Page 598 - Cardiac Nursing

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574 PA R T I V / Pathophysiology and Management of Heart Disease
associated with both severe IR and fatal hyperglycemia. Such as- in hemoglobin in patients with HF has been shown to be an in-
sociation gives pause to examine the mechanistic impact of IR on dependent predictor of mortality and rehospitalization in many
the myocardium. A more common thought is that HF predisposes studies, 49,57,119 it is difficult to determine if the HF outcome is wors-
a person to developing IR or Type II DM. There are data to sug- ened by the anemia or the anemia is secondary to worsening HF.
gest that 43% of patient with HF exhibit abnormal glucose me- There are currently no recommendations to treat anemia in patients
tabolism. 103 A recent prospective study suggested a one standard with HF. Diagnosis and evaluation of potential reversible causes,
deviation decrease in insulin sensitivity increased the risk of HF such as nutritional deficiencies, should be undertaken, but given the
by one third. 104 Previous studies have shown that even a 1% in- absence of long-term clinical trials, aggressive treatment with trans-
crease in hemoglobin A1c increases the risk of HF by 15%. 105 fusions or exdogenous erythropoetin is not recommended. 120
One must recognize that while systemic IR (Type II DM) is asso- Interestingly, perhaps an alternative hypothesis may be that the
ciated with increased mortality in patients with HF, 106 systemic anemia associated with HF is an adaptive mechanism. Hemoglobin
and myocardial IR may be different. Interestingly, cardiac is high in oxidative stress and as such reduction in trafficking of
positron emission tomography studies suggest that a failing my- such an agent may be in fact a compensatory mechanism. Further
ocardium has reduced glucose uptake in favor of free fatty acid up- work in this area is ongoing and highlights an important point that
take; in patients with Type II DM, myocardial glucose uptake is observations made in the patient with HF cannot automatically be
even lower. 107 converted to treatment options without prospective, well-done ran-
domized clinical trials. 118
Smoking Cessation. Cessation of smoking has a dramatic
effect on improvement in health status. Smoking contributes to Depression. Patients living with HF have a significant bur-
32% of all deaths due to cardiovascular disease in the United den of symptoms. Optimizing their health status is an important
States. 108 Patients with HF who continue to smoke have an ap- goal of therapy, yet specific factors influencing health status are
proximately 30% to 50% higher risk hospitalization for HF, MI, just now being studied. Significant depressive symptoms is re-
121,122
and death than patients who do not smoke. 109,110 While many ported by approximately 30% to 50% of patients with HF.
patients with HF who have smoked long periods of time may These depressed patients report a significantly higher symptom
question the benefit of quitting seemingly late in the course of burden, lower physical and social function, and lower quality of
their lives, there is strong evidence to support that within 2 years life compared to nondepressed patients with HF. In fact, depres-
of quitting, the increased relative risk of both hospitalization for sive symptoms are some of the strongest predictors of decline in
121
HF and MI drop similar to those levels in persons who have never health status in patients with HF. Symptoms of depression
smoked. 110 In fact mortality benefits associated with smoking ces- have been associated with a 56% increase likelihood of death or
sation exceed those of many of the standard pharmacologic treat- hospitalization for HF even after controlling for other markers of
123
ment regimes, such as ACE-I and -blocker therapy in patients disease severity. What remains unclear and is the focus of on-
with HF. The benefits of smoking cessation accrue rapidly (within going study are the effect of interventions aimed at treatment of
124,125
one year) in patients with HF. Despite this clear benefit, many depression in this population.
nurses and health care providers are hesitant to address this issue Sleep Disturbances. The link between sleep disordered
with this patient population. 111 Data suggest that only 9% of breathing and HF has recently been made. Patients with obstructive
smokers hospitalized with HF are counseled to quit smoking. 112 sleep apnea have a 2.4 times higher risk of developing HF inde-
However, there is mounting evidence that smokers who received pendent of other risk factors. Interestingly, the risk of HF associ-
42
assistance from a nurse have a 28% greater probability of quit- ated with obstructive sleep apnea exceeds that of hypertension,
ting. 113 Documentation of assessment of tobacco use and subse- CAD, and stroke. Respiratory events during sleep have long been
quent smoking cessation counseling is now an indicator of quality known to cause hypoxemia, systemic and pulmonary hypertension,
under new Joint Commission on the Accreditation of Healthcare sympathetic activation and reduced stroke volume. 126 Patients
Organizations standards of practice for all patients hospitalized for with sleep apnea have dynamic ST-segment and T-wave changes
HF (Chapter 34). 114
on ambulatory ECG monitoring consistent with myocardial is-
chemia. 127,128 While the many mechanisms that might link the
Anemia. Anemia is a common problem in patients with HF broad spectrum of sleep disturbances to clinical HF remain un-
and reduced LVEFs. Some estimates suggest that the incidence certain, several hypotheses are plausible. Obstructive sleep apnea
is as high as 60%. 115 While the precise prevalence is unknown, is associated with sympathetic hyperactivity, 129 which can cause
anemia does appear more common in HF patient groups with hypoxia—a putative atherogenic factor 130 —and pulmonary hy-
other comorbidities, such as renal dysfunction and advanced pertension; 131 sympathetic hyperactivity and pulmonary hyper-
age. Anemia occurs secondary to a deficiency in new erythrocyte tension both lead to and exacerbate the syndrome of HF. While
production relative to the rate of removal of aged erythrocytes. there is no current evidence that treating sleep disorders will pre-
Erythropoetin, primarily produced by the kidneys, is the key vent HF, data are beginning to suggest that treatment of HF with
component in red blood cell mass. Abnormalities that impact re- continuous positive airway pressure improves outcomes in patients
nal perfusion impact the body’s response to erythropoetin. In ad- with documented sleep apnea. 132
dition, iron deficiency is present in about 30% of anemic patients
with HF. 116 Age, female sex, decreased GFR, decreased body mass Cognitive Dysfunction. Cognitive dysfunction, including
index, use of ACE-I, increased jugular venous pressure, and lower impairments in memory, attention, learning, psychomotor ability,
extremity edema have all been associated with anemia. 117,118 perceptual skills, and language are common in patients with HF. 133
Chronic anemia is associated with sodium and water retention, Difficulties with memory and concentration are very common in
reduction of renal blood flow, and neurohormonal activation—all patients with HF. 134 It has been reported recently that 30% to
defining characteristics of the syndrome of HF. While reduction 50% of patients with HF will have diminished cognition. 134,135