Page 607 - Cardiac Nursing

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LWBK340-c24_ pp555-594.qxd 30/06/2009 01:43 PM Page 583 Aptara
C HAPTER 24 / Heart Failure and Cardiogenic Shock 583
the volume of blood returning to the systemic circulation. This In cardiogenic shock, failure of the left ventricle leads to acute
loss of circulating blood volume and impaired capillary flow re- cardiogenic pulmonary edema. Because of the increase in LV end-
sults in reduced venous return, further reducing cardiac output diastolic pressure, there is an increase in LA pressure and dilation.
and arterial pressure. This situation creates a positive feedback Pressure is increased within the pulmonary capillary bed, forcing
mechanism in which the low-flow state produces a further reduc- plasma or whole blood into the pulmonary interstitial compart-
tion in flow. 197 ment and, finally, into the pulmonary alveoli.
Respiratory rate and depth are initially increased in all forms
of shock, and patients may experience dyspnea or air hunger.
Diagnosis and Clinical Manifestations
This increased ventilation represents the body’s attempt to elim-
The diagnosis of shock is made by the history, physical examina- inate lactic acid resulting from decreased tissue perfusion. In-
tion, and collection of data from adjunctive diagnostic tests. creased respiratory depth also enhances blood return to the right
heart. Arterial blood gases initially reveal respiratory alkalosis. As
History shock progresses, a combined metabolic and respiratory acidosis
Most patients who present with cardiogenic shock have either a follows.
history of cardiovascular disease or risk factors for cardiovascular Neuroregulatory Assessment. Decreased cerebral blood
disease. Obtaining a thorough medical and surgical history is flow and coagulopathy can lead to a cerebral infarction or cerebral
vital to plan life-saving interventions. Much like chronic HF, a thrombus formation. Alterations in cellular metabolism through-
history may provide possible causes of the acute decompensa- out the body, metabolic acidosis, and the accumulation of toxins
tion.
further depress cerebral function. Lethargy, stupor, and coma de-
velop as shock progresses. Finally, in the irreversible stage of
Physical Examination shock, the vasomotor center in the brain is disrupted, causing fail-
Ongoing assessment of the patient at risk for or in shock, with ure of the circulatory mechanisms. 196
early detection of subtle changes in the patient’s condition, is Level of consciousness is an indicator of the adequacy of cerebral
essential. Subjective and objective data must be correlated with blood flow. With cerebral ischemia, the patient initially exhibits hy-
adjunctive clinical measurements, such as the measurement of pervigilance, restlessness, agitation, and mild confusion. Persistent
cardiac output and oxygen consumption. The clinical assess- cerebral hypoxia results in progressive unresponsiveness to verbal
ment of the patient provides the basis for medical and nursing stimuli with eventual coma.
interventions.
Gastrointestinal Assessment. Compensatory vasoconstric-
Cardiovascular Assessment. Low blood pressure is one of
tion in shock may result in mucosal ischemia, an ileus, and full-
the defining characteristics of shock. A MAP of 65 mm Hg is re-
thickness gangrene of the bowel. If the bowel wall becomes
quired to maintain adequate myocardial and renal perfusion.
disrupted, the normal bacterial flora of the intestines enters the
Shock is defined clinically as the pathophysiologic state that re-
abdomen and can then enter the circulation. Gastrointestinal
sults from a MAP of less than 65 mm Hg over time. Narrowing
bleeding may also occur. Factors that cause damage to the liver in-
of the pulse pressure indicates arteriolar vasoconstriction and a de-
creasing cardiac output. 1,197 Heart rate usually increases in re- clude decreased blood flow, splanchnic vasoconstriction, pooling
of blood in the microcirculation, right HF, and bacterial invasion.
sponse to sympathetic stimulation to compensate for decreased
The subsequent changes include loss of reticuloendothelial (tissue
stroke volume and to maintain cardiac output. In cardiogenic
macrophage) system function, increasing the risk of infection; a
shock the pulse is weak and thready.
Distended neck veins may be seen with cardiogenic shock. 44 decreased lactic acid conversion, contributing to metabolic acido-
sis; altered protein, fat, and carbohydrate metabolism; and altered
The presence of an RV heave, jugular venous V waves, and right- 197
bilirubin function. Jaundice, increased serum bilirubin levels,
sided S 3 or S 4 gallops may suggest pulmonary emboli. Distant
and increased serum enzymes are early indicators of liver damage
heart sounds and an exaggerated pulsus paradoxus ( 10 mm Hg)
associated with shock. Serum globulin is increased, and serum
suggest cardiac tamponade. A laterally displaced and sustained LV 196
albumin is decreased.
apical impulse with left-sided S 3 and/or S 4 suggests LV dysfunc-
tion. 44 Renal Assessment. Adequate renal perfusion produces a min-
imum of 400 mL urine/24 hours, or 20 mL/h. Impaired renal per-
Pulmonary Assessment. The lungs are fairly resistant to fusion in shock results in hourly urine outputs of less than 20
short-term ischemia. Thus, it is unlikely that low blood flow is the mL/h. 198 The excretion of high volumes of low solute urine may
sole cause of pulmonary insufficiency associated with shock. Other also represent renal hypoperfusion. Prolonged hypoperfusion may
contributory factors have been implicated, including thromboem- lead to acute tubular necrosis and acute renal failure. Urine output
boli or fat emboli in the pulmonary tree, and the toxic effects of is an indicator of the adequacy of renal perfusion and may decrease
fibrin degradation products that result from intravascular coagula- early in cardiogenic shock. Oliguria is defined by a urine output of
tion and serum complement depletion with sequestration of gran- less than 20 mL/h. Urine osmolarity and specific gravity increase,
ulocytes in the lung. These factors lead to increased pulmonary and urine sodium decreases with decreased urine output. An
capillary permeability. As the ensuing alveolar edema impairs sur- elevated serum creatinine is an early, nonspecific indicator of im-
factant production, massive atelectasis develops, clinically termed paired renal perfusion.
shock lung, systemic inflammatory response syndrome, adult res-
piratory distress syndrome, or primary pulmonary edema. These Integumentary Assessment. Skin appearance and tempera-
conditions are characterized by severe hypoxemia, dyspnea, a ture provide a clinical measure of peripheral circulation. Progres-
marked reduction in lung compliance, and the presence of exten- sive peripheral vasoconstriction results in a change from the initial
sive lung infiltrates. 196 normal skin appearance to cool, moist, pale skin with mottling. In