Page 579 - Cardiac Nursing

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CHAPTER
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H H H H Heart Failure and Cardiogenic Shock
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Laurie A. Soine
syndrome haave evolved secondary to the tools available to ddetect
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HEART FAILURE andd mark the diseasse progreession. During the nineteenthh century y
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thhe ltered architectuurre of the failing heart was implicated as the
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H Heart ffailuree (HF) is a pa hophhy isi lologiic state inn whichh an abbnor- cause of patient’s symptoms. In 1832, James Hope first described
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malityy of cardiac function is responsible for inadequate systemic ba backward failure s the failure that results as thhe ventricle fails to
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perfusion. HF is not an event or disease but rather a constellation pump its volume, causing blood accumulation and subsequent
of signs and symptoms that represent the final pathway of a het- increase in ventricular, atrial, and venous pressures. A primary
erogeneous group of diseases, the end result of most cardiovascular cause of backward failure was mechanical cardiac obstruction.
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disease states. The extent and severity by which cardiac function The term forward failure, proposed by MacKenzie in 1913, was
is impaired varies greatly. It is the primary reason people over the applied to a situation in which the primary pathologic process
age of 65 are hospitalized in the United States. 2,3 Three-month re- was decreased cardiac output, which ultimately leads to a de-
hospitalization rates for recurrent failure are as high as 79%. 3 crease in vital organ perfusion, and to water and sodium reten-
The prevalence of the syndrome of HF has increased dra- tion. MacKenzie was the first to propose that intrinsic myocar-
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matically throughout the world over the last decade, attributa- dial abnormalities lead to the death of patients with this
ble to both the general aging of the worlds’ population and ad- syndrome. By the mid-1920s Starling and colleagues revolu-
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vances in the treatment of acute cardiac disease. Over 5 million tionized the understanding of the syndrome with their animal
people carry the diagnosis, with approximately 550,000 new studies describing the effect of alterations in pressure and flow on
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cases diagnosed annually. While the syndrome of HF has been myocardial performance. This work formed the basis upon which
extensively researched and intensively studied, it remains a sig- the syndrome was understood until almost the end of the twen-
nificant and growing health problem in the United States and tieth century. The hemodynamic derangement secondary to pres-
worldwide. There is an increasing incidence of HF in the aging sure and flow abnormalities became the accepted paradigm, ex-
population, with a prevalence of approximately 10% by age 70 plaining the therapeutic interventions of the time. If pressure and
years. For HF occurring in the absence of myocardial infarc- volume where the two components of myocardial contractility—
tion (MI), the lifetime risk is 1 in 9 for men and 1 in 6 for causing reduced cardiac output, therapeutic interventions were
women; the increase in HF is largely attributable to hyperten- aimed at accurately assessing and altering hemodynamics. While
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sion. The American Heart Association estimates that greater we now know that cardiac hemodynamics play a role in the syn-
than $33 billion is spent on the syndrome of HF annually. 4 drome of HF, therapeutic intervention targeted at normalization
As many as 20 million people in the United States who have of hemodynamic derangement did not translate to improved
asymptomatic impairment of cardiac function are likely to outcomes in patients.
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develop symptoms of HF within 5 years. In the past decade, ex- Advances in cellular biochemistry and biophysics in the
perimental and clinical studies have demonstrated altered neuro- 1970s to 1980s lead to a widening of the lens through which
hormonal activity as a major pathophysiologic component of HF. the complexity and progression of the HF syndrome emerged.
The quality of life, exercise capacity, and perhaps the life ex- Patients with HF were noted to have markedly elevated levels
pectancy of patients with HF can be altered by the introduction of stress hormones such as norepinephirine. These discoveries
of appropriate medical and nursing interventions. led some to hypothesize that while myocardial dysfunction be-
This chapter reviews major physiologic and pathophysiologic gins the syndrome, progression and subsequent death of the pa-
concepts of chronic HF as a basis for understanding its underlying tients may be attributable to dramatic neurohormonal abnor-
causes as well as its clinical and physical findings. Emphasis also is malities. By the early 1990s studies of medications aimed at
placed on the various diagnostic tests, the vast array of pharmaco- altering the neurohormonal milieu within the body solidly sup-
logic agents, and medical and nursing interventions in the adult pa- ported the neurohormonal/neuroendocrine hypothesis that re-
tient with ventricular dysfunction. With this knowledge, the nurse mains the target of many of our current interventions. How-
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is able to develop and implement a plan of care, to identify patients ever, by the turn of the twentieth century advances in the ability
at risk for developing the syndrome, and to optimize the functional to measure molecular changes in myocytes has lead to an ever
capacity and outcome of patients living with the syndrome of HF. complex understanding of the collection of complex genetic
Although pharmacologic agents are reviewed in this chapter, refer to and molecular disorders that lead to and perpetuate the syn-
current sources of information for specifics of use and dose. drome.
Historic Perspective Etiologies and Definitions
The understanding of the syndrome of HF has evolved dramat- HF is a complex clinical syndrome manifested by shortness of
ically in the last 100 years. Advances in our understanding of the breath, fatigue, and characterized by abnormalities of left ventricular
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