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C HAPTER 24 / Heart Failure and Cardiogenic Shock 569
Mean BNP levels for normal LV function 20%. 58 Historically, mortality has been linked to NYHA func-
versus LV dysfunction tional class (i.e., patient’s symptoms); newer algorithms include
1500
laboratory measures and quantitative data regarding LV status.
Clinical factors associated with a lower survival rates include older
1200 age; hyponatremia, decreased hematocrit; widened QRS; and
worsening LVEF, NYHA functional class, peak exercise oxygen
BNP pcg/dL 900 demonstrated an association between elevated circulating neuro-
43
While studies have
uptake (V O2 max), and renal function.
hormones (BNP, ET, and NE) and outcome, neurohormonal lev-
600
els are not used commonly in the clinical area to predict survival.
Sudden cardiac death (SCD; Chapter 27) remains an ever-present
risk. It is estimated that approximately 50% of patients with sys-
300
tolic dysfunction will die of a sudden tachycardic or bradycardiac
rhythm. Predicting SCD in this population has proven difficult;
0 thus, primary prevention measures, such as implantation of im-
Normal Systolic Diastolic Systolic &
N
N = 53
N = 105 N N = 42 Diastolic plantable cardioverter defibrillators (ICDs) is indicated in patients
N
N
N = 14 with LVEF less than 0.35. 59
■ Figure 24-11 BNP values for the different subclasses of LV dys- As imperfect as the ability to predict the outcome for individ-
function. Normal BNP levels are less than 100 pg/mL. (From Maisel, ual patients, candid discussions regarding prognosis must occur
A. S., Koon, J., Krishnaswamy, P., et al. [2001]. Utility of B-natri- between providers, families, and patients such that expectations
uretic peptide as a rapid, point-of-care test for screening patients un- can be aligned and plans made. As the tools to detect, quantify, di-
dergoing echocardiography to determine left ventricular dysfunction. agnose, and treat the syndrome of HF improve, the life trajectory
American Heart Journal, 141[3], 369.) of patients has improved. 43
Approach to Treatment
pressures. It is increased in patients with systolic and diastolic dys-
function, and although it cannot distinguish between the two dys- Patients with LV dysfunction often present with exercise intoler-
functions, it is being widely investigated as a biochemical marker for ance, shortness of breath, and/or fluid retention. Incidental find-
morbidity and mortality. 50–52 It is very helpful in differentiating ings of dysfunction also may be found in asymptomatic patients.
dyspnea caused by HF from other causes. The normal level of BNP All patients presenting with HF should undergo a detailed evalu-
is less than 100 pg/mL (Fig. 24-11). ation to: (1) determine the type of cardiac dysfunction, (2) un-
Although not a general test for HF, plasma homocysteine has cover correctable causative factors, (3) determine prognosis, and
been recently associated with an increased risk of vascular disease. (4) guide treatment. Recognition of signs and symptoms resulting
There is some evidence that increased plasma homocysteine level in- from an inadequate cardiac output and from systemic and pul-
dependently predicts risk of the development of HF in adults with- monary congestion is accomplished through a careful history,
out previous MI. 53 physical examination, routine laboratory analyses, and diagnostic
studies. 1
Prognosis There are various principles that guide management of HF.
The first and most important step begins with early identification
Despite many advances in the treatment of HF in the last decade of patients who we know to be at risk for developing the syn-
it remains a highly lethal syndrome, with more than 50,000 drome. The first step is identification and correction of the under-
deaths reported annually in the United States. 54 Most patients lying pathogenic processes, as appropriate, such as aggressive med-
with HF will die from the syndrome. The mode of death is typi- ical management of hypertension, coronary revascularization
cally either secondary to progressive LV dysfunction with systemic procedures for CAD or surgical correction of structural abnormal-
1
malperfusion or via a sudden arrhythmic event. Two-year mortal- ities. The second step is the removal of the compounding or pre-
ity rates of approximately 20% and 6-year rates of 50% have been cipitating causes, such as infection, arrhythmia, and pulmonary
reported in population-based studies. 55 A large community-based emboli. The third step is the treatment and control of HF. Ther-
cohort study revealed that the number of new cases of HF has not apy for HF is directed at reducing the workload of the heart and
declined over the past 20 years but survival has. The incidence of manipulating the various factors that determine cardiac perform-
HF was highest among men and survival after onset was worse in ance, such as contractility, heart rate, preload, and afterload. The
men. However, the largest survival gains over the last 20 years greatest advance has been in agents that inhibit harmful neuro-
were seen in the men and younger patients, with less improve- hormonal systems that are activated in support of the failing heart,
ment in women and patients over the age of 75. 56 specifically the RAAS and sympathetic nervous system. 60 Treat-
While complex algorithms and computer tools have been cre- ment of HF is based on the manner in which the patient clinically
ated and tested in the last few years to aid in estimating progno- presents, which may encompass the extremes from asymptomatic
sis, 57 it is important to remember that likelihood of survival can LV failure to acute cardiogenic shock.
only be determined in populations not in individuals. A large, HF ranges clinically from acute cardiogenic shock, acute de-
population-based study examined the association between appli- compensation of chronic HF, to compensated chronic HF. The
cation of the AHA/ACC HF staging system and survival. The fol- goal of therapy is support of pump function, which may include
lowing 5-year survival rates in patients were determined: stage 0, positive inotropic agents, vasodilator therapy, and/or, if extremely
99%; stage A, 97%; stage B, 96%; stage C, 75%; and stage D, severe, mechanical devices. In the case of ischemia caused by CAD,