Porth's Essentials of Pathophysiology, 4e

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Circulatory Function

U N I T 5

As shock progresses, the respirations become rapid and deep to compensate for the increased production of acid and decreased availability of oxygen. Decreased intravascular volume results in decreased venous return to the heart and a decreased central venous pressure (CVP). The pulse becomes weak and thready, indicat- ing vasoconstriction and reduced filling of the vascular compartment. When shock becomes severe, the periph- eral veins may collapse. Sympathetic stimulation leads to intense vasoconstriction of the skin vessels, which results in cool and mottled skin. In hemorrhagic shock, the loss of red blood cells results in pallor of the skin and mucous membranes. Urine output decreases very quickly in hypovolemic shock. Compensatory mechanisms decrease renal blood flow as a means of diverting blood flow to the heart and brain. Oliguria of 20 mL/hour or less indicates inadequate renal perfusion. Continuous measurement of urine output is essential for assessing the circulatory and volume status of the person in shock and monitor- ing the response to fluid replacement. Restlessness, agitation, and apprehension are com- mon in early shock because of increased sympathetic outflow and increased levels of epinephrine. As the shock progresses and blood flow to the brain decreases, restlessness is replaced by altered arousal and menta- tion. Loss of consciousness and coma may occur if the person does not receive or respond to treatment. Treatment. The treatment of hypovolemic shock is directed toward correcting or controlling the underlying cause (replacing or shifting volume) and improving tis- sue perfusion. Ongoing loss of blood must be corrected, such as in surgery. Oxygen is administered to increase oxygen delivery to the tissues. Medications usually are administered intravenously. Frequent measurements of heart rate and cardiac rhythm, blood pressure, and urine output are used to assess the severity of circulatory compromise and to monitor treatment. Restoration of vascular volume can be accomplished through intravenous administration of fluids, blood and blood products. 52 The crystalloids (e.g., isotonic saline and Ringer lactate) are readily available and effective, at least temporarily. Colloids or plasma volume expand- ers (e.g., pentastarch and colloidal albumin) have a high molecular weight, do not necessitate blood typ- ing, and remain in the vascular space for longer periods than crystalloids such as dextrose and saline, but are considerably more expensive. 52,53 Blood or blood prod- ucts (packed or frozen red cells) are administered based on hematocrit and hemodynamic findings. Fluids and blood are best administered based on volume indicators such as CVP and urine output. Vasoactive medications are agents capable of con- stricting or dilating blood vessels. Considerable con- troversy exists about the advantages or disadvantages related to the use of these drugs. As a general rule, vasoconstrictor agents are not used as a primary form of therapy in hypovolemic shock, and may be detrimen- tal. 54 Replacing volume is the first priority but vaso- pressor and inotropic agents may be used as an adjunct

to help restore tissue perfusion and normalize cellular metabolism. These agents are given only when volume deficits have been corrected yet hypotension persists. Cardiogenic Shock Cardiogenic shock occurs when the heart fails to pump blood sufficiently to meet the body’s demands (see Fig. 20-7). Clinically, it is defined as decreased cardiac output, hypotension, hypoperfusion, and indications of tissue hypoxia despite an adequate intravascular vol- ume. 55,56 Cardiogenic shock most commonly occurs from an acute myocardial infarction, 57 but may also occur from non-ischemic causes including myocardial contu- sion, acute mitral valve regurgitation due to papillary muscle rupture, sustained arrhythmias, severe dilated cardiomyopathy, and cardiac surgery. Cardiogenic shock can also occur with other types of shock because of inadequate coronary blood flow. Approximately 3% to 6% of the patients with ST elevation MI (STEMI) develop cardiogenic shock despite receiving reperfusion therapy (see Chapter 19). 55–57 Most patients who die of cardiogenic shock have had extensive damage to the left ventricle because of a recent infarct or reinfarction. Regardless of cause, in persons with cardiogenic shock there is failure to eject blood from the heart, hypoten- sion, and inadequate cardiac output. Compensatory neu- rohumoral responses take place, which include activation of the sympathetic and renin-angiotensin systems lead- ing to vasoconstriction, tachycardia, and fluid retention. Increased systemic vascular resistance often contributes to the deterioration of cardiac function by increasing after- load or the resistance to ventricular systole. Preload, the filling pressure, also is increased as blood returning to the heart is added to blood that previously was not pumped forward, resulting in an increase in end-systolic ventricu- lar volume. Increased resistance to ventricular systole (i.e., afterload) combined with decreased myocardial contrac- tility causes an increase in end-systolic ventricular volume and preload, further complicating cardiac status. Manifestations. The signs and symptoms of cardio- genic shock are consistent with those of end-stage heart failure. The lips, nail beds, and skin may become cya- notic because of stagnation of blood flow and increased extraction of oxygen from the hemoglobin as it passes through the capillary bed. Mean arterial and systolic blood pressures decrease due to poor stroke volume, and there is a narrow pulse pressure and near-normal diastolic blood pressure because of arterial vasoconstric- tion. Urine output decreases because of lower renal per- fusion pressures and the increased release of aldosterone. Elevated preload is reflected in a rise in CVP and pul- monary capillary wedge pressure of at least 15 mm Hg. Neurologic changes, such as alterations in cognition or consciousness, may occur because of low cardiac output and poor cerebral perfusion. Treatment. Treatment of cardiogenic shock requires striking a precarious balance between improving car- diac output, reducing the workload and oxygen needs