Page 604 - Cardiac Nursing

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580 PA R T I V / Pathophysiology and Management of Heart Disease
increase in intensity in an attempt to restore adequate tissue per- A reduction in arterial blood pressure secondary to decreased
fusion. 190 The compensatory mechanisms are directed at the blood volume, decreased cardiac output, or increased venous
restoration and maintenance of adequate blood volume, cardiac capacitance initiates the body’s compensatory mechanisms to
output, and vascular tone. The initial compensatory mechanisms maintain adequate tissue perfusion. These mechanisms serve to in-
vary with the primary pathophysiologic derangement, but the in- crease cardiac output and arterial blood pressure through increas-
termediate and final stages are similar. The initial compensatory ing heart rate, enhancing myocardial contractility, providing selec-
mechanisms in cardiogenic shock are an increased heart rate and tive vasoconstriction, conserving sodium and water, and shifting
increased SVR. fluid from the interstitial to the intravascular space.
Specialized nerve endings (mechanoreceptors) in the carotid
Initial Stage sinus, aortic arch, heart, and lungs sense the decrease in blood
In cardiogenic shock, the decreased coronary blood flow results in pressure and transmit their impulses to the vasomotor center.
profound local compensatory events. Figure 24-15 graphically dis- The vasomotor center stimulates the sympathetic nervous sys-
plays the compensatory mechanisms activated in the initial states tem, inhibits the parasympathetic nervous system, and initiates
of an acute reduction in cardiac output. There is an increase in my- the secretion of catecholamines from the adrenal gland. Sympa-
ocardial oxygen extraction and dilatation of the coronary arteries. thetic nervous system stimulation unopposed by parasympathetic
The myocardial cells shift to anaerobic metabolism and use glycol- effects results in increased heart rate, increased myocardial con-
ysis in the production of adenosine triphosphate (ATP). 196,197 tractility, and selective vasoconstriction. Reflexes of the sympa-
These events occur immediately in response to myocardial is- thetic nervous system are active within 30 seconds of an acute
chemia. If compensatory mechanisms are inadequate, myocardial decrease in circulating blood volume and are able to compensate
contractility decreases, leading to a decrease in cardiac output and for a 20% loss in blood volume by increasing cardiac output by
systemic hypoperfusion. 20% to 25%. 196 In response to ischemia and sympathetic

■ Figure 24-15 In the initial stage of shock, all three types of shock lead to a decrease in mean arterial pres-
sure. Compensatory mechanisms attempt to reduce the effects of this decreased mean arterial pressure and, if
successful, lead to an increase in cardiac output and mean arterial pressure.