further deprive body cells of oxygen and nutrients needed for
tal gene expression, contractile defects, and progressive myocyte cell growth and result in microcirculatory insufficiency. The mi-
loss through apoptosis. 198 In addition to the direct detrimental crocirculation responds by vasodilatation to secure the necessary
effects of myocardial ischemia, there is some evidence that a pep- nutrients and oxygen for the deprived cells. Microcirculatory va-
tide secreted by the pancreas, the myocardial depressant factor, sodilatation, in association with systemic vasoconstriction, results
may further depress myocardial function. 11 Myocardial depres- in the sequestration of blood in the capillary beds, further limiting

■ Figure 24-17 In the irreversible stage of shock, a prolonged decrease in cardiac output and mean arterial
pressure leads to cellular necrosis and multiple organ failure.