Вы находитесь на странице: 1из 12

Cover

Pathophysiological
Relationships Between
Heart Failure and
Depression and Anxiety
DEBORAH W. CHAPA, PhD, ACNP-BC
BIMBOLA AKINTADE, PhD, ACNP-BC, MBA, MHA
HEESOOK SON, RN, PhD, MPH
PATRICIA WOLTZ, RN, MS
DENNIS HUNT, EDD, CSCS
ERIKA FRIEDMANN, PhD
MARY KAY HARTUNG, MALS, MSPH
SUE ANN THOMAS, RN, PhD

Depression and anxiety are common comorbid conditions in patients with heart failure. Patients with heart
failure and depression have increased mortality. The association of anxiety with increased mortality in patients
with heart failure is not established. The purpose of this article is to illustrate the similarities of the underly-
ing pathophysiology of heart failure, depression, and anxiety by using the Biopsychosocial Holistic Model of
Cardiovascular Health. Depression and anxiety affect biological processes of cardiovascular function in patients
with heart failure by altering neurohormonal function via activation of the hypothalamic-pituitary-adrenal
axis, autonomic dysregulation, and activation of cytokine cascades and platelets. Patients with heart failure
and depression or anxiety may exhibit a continued cycle of heart failure progression, increased depression, and
increased anxiety. Understanding the underlying pathophysiological relationships in patients with heart failure
who experience comorbid depression and/or anxiety is critical in order to implement appropriate treatments,
educate patients and caregivers, and educate other health professionals. (Critical Care Nurse. 2014;34[2]:14-25)

H
eart failure is an epidemic with national and global implications. Compared with
the situation in other cardiac diseases, the incidence and prevalence of heart failure
continue to increase despite recent advancements in understanding and treatment.
Increased survival after myocardial infarction, aging of the population, and increased
incidence of diabetes are contributing factors.1 In the United States, heart failure is

CNE Continuing Nursing Education


This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,
which tests your knowledge of the following objectives:

1. Describe the biopsychosocial holistic model for cardiovascular health


2. Identify 2 neurohormonal pathways and their impact in heart failure
3. Identify nursing implications for heart failure, depression, and anxiety

©2014 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2014938

14 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


the primary diagnosis in more than 1 million hospital- in depression symptoms were significantly predictive of
izations, and the estimated cost is $40 billion annually.1 higher mortality rates. In 2 studies31,37 no relationship
Depression is a common comorbid condition in was detected between depressive symptoms and mortal-
patients with heart failure.2 Prevalence of depression ity. In one of these studies,37 a questionnaire with only 4
was 23.8%3 to 67%4 in 8 studies of inpatients with heart items was used to assess both anxiety and depression, a
failure5-10 and 16.7%11 to 70%12 in 22 studies of outpatients method that decreases sensitivity and specificity of the
with heart failure.11-32 The wide range reflects the inpa- assessment. In the other study,31 the sample size was
tients and outpatients assessed and the methods used small (n=111), mortality was low, and none of the patients
to determine depression, including diagnostic inter- had indications of severe depression. The association
views and a variety of both brief and extensive symptom between anxiety and mortality was recently examined in
inventories. The prevalence of depression in all studies only 2 studies.31,34 In one study,31 the investigators found
of patients with heart failure is greater than the preva- no relationship between anxiety and mortality. This study
lence in the general population.33 was underpowered, and only 10% of the sample reported
Compared with depression, anxiety is less commonly moderate to severe symptoms of anxiety. In the other
examined in patients with heart failure.2 The prevalence study,34 patients with heart failure and high anxiety had
of anxiety in patients with heart failure was determined a significantly shorter period of event-free survival than
in 14 studies.2,16-21,25-35 Prevalence was 14.8% in the 1 study21 did patients with heart failure and lower anxiety. Event-
of inpatients and 11%25 to 54%34 in the 13 studies of out- free survival was defined as the period without rehospi-
patients. A total of 8 different instruments were used to talization or death. The results did not indicate a direct
assess anxiety in these 14 studies, resulting in the wide association between anxiety and mortality in patients
range of prevalence. The Brief Symptom Inventory was with heart failure.
used in the 3 studies16,28,34 with the highest prevalence rates. Depression contributes to increased mortality in
The Hamilton Anxiety and Depression Scale was used in patients with heart failure. The association between
5 studies26,29-31,35; the prevalence of anxiety was 21% to increased anxiety and mortality has not been estab-
30%. Regardless of the method of assessment, the preva- lished. More studies on the association in patients with
lence of anxiety in patients with heart failure was greater heart failure are needed.
than the prevalence of 11.3% in the general population.33 In this article, we use the Biopsychosocial Holistic
The association between depression and mortality Model of Cardiovascular Health to describe the relation-
in patients with heart failure was examined in 9 stud- ships of the underlying pathophysiology of heart failure,
ies.13,22,25,31,36-40 In most studies (7 of 9),13,22,25,36,38-40 increases depression, and anxiety. Patients with heart failure who

Authors
Deborah Chapa is an assistant professor and coordinator of bachelor of nursing science to doctor of nursing practice at George Washington
University, School of Nursing, Washington, DC. She is also an acute care nurse practitioner.
Bimbola Akintade is an assistant professor in the trauma, critical care, emergency department and clinical nurse specialist nurse practitioner
program at the University of Maryland, School of Nursing, and an acute care nurse practitioner at Washington Hospital Center, Baltimore,
Maryland.
Heesook Son is an assistant professor at Chung-Ang University School of Nursing, Seoul, South Korea.
Patricia Woltz is director of nursing research at the University of Maryland Medical Center in Baltimore.
Dennis Hunt is an assistant professor, physical therapy and human performance, and director of the exercise science program at Florida Gulf
Coast University, Fort Meyers, Florida.
Erika Friedmann is a professor at the University of Maryland, School of Nursing.
Mary Kay Hartung was a health sciences librarian at Florida Gulf Coast University. She is now retired.
Sue Ann Thomas is a professor emeritus of nursing at the University of Maryland School of Nursing.
Corresponding author: Deborah W. Chapa, PhD, ACNP-BC, Assistant Professor, George Washington University, School of Nursing, 2010 M St NW, Ste 300, Washington, DC
20036 (e-mail: dchapa@gwu.edu).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)
362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

www.ccnonline.org CriticalCareNurse Vol 34, No. 2, APRIL 2014 15


are depressed or anxious may be trapped in a harmful
loop in which depression and anxiety symptoms might Biological realm Psychological realm

be worsened by the synergistic pathophysiological Age Anxiety


changes associated with heart failure. Sex Depression
Cardiovascular
Race/ethnicity health Stress
Biopsychosocial Holistic Model of Genomics
Cardiovascular Health
Thomas et al41 have proposed a holistic model of car- Social realm
diovascular health based on the biopsychosocial model.42 Social support
Engel42 believed that treatment directed at the biological Pet ownership
factors alone would not restore health. The biopsycho- Socioeconomic status
social holistic model is an interactive biological, psycho-
logical, and social model in which factors work together Figure 1 Biopsychosocial holistic model of cardiovascular
health.
within a person to affect cardiovascular health (Figure 1).
Unlike the situation in a biomedical model of disease,
health is considered a process in which acute and damage to heart muscle impairs the heart’s pumping or
chronic shifts in each realm interact to either enhance filling ability.53 Current understanding of heart failure
or inhibit pathological processes and thus affect health. involves a neurohormonal model. Many of the neurohor-
Interaction between the biological and psychological mones involved in heart function, such as norepineph-
realms is illustrated by increased mortality in patients rine, angiotensin II, aldosterone, and tumor necrosis
with depression and heart failure.13,22,25,31,36-40 An example factor α (TNF-α), are synthesized both within endocrine
of the interaction between the psychological and the organs, from which they are released into the circulation,
social realms is the independent association between and within the myocardium, where they cause interac-
increased anxiety and low social support that is predic- tions between and within myocardial cells.54-56 The Table
tive of readmission of heart failure patients.23 Another lists the major neurohormones involved in heart failure,
example of the interaction of all 3 realms is the relation- depression, and anxiety and their effects. Increases in
ship of dog ownership and cardiovascular health.43 neurohormones initially are an adaptive physiological
Depression and anxiety affect biological processes of response. However, in heart failure, long-term activation
cardiovascu- of these biochemical messengers results in direct end-
Dysregulation of the autonomic nervous lar function organ damage to the heart and vasculature.57 Neurohor-
system is a predictor of progression of heart in patients mone dysregulation also occurs in depression and anxiety.58
failure, mortality, and sudden cardiac death. with heart Neurohormone dysregulation in depression and anxiety
failure by also includes increases in corticotropin-releasing factor,
altering neurohormonal function via activation of the norepinephrine, angiotensin II, and aldosterone.58 In
hypothalamic-pituitary-adrenal (HPA) axis,44,45 auto- many instances, the pathological processes of anxiety
nomic dysregulation,46,47 and activation of cytokine cas- parallel those of depression, although some cardiac
cades and platelets.48-50 Conversely, neurohormonal effects of anxiety are thought to be due to an exaggerated
dysfunctions due to heart failure may increase the risk sensitivity to exogenous stress.58
for depression and anxiety in patients with this cardio- Figure 2 is a simplified representation of the complex
vascular abnormality.44-47,51,52 pathophysiological mechanisms that link depression,
anxiety, and heart failure. An overview of the pathophys-
Role of Neurohormones iological mechanisms that link the elements of the model
Heart failure is a progressive, complex pathophysio- together are discussed in the following sections.
logical state.53 The usual clinical manifestation of heart
failure is left ventricular dysfunction that occurs after Activation of the HPA Axis
some index event, such as myocardial infarction, uncon- In response to mental and physical stress, activation
trolled hypertension, or hereditary causes, in which of the HPA axis occurs, leading to the following reactions.

16 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


Table Major hormones involved in heart failure, depression, and anxiety

Neurohormone Site Action/effect


Corticotropin-releasing factor Synthesized in hypothalamus and Signals hypothalamic neurons to synthesize and release adreno-
peripheral cells such as corticotropin from the anterior part of the pituitary gland
T lymphocytes Corticotropin then stimulates release of cortisol and aldosterone
Cortisol Produced in the adrenal cortex Increases glucose through gluconeogenesis
Suppresses the immune system
Aids in fat, protein, and carbohydrate metabolism
Decreases bone formation
Inhibits peripheral utilization of glucose (insulin resistance)
Increases blood pressure by increasing sensitivity of the
vasculature to epinephrine and norepinephrine
Promotes anti-inflammatory mechanism that reduces histamine
secretion
Norepinephrine Produced in adrenal medulla and Increases blood pressure by increasing vascular tone
released from cells in adrenal Directly increases heart rate
medulla and postganglionic Causes release of glucose from energy stores
parasympathetic neurons Increases blood flow to skeletal muscle
Increases oxygen supply to the brain
Epinephrine Produced and released mainly in Increases heart rate
adrenal medulla but also heart Increases blood vessel diameter
and brain Promotes bronchodilation
Stimulates glycogenolysis in the liver and muscle
Inhibits insulin secretion
Increases levels of blood glucose and fatty acids
Aldosterone Produced by adrenal cortex Promotes conservation of sodium
Promotes secretion of potassium
Increases water retention
Increases blood volume and therefore blood pressure
Angiotensin II Produced by conversion of Causes vasoconstriction of systemic arterioles, resulting in
angiotensin I by angiotensin- elevated arterial blood pressure
converting enzyme Aids in norepinephrine release and reuptake
Increases circulating levels of antidiuretic hormone, resulting in
increases in vasoconstriction and inhibition of water excretion
Cytokines Produced by macrophages Promote immunosuppression
Promote inflammation
Promote cardiac remodeling

The hypothalamus releases corticotropin-releasing factor. sites where the hormone is produced.66 Increased levels
This factor signals hypothalamic neurons to synthesize of aldosterone in the circulation or in heart tissue stimu-
and release corticotropin and also signals cells in the ante- late excessive production of collagen, which leads to car-
rior part of the pituitary gland to release corticotropin.59 diac fibrosis and cardiac remodeling.66 Further, cortisol
Corticotropin stimulates release of cortisol and aldos- may mimic the effects of aldosterone in patients with
terone from the adrenal cortex.60 Hypercortisolemia con- heart failure because of changes caused by damage to
tributes to abdominal obesity,61 hypertension,62 insulin myocardial tissue.66 Elevated serum levels of cortisol and
resistance,63 and inflammation. Aldosterone promotes aldosterone are independent predictors of mortality in
water reabsorption, conservation of sodium, and secre- patients with heart failure.67
tion of potassium, increasing circulating blood volume Aldosterone level is also elevated in patients with
and ultimately increasing blood pressure.64,65 depression and may precipitate depression.67 Little is
The HPA axis is activated by a failing ventricle. There- known about the relationship between aldosterone and
fore, with increased severity of heart failure, production anxiety. No studies on the relationship and changes of
of aldosterone increases. Aldosterone is also produced aldosterone level and anxiety or aldosterone in heart
within the heart and works directly on heart tissue at the failure, depression, and anxiety are available.

www.ccnonline.org CriticalCareNurse Vol 34, No. 2, APRIL 2014 17


Increased free fatty acids
Increased sodium and water Hypothalamic-
retention pituitary-
adrenal axis

Increased thrombus Heart failure Reduced heart rate


formation Platelet Autonomic variability
Increased heart activation Depression dysregulation Increased
muscle contractility catecholamine levels
Anxiety

Cytokine
Immunosuppression,
cascade
inflammation, myocardial
Pathophysiological processes explained in this remodeling
diagram may ultimately lead to increased
mortality, increased sudden cardiac death,
and increased ventricular arrhythmias.

Figure 2 Proposed pathophysiological mechanisms linking depression to heart failure.

Hyperactivity of the HPA axis mediates hyperactivity anxiety or depression have both abnormalities, and this
of the sympathetic nervous system and increases circu- combination is also associated with increased severity of
lating levels of norepinephrine and epinephrine. Levels anxiety and depression.45
of circulating norepinephrine and epinephrine fluctuate Patients with heart failure who have signs and symp-
in patients with heart failure.68 In patients with heart toms of depression and increased levels of norepinephrine
failure, high norepinephrine levels are predictive of poor and epinephrine have greater than normal responsive-
prognosis. Patients with decompensated heart failure ness to β-adrenergics such as epinephrine. Increased
have increased levels of norepinephrine and epineph- β-adrenergic sensitivity is postulated to be associated
rine. However, patients with chronic but stable heart with cardiac remodeling and progression of heart failure.72
failure usually have increased levels of circulating norep- Anxiety reduces compliance with medications, resulting
inephrine but no marked changes in levels of circulating in shorter event-free survival.73 No published studies on
epinephrine. Myocardial levels of norepinephrine may the combination of anxiety, epinephrine, and heart fail-
be reduced in the later stages of heart failure.69 ure are available.
Patients with depression and anxiety also have
increased levels of norepinephrine and epinephrine.45 Autonomic Dysregulation and
Emerging evidence on norepinephrine in depression Sudden Cardiac Death
indicates that the hormone has a determinant role in The autonomic nervous system regulates cardiovas-
regulating cognition, motivation, and intellect, provid- cular homeostasis via sympathetic and parasympathetic
ing the fundamentals for social relationships.70 Epineph- nerves. Norepinephrine and epinephrine are the major
rine also regulates attention, mental focus, arousal, and catecholamines released by the autonomic nervous sys-
cognition.71 One-quarter to one-half of individuals with tem (see preceding section on activation of the HPA

18 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


axis). Heart rate varies frequently over time in response also causes vasoconstriction of systemic arterioles, result-
to changes in the physical and mental needs of the body. ing in elevated arterial blood pressure. Other potent
Ventricular rate can be calculated by measuring the RR effects of angiotensin II in patients with heart failure are
interval on an electrocardiogram. Changes in the RR inhibition of the release and reuptake of norepinephrine
interval are described as either an increase or a decrease and increases in circulating levels of antidiuretic hormone,
in heart rate variability. Heart rate variability can reflect which also increase vasoconstriction and inhibition of
increased sympathetic activity, decreased parasympa- water excretion.78,79
thetic activity, or a balance of the 2 activities.74 There- Other important pathophysiological complications
fore, heart rate variability, a measure of beat-to-beat due to angiotensin II and aldosterone are release of
alterations in heart rate, is used to measure autonomic inflammatory cytokines, activation of macrophages at
neurocardiogenic dysfunction.74 sites of injury, attraction of neutrophils and macrophages,
Dysregulation of the autonomic nervous system is a increased
predictor of progression of heart failure,75 mortality, and growth of Increased activation if the HPA axis, autonomic
sudden cardiac death.75 Decreased heart rate variability fibroblasts, dysregulation, activation of RAAS, and cytokine
is associated with increased severity of heart failure and and syn- cascades occur in patients with heart failure
increased dysrhythmia in patients with depression76 and thesis of who are depressed or anxious.
anxiety.45 In patients with depression, an imbalance exists collagen
between sympathetic and parasympathetic tone. Induc- fibers. Deposition of fibroblasts and collagen results in
tion of depression, defined as anhedonia in a rodent model, ventricular hypertrophy and fibrosis of the myocardial
increased susceptibility to ventricular arrhythmias.77 wall, leading to inappropriate heart remodeling and sub-
Risk of sudden cardiac death may be increased in sequent systolic and diastolic ventricular dysfunction.80
patients with anxiety because of an increased risk for The RAAS is activated in both patients with depres-
ventricular arrhythmias. Higher anxiety scores have been sion and patients with anxiety.81 In a study by Häfner et
related to lower heart rate variability and increased risk al,82 depressive symptoms alone were not linked to
of sudden cardiac death.45 The combined impact of auto- increased activation of RAAS, but patients with chronic
nomic dysregulation in patients with heart failure who stress and depressive symptoms had activation of the
have depression or anxiety disorders has not been estab- system. No investigators have examined the RAAS and
lished. According to the biopsychosocial holistic model, depression and heart failure or RAAS and anxiety and
the biological factor of autonomic dysregulation is asso- heart failure.
ciated with heart failure and with depression and anxiety.
Activation of Cytokine Cascades
Renin-Angiotensin-Aldosterone System Cytokines are widely secreted peptides that mediate
The release of aldosterone is also initiated by the renin- and regulate cellular immune function. Cytokines exert
angiotensin-aldosterone system (RAAS). The release of both proinflammatory and anti-inflammatory control
renin, an enzyme synthesized, stored, and released by over physiological conditions. Like the neurohormones
juxtaglomerular cells in the kidney, is stimulated by the previously discussed, under normal physiological condi-
sympathetic nervous system, renal artery hypotension, tions, cytokines limit the potentially injurious effects of
and decreased amounts of sodium delivered to the distal sustained inflammatory reactions.83 When proinflamma-
tubules of the kidney.78,79 After release by juxtaglomerular tory cytokines are unchecked by anti-inflammatory
cells, renin moves into the bloodstream, leading to con- cytokines, illness such as heart failure may result. Proin-
version of the inactive plasma protein angiotensinogen flammatory cytokines have direct toxic effects on the
to angiotensin I. Then, angiotensin-converting enzyme heart and are hypothesized to be responsible for myocar-
converts angiotensin I to angiotensin II. After this con- dial remodeling and progression of heart failure.84
version, angiotensin II stimulates the adrenal cortex to TNF-α and interleukin-6 (IL-6) are proinflammatory
release aldosterone. Aldosterone is metabolized in the cytokines that produce abnormal endothelium-dependent
liver. In patients with heart failure and resulting liver con- vasodilation and myocardial dysfunction.84 High levels
gestion, aldosterone levels are increased. Angiotensin II are independent predictors of mortality in patients with

www.ccnonline.org CriticalCareNurse Vol 34, No. 2, APRIL 2014 19


heart failure.85 Increased plasma levels of IL-6 in patients poor prognosis at 30 and 180 days.93 Patients with depres-
with heart failure are associated with activation of the sion and anxiety have elevated levels of C-reactive pro-
sympathetic nervous system.84 TNF-α initiates processes tein.94 According to the biopsychosocial holistic model,
that result in left ventricular dysfunction, pulmonary the biological factors of cytokines, levels of C-reactive
edema, and cardiomyopathy. Elevated levels of periph- protein, and heart failure interact with the psychological
erally circulating TNF-α are associated with increased factors of depression and anxiety, compounding the possi-
severity of heart failure.85 Three sources of TNF-α after bility for a poor prognosis in patients with heart failure
myocardial injury in heart failure are proposed: (1) who are depressed or anxious or both.
TNF-α produced locally in the myocardium triggers the
HPA axis and leads to secondary activation of the immune Platelet Activation
system in the periphery86; (2) decreased cardiac output The biological factor of heart failure and the psycho-
causes underperfusion of systemic tissues and leads to logical processes of depression and anxiety increase platelet
elaboration of the factor87; and/or (3) activation of the reactivity.48-50 In heart failure, through a complex process
immune system occurs in response to injury from some that includes a cascade of neurohormones, activated
index event.88 platelets interact with leukocytes to adhere to endothelial
Complex and not fully understood, depression is cells in the vasculature and promote thrombosis.95 Through
accompanied by moderate activation of proinflamma- stimulation of platelet receptors for norepinephrine and
tory cytokines, in particular TNF-α, IL-1, and IL-6.89 epinephrine, elevated levels of circulating catecholamines
Receptors for these cytokines have been found in the potentiate platelet responses.95 Platelet activation is
hippocampus and hypothalamus. Levels of TNF-α were increased in depression.48 No published articles on platelet
significantly higher in outpatients with depression and activation in anxiety or on platelet activation in depres-
heart failure than in outpatients with heart failure and sion and anxiety and heart failure are available.
no depression.88 In addition, levels of IL-6 were higher
in patients with depression and heart failure who were Summary of Pathophysiological
hospitalized.89 Cytokines can be also triggered by mental Mechanisms That Link Depression and
stress and are associated with anxiety and fear in healthy Anxiety to Heart Failure
people without Increased activation if the HPA axis, autonomic dys-
Improvement in depression and anxiety heart failure.90 regulation, activation of RAAS, and cytokine cascades
is associated with improvement in med- Administration occur in patients with heart failure who are depressed or
ication compliance and health outcomes of cytokines to anxious. Because of the combined effects of emotional
in patients with cardiovascular disease. patients can pro- distress and heart failure, patients with heart failure who
duce “sickness are depressed or anxious may be at greater risk than
behavior,” which is characterized by marked behavioral patients who are not depressed or anxious for progres-
symptoms of depression and anxiety that include increased sion of heart failure. The substantial research supporting
sleep, decreased appetite, malaise, decreased motivation, increased mortality in depressed patients with heart fail-
impairment in cognition, and depressed memory.91 ure provides noncausal evidence of the relationship.
C-reactive protein is found in the blood and is known
as an acute-phase protein, or a marker of inflammation. Effects of Selective Serotonin
The release of IL-6 triggers the synthesis of C-reactive Reuptake Inhibitors and Exercise
protein by the liver. Serum levels of C-reactive protein A recent systematic review96 of studies from 1996 to
are elevated in cardiovascular disease, and research on 2011 provided an evaluation of the effects of interven-
C-reactive protein in patients with heart failure is increas- tion on depression in patients with heart failure. Evidence
ing. Increased levels of C-reactive protein are associated was strong for the use of selective serotonin reuptake
with increased severity of heart failure and can independ- inhibitors, and moderate evidence supported use of
ently increase morbidity and mortality in patients with exercise to reduce depression in patients with heart fail-
heart failure.92 After an episode of acute heart failure, ure. Disease management programs for patients with
levels of C-reactive protein increase and contribute to a heart failure did not improve depressive symptoms.

20 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


The effect of selective serotonin reuptake inhibitors on physical activity patterns for patients with heart failure
depression in patients with heart failure was examined in is essential. Nurses who care for patients with heart failure
4 double-blind, placebo-controlled randomized trials.97-100 can benefit from an understanding of pathophysiology,
Use of paroxetine98 and sertraline99 reduced depression in signs and symptoms, depression, and anxiety. Signs and
2 of the trials, whereas use of sertraline97 and citalopram100 symptoms of heart failure can mimic signs and symptoms
yield no improvement in 2 other trials. The limitation of of depression and anxiety, and shared pathophysiologi-
the 2 studies in which no difference occurred was that the cal mechanisms may potentiate comorbid progression.
control groups in both studies inadvertently received ther- Improvement in depression and anxiety is associated
apeutic interventions. The strength of the evidence is high with improvement in medication compliance and health
that paroxetine and sertraline are effective in treating outcomes in patients with cardiovascular disease.115
depression in patients with heart failure.96
The effects of an exercise program on depression in Patient and Family Education
patients with heart failure were examined in 7 studies.101-107 Patients and their families may lack understanding
The exercise programs varied by type, intensity, frequency, of the diagnoses of depression and anxiety, the underly-
duration, and patients’ adherence. Despite the differences, ing pathophysiology, and the interrelationships between
the strength of the evidence was moderate that exercise depression, anxiety, and heart failure. Patients and their
is effective at decreasing depressive symptoms in patients family mem-
with heart failure. The recently completed HF-ACTION bers also Similar pathophysiological processes in
(Heart Failure: A Controlled Trial Investigating Outcomes require edu- depression, anxiety, and heart failure
of Exercise Training) indicated that regular exercise con- cation about suggest that the onset and progression of
fers a modest reduction in the risk for all-cause mortality treatment these conditions may be linked.
or hospitalization in patients with heart failure.108 The options for
same trial indicated a significant reduction in depressive depression that include selective serotonin reuptake
symptoms, illustrating that exercise may be an effective inhibitors (paroxetine and sertraline), exercise, and
intervention for reducing depressive symptoms and pre- physical activity. Important information for patients and
venting worsening of depressive symptoms of patients families about these treatments includes the side effects,
with heart failure.109 Physical activity also enhances anti- the length of treatment required for anticipated benefits
inflammatory responses and reduces proinflammatory to begin, and the possibility that more than 1 treatment
responses.110 Currently, physical activity is recommended may be required to obtain effective results. Patients and
as safe and effective in patients with heart failure.111 their families should be encouraged by the knowledge
Multidisciplinary, multicomponent disease manage- that an improvement in quality of life often accompanies
ment programs for patients with heart failure were exam- improvement in the signs and symptoms of depression
ined in 7 studies.112-118 The results were strong evidence and anxiety.119
that disease management programs do not decrease depres-
sive symptoms in patients with heart failure. The objec- Implications for Nursing Research
tive of disease management programs is not reduction Similar pathophysiological processes in depression,
in depression, and these programs may have other bene- anxiety, and heart failure suggest that the onset and pro-
fits for patients with heart failure. gression of these conditions may be linked. Although
Currently no clinical guidelines for diagnosing and anxiety in heart failure is common, few investigators
treating depression in patients with heart failure are avail- have evaluated anxiety in patients with heart failure.
able.111 Further research is needed to establish effective More research on anxiety in patients with heart failure is
treatments for depression in patients with heart failure. needed. Research on the pathophysiological changes that
occur in patients with heart failure who are depressed and
Nursing Implications anxious is critical. Evidence-based treatments for depres-
Screening and Assessment sion and anxiety in patients with heart failure have not
Development of a comprehensive evidence-based been established. Research is needed to determine which
assessment tool that includes depression, anxiety, and treatments are most effective and whether the treatment

www.ccnonline.org CriticalCareNurse Vol 34, No. 2, APRIL 2014 21


of depression and anxiety will improve morbidity and predictive of depressive symptoms in patients hospitalized for heart fail-
ure. Cardiol J. 2011;18(1):18-25.
mortality in patients with heart failure. 6. Sharma V, Zehtabchi S, Rojas N, Birkhahn R. Ethnic variations in qual-
ity of life and depressive symptoms among black Americans with acute
decompensated heart failure. J Natl Med Assoc. 2009;101:985-991.
Conclusion 7. Lesman-Leegte I, Jaarsma T, Sanderman R, Hillege HL, van Veldhuisen
DJ. Determinants of depressive symptoms in hospitalised men and
Increasing evidence supports depression and anxiety women with heart failure. Eur J Cardiovasc Nurs. 2008;7:121-126.
8. Johansson P, Lesman-Leegte I, Svensson E, Voors A, van Veldhuisen DJ,
as frequent comorbid conditions in patients with heart Jaarsma T. Depressive symptoms and inflammation in patients hospital-
failure. Major pathophysiological changes that occur in ized for heart failure. Am Heart J. 2011;161(6):1053-1059.
9. Jenner RC, Strodl ES, Schweitzer RD. Anger and depression predict hos-
depression and anxiety have potentially deleterious effects pital use among chronic heart failure patients. Aust Health Rev. 2009;33:
541-548.
on the heart. Using a holistic model to understand the 10. Angermann CE, Gelbrich G, Störk S, et al; Competence Network Heart
integration of mind and body in health status, nurses Failure. Somatic correlates of comorbid major depression in patients with
systolic heart failure. Int J Cardiol. 2011;147:66-73.
can improve assessment and treatment of patients with 11. Holzapfel N, Müller-Tasch T, Wild B, et al. Depression profile in patients
heart failure who are depressed and anxious. The most with and without chronic heart failure. J Affect Disord. 2008;105(1-3):53-62.
12. Macabasco-O’Connell A, Crawford MH, Stotts N, Stewart A, Froelicher
effective treatments for depression and anxiety in patients ES. Gender and racial differences in psychosocial factors of low-income
patients with heart failure. Heart Lung. 2010;39:2-11.
with heart failure have not been established. Research 13. Frasure-Smith N, Lespérance F, Habra M, et al; Atrial Fibrillation and
is needed on the physiological changes that occur in Congestive Heart Failure Investigators. Elevated depression symptoms
predict long-term cardiovascular mortality in patients with atrial fibril-
patients with heart failure who are depressed and anxious. lation and heart failure. Circulation. 2009;120:134-140, 3 p following 140.
14. Schiffer AA, Pedersen SS, Broers H, Widdershoven JW, Denollet J. Type-
Research is needed to determine which treatments are D personality but not depression predicts severity of anxiety in heart
most effective and whether the treatment of depression failure patients at 1-year follow-up. J Affect Disord. 2008;106:73-81.
15. Moser DK, Dracup K, Evangelista LS, et al. Comparison of prevalence of
and anxiety will improve morbidity and mortality in symptoms of depression, anxiety, and hostility in elderly patients with
heart failure, myocardial infarction, and a coronary artery bypass graft.
patients with heart failure, depression, and anxiety. CCN Heart Lung. 2010;39(5):378-385.
16. Chung ML, Moser DK, Lennie TA, Rayens MK. The effects of depressive
Acknowledgment symptoms and anxiety on quality of life in patients with heart failure
The authors would like to thank Lori Lupe, DNP, MSN, CCRN, Executive Director and their spouses: testing dyadic dynamics using Actor-Partner Interde-
of Acute Care and Emergency Department at University of Miami Hospital, pendence Model. J Psychosom Res. 2009;67:29-35.
for her help in editing an early version of this paper. 17. Gottlieb SS, Kop WJ, Ellis SJ, et al; HF-ACTION Investigators. Relation
of depression to severity of illness in heart failure (from Heart Failure
Financial Disclosures And a Controlled Trial Investigating Outcomes of Exercise Training [HF-
None reported. ACTION]). Am J Cardiol. 2009;103(9):1285-1289.
18. Cully JA, Jimenez DE, Ledoux TA, Deswal A. Recognition and treatment
of depression and anxiety symptoms in heart failure. Prim Care Com-
panion J Clin Psychiatry. 2009;11(3):103-109.
19. Kato N, Kinugawa K, Yao A, Hatano M, Shiga T, Kazuma K. Relationship
Now that you’ve read the article, create or contribute to an online discussion of depressive symptoms with hospitalization and death in Japanese
about this topic using eLetters. Just visit www.ccnonline.org and select the arti- patients with heart failure. J Card Fail. 2009;15:912-919.
cle you want to comment on. In the full-text or PDF view of the article, click 20. Rohyans LM, Pressler SJ. Depressive symptoms and heart failure: exam-
“Responses” in the middle column and then “Submit a response.” ining the sociodemographic variables. Clin Nurse Spec. 2009;23:138-144.
21. Hägglund L, Boman K, Lundman B, Brulin C. Depression among elderly
people with and without heart failure, managed in a primary healthcare
setting. Scand J Caring Sci. 2008;22(3):376-382.
22. Song EK, Moser DK, Lennie TA. Relationship of depressive symptoms
To learn more about caring for patients with heart failure, read to the impact of physical symptoms on functional status in women with
“Parallel Paths to Improve Heart Failure Outcomes: Evidence heart failure. Am J Crit Care. 2009;18:348-356.
Matters” by Albert in the American Journal of Critical Care, July 23. Tsuchihashi-Makaya M, Kato N, Chishaki A, Takeshita A, Tsutsui H.
2013;22:289-296. Available at www.ajcconline.org. Anxiety and poor social support are independently associated with
adverse outcomes in patients with mild heart failure (HF). Circulation.
2009;73:280-287.
References 24. Hansen RA, Dusetzina SB, Song L, Gaynes BN, Tu W, Murray MD.
1. Go AS, Mozaffarian D, Roger VL, et al; American Heart Association Sta- Depression affects adherence measurement but not the effectiveness of
tistics Committee and Stroke Statistics Subcommittee. Heart disease and an adherence intervention in heart failure patients. J Am Pharm Assoc.
stroke statistics—2013 update: a report from the American Heart Asso- 2009;49(6):760-768.
ciation [published correction appears in Circulation. 2013;127(23):e841]. 25. Schiffer AA, Pelle AJ, Smith OR, Widdershoven JW. Somatic versus cog-
Circulation. 2013;127(1):e6-e245. doi:10.1161/CIR.0b013e31828124ad. nitive symptoms of depression as predictors of all-cause mortality and
2. Yohannes AM, Willgoss TG, Baldwin RC, Connolly MJ. Depression and health status in chronic heart failure. J Clin Psychiatry. 2009:70:1679-1673.
anxiety in chronic heart failure and chronic obstructive pulmonary dis- 26. Hallas CN, Wray J, Andreou P, Banner NR. Depression and perceptions
ease: prevalence, relevance, clinical implications and management prin- about heart failure predict quality of life in patients with advanced heart
ciples. Int J Geriatr Psychiatry. 2010;25:1209-1221. failure. Heart Lung. 2011;40:111-121.
3. Zuluaga MC, Guallar-Castillon P, Rodriguez-Pascual C, Conde-Herrera 27 Holzapfel N, Löwe B, Wild B, et al. Self-care and depression in patients
M, Conthe P, Rodriguez-Artalejo F. Mechanisms of the association with chronic heart failure. Heart Lung. 2009;38(5):392-397.
between depressive symptoms and long-term mortality in heart failure. 28. Evangelista LS, Ter-Galstanyan A, Moughrabi S, Moser DK. Anxiety and
Am Heart J. 2010;159:231-237. depression in ethnic minorities with chronic heart failure. J Card Fail.
4. Mbakwem AC, Aina OF. Comparative study of depression in hospital- 2009;15(7):572-579.
ized and stable heart failure patients in an urban Nigerian teaching 29. von Känel R, Saner H, Kohls S, et al. Relation of heart rate recovery to
hospital. Gen Hosp Psychiatry. 2008;30:435-440. psychological distress and quality of life in patients with chronic heart
5. Pena FM, Modenesi Rde F, Piraciaba MC, et al. Prevalence and variables failure. Eur J Cardiovasc Prev Rehabil. 2009;16(6):645-650.

22 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


30. Shen BJ, Eisenberg SA, Maeda U, Farrell KA. Depression and anxiety 53. Mann DL, Bristow MR. Mechanisms and models in heart failure: the
predict decline in physical health functioning in patients with heart fail- biomechanical model and beyond. Circulation. 2005;111(21):2837-2849.
ure. Ann Behav Med. 2011;41:373-382. 54. Katada J, Meguro T, Saito H, et al. Persistent cardiac aldosterone syn-
31. Volz A, Schmid JP, Zwahlen M, Kohls S, Saner H, Barth J. Predictors of thesis in angiotensin II type 1A receptor-knockout mice after myocardial
readmission and health related quality of life in patients with chronic infarction. Circulation. 2005;111(17):2157-2164.
heart failure: a comparison of different psychosocial aspects. J Behav Med. 55. Lee CS, Tkacs NC. Current concepts of neurohormonal activation in
2011;34(1):13-22. heart failure: mediators and mechanisms. AACN Adv Crit Care. 2008;
32. Luyster FS, Hughes JW, Gunstad J. Depression and anxiety symptoms 19(4):364-385.
are associated with reduced dietary adherence in heart failure patients 56. Raizada V, Skipper B, Luo W, Griffith J. Intracardiac and intrarenal
treated with an implantable cardioverter defibrillator. J Cardiovasc Nurs. renin-angiotensin systems: mechanisms of cardiovascular and renal
2009;24:10-17. effects. J Investig Med. 2007;55(7):341-359.
33. Strine TW, Mokdad AH, Balluz LS, et al. Depression and anxiety in the 57. Johnson AK, Grippo AJ. Sadness and broken hearts: neurohumoral
United States: findings from the 2006 Behavioral Risk Factor Surveil- mechanisms and co-morbidity of ischemic heart disease and psycholog-
lance System. Psychiatr Serv. 2008;59(12):1383-1390. ical depression. J Physiol Pharmacol. 2006;57(suppl 11):5-29.
34. De Jong MJ, Chung ML, Wu JR, Riegel B, Rayens MK, Moser DK. Link- 58. Thurston RC, Rewak M, Kubzansky LD. An anxious heart: anxiety and
ages between anxiety and outcomes in heart failure. Heart Lung. 2011;40: the onset of cardiovascular diseases. Prog Cardiovasc Dis. 2013;55(6):
393-404. 524-537. doi:10.1016/j.pcad.2013.03.007.
35. Damen NL, Pelle AJ, Szabó BM, Pedersen SS. Symptoms of anxiety and 59. Januzzi JL Jr, Stern TA, Pasternak RC, DeSanctis RW. The influence of
cardiac hospitalizations at 12 months in patients with heart failure. J Gen anxiety and depression on outcomes of patients with coronary artery
Intern Med. 2012;27:345-350. disease. Arch Intern Med. 2000;160(13):1913-1921.
36. Zuluaga MC, Guallar-Castillon P, Rodriguez-Pascual C, Conde-Herrera M, 60. Strohle A, Holsboer F. Stress responsive neurohormones in depression
Conthe P, Rodriguez-Artalejo F. Mechanisms of the association between and anxiety. Pharmacopsychiatry. 2003;36(suppl 3):S207-S214.
depressive symptoms and long-term mortality in heart failure. Am Heart 61. Westerbacka J, Yki-Järvinen H, Vehkavaara S, et al. Body fat distribution
J. 2010;159:231-237. and cortisol metabolism in healthy men: enhanced {Greek beta} 5 -
37. Pelle AJ, Pedersen SS, Schiffer AA, Szabo B, Widdershoven JW, Denollet J. reductase and lower cortisol/cortisone metabolite ratios in men with
Psychological distress and mortality in systolic heart failure. Circ Heart fatty liver. J Clin Endocrinol Metab. 2003;88(10):4924-4931.
Fail. 2010;3:261-267. 62. Kelly JJ, Mangos G, Williamson PM, Whitworth JA. Cortisol and hyper-
38. Lupón J, González B, Santaeugenia S, et al. Prognostic implication of tension. Clin Exp Pharmacol Physiol Suppl. 1998;25:S51-S56.
frailty and depressive symptoms in an outpatient population with heart 63. Muoio DM, Newgard CB. Mechanisms of disease: molecular and meta-
failure. Rev Esp Cardiol. 2008;61:835-842. bolic mechanisms of insulin resistance and beta-cell failure in type 2
39. Sherwood A, Blumenthal JA, Hinderliter AL, et al. Worsening depressive diabetes. Nat Rev Mol Cell Biol. 2008;9(3):193-205.
symptoms are associated with adverse clinical outcomes in patients with 64. Briet M, Schiffrin B. Aldosterone: effects on the kidney and the cardio-
heart failure. J Am Coll Cardiol. 2011;57:418-423. vascular system. Nat Rev Nephrol. 2010;6(5):261-273.
40. Kato N, Kinugawa K, Yao A, Hatano M, Shiga T, Kazuma K. Relationship 65. Bauersachs J. Aldosterone antagonism in heart failure: improvement of
of depressive symptoms with hospitalization and death in Japanese cardiac remodeling, endothelial dysfunction and platelet activation. Eur
patients with heart failure. J Card Fail. 2009;15:912-919. J Clin Invest. 2004;34(10):649-652.
41. Thomas SA, Chapa DW, Friedmann E, et al. Depression in patients with 66. Güder G, Bauersachs J, Frantz S, et al. Complementary and incremental
heart failure: prevalence, pathophysiological mechanisms, and treatment. mortality risk prediction by cortisol and aldosterone in chronic heart
Crit Care Nurse. 2008;28(2):40-55. failure. Circulation. 2007;115(13):1754-1761.
42. Engel GL. The need for a new medical model: a challenge for biomedi- 67. Hlavacova N, Wes PD, Ondrejcakova M, et al. Subchronic treatment with
cine. Science. 1977;196:129-136. aldosterone induces depression-like behaviours and gene expression
43. Levine G, Allen K, Braun L, et al; American Heart Association Council changes relevant to major depressive disorder. Int J Neuropsychopharmacol.
on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing. 2012;15(2):247-265.
Pet ownership and cardiovascular risk: a scientific statement from the 68. Eisenhofer G, Friberg P, Rundqvist B, et al. Cardiac sympathetic nerve
American Heart Association. Circulation. 2013;127(23):2353-2363. function in congestive heart failure. Circulation. 1996;93(9):1667-1676.
doi:10.1161/CIR.0b013e31829201e1. 69. Latini R, Masson S, Anand I, et al; Val-HeFT investigators. The compar-
44. Holsboer F, Ising M. Central CRH system in depression and anxiety— ative prognostic value of plasma neurohormones at baseline in patients
evidence from clinical studies with CRH1 receptor antagonists. Eur J with heart failure enrolled in Val-HeFT. Eur Heart J. 2004;25(4):292-299.
Pharmacol. 2008;583(2-3):350-357. 70. Moret C, Briley M. The importance of norepinephrine in depression.
45 Cameron OG, Abelson JL, Young EA. Anxious and depressive disorders Neuropsychiatr Dis Treat. 2011;7(suppl 1):9-13. doi:10.2147/NDT.S19619.
and their comorbidity: effect on central nervous system noradrenergic 71. Dornelles A, de Lima MN, Grazziotin M, et al. Adrenergic enhancement
function. Biol Psychiatry. 2004;(11):875-783. of consolidation of object recognition memory. Neurobiol Learning Mem.
46. Licht CM, de Geus EJ, Zitman FG, Hoogendijk WJ, van Dyck R, Penninx 2007;88(1):137-142. doi:10.1016/j.nlm.2007.01.005.
BW. Association between major depressive disorder and heart rate vari- 72. Redwine LS, Wirtz PH, Hong S, et al. Depression as a potential modula-
ability in the Netherlands Study of Depression and Anxiety (NESDA). tor of beta-adrenergic-associated leukocyte mobilization in heart failure
Arch Gen Psychiatry. 2008;65(12):1358-1367. doi:10.1001/archpsyc.65.12 patients. J Am Coll Cardiol. 2010;56(21):1720-1727. doi:10.1016/j.jacc.2010
.1358. .04.064.
47. Licht CM, de Geus EJ, van Dyck R, Penninx BW. Association between 73. Cully JA, Jimenez DE, Ledoux TA, Deswal A. Recognition and treatment
anxiety disorders and heart rate variability in the Netherlands Study of of depression and anxiety symptoms in heart failure. Prim Care Compan-
Depression and Anxiety (NESDA). Psychosom Med. 2009;71(5):508-518. ion J Clin Psychiatry. 2009;11(3):103-109.
48. Morel-Kopp MC, McLean L, Chen Q, et al. The association of depression 74. Malik M. Heart rate variability. Ann Noninvasive Electrocardiol. 1996;1:
with platelet activation: evidence for a treatment effect. J Thromb Haemost. 151-181.
2009;7(4):573-581. 75. Landolina M, Gasparini M, Lunati M, et al; InSync/InSync ICD Italian
49. Leo R, Di Lorenzo G, Tesauro M, et al. Association between enhanced Registry Investigators. Heart rate variability monitored by the implanted
soluble CD40 ligand and proinflammatory and prothrombotic states in device predicts response to CRT and long-term clinical outcome in patients
major depressive disorder: pilot observations on the effects of selective with advanced heart failure. Eur J Heart Fail. 2008;10(11):1073-1079.
serotonin reuptake inhibitor therapy. J Clin Psychiatry. 2006;67(11): doi:10.1016/j.ejheart.2008.08.011.
1760-1766. 76. Guzzetti S, La Rovere MT, Pinna GD, et al. Different spectral compo-
50. Zafar MU, Paz-Yepes M, Shimbo D, et al. Anxiety is a better predictor nents of 24 h heart rate variability are related to different modes of
of platelet reactivity in coronary artery disease patients than depression. death in chronic heart failure. Eur Heart J. 2005;26(4):357-362.
Eur Heart J. 2010;31(13):1573-1582. 77. Grippo AJ, Santos CM, Johnson RF Increased susceptibility to ventricu-
51. Friedmann E, Thomas SA, Liu F, Morton PG, Chapa D, Gottlieb SS. lar arrhythmias in a rodent model of experimental depression. Am J
Relationship of depression, anxiety, and social isolation to chronic heart Physiol Heart Circ Physiol. 2004;286(2):H619-H626.
failure outpatient mortality. Am Heart J. 2006;152(5):940-948. 78. Weber KT. Aldosterone in congestive heart failure. N Engl J Med. 2001;
52. Friedmann E, Thomas SA, Stein PK, Kleiger RE. Relation between pet 345(23):1689-1697.
ownership and heart rate variability in patients with healed myocardial 79. Rousseau MF, Gurné O, Duprez D, et al; Belgian RALES Investigators.
infarcts. Am J Cardiol. 2003;91(6):718-721. Beneficial neurohormonal profile of spironolactone in severe congestive

www.ccnonline.org CriticalCareNurse Vol 34, No. 2, APRIL 2014 23


heart failure: results from the RALES neurohormonal substudy. J Am 103. Kulcu DG, Kurtais Y, Tur BS, Gülec S, Seckin B. The effect of cardiac
Coll Cardiol. 2002;40(9):1596-1601. rehabilitation on quality of life, anxiety and depression in patients with
80. Sata Y, Krum H. The future of pharmacological therapy for heart failure. congestive heart failure: a randomized controlled trial, short term results.
Circ J. 2010;74(5):809-817. Eura Medicophys. 2007;43(4):489-497.
81. Künzel HE. Psychopathological symptoms in patients with primary 104. Jolly K, Taylor RS, Lip GY, et al. A randomized trial of the addition of
hyperaldosteronism—possible pathways. Horm Metab Res. 2012;44(3): home-based exercise to specialist heart failure nurse care: the Birmingham
202-207. Rehabilitation Uptake Maximisation study for patients with Congestive
82. Häfner S, Baumert J, Emeny RT, et al; MONICA/KORA Study Investiga- Heart Failure (BRUM-CHF) study. Eur J Heart Fail. 2009;11(2):205-213.
tors. To live alone and to be depressed, an alarming combination for the 105. Karapolat H, Demir E, Bozkaya YT, et al. Comparison of hospital-based
renin-angiotensin-aldosterone-system (RAAS). Psychoneuroendocrinology. versus home-based exercise training in patients with heart failure:
2012;37(2):230-237. effects on functional capacity, quality of life, psychological symptoms,
83. Steinke JW, Borish L. Cytokines and chemokines. J Allergy Clin Immunol. and hemodynamic parameters. Clin Res Cardiol. 2009;98(10):635-642.
2006;117(2 suppl mini-primer):S441-S445. 106. Yu DS, Lee DT, Woo J, Hui E. Non-pharmacological interventions in
84. Hedayat M, Mahmoudi MJ, Rose NR, Rezaei N. Proinflammatory older people with heart failure: effects of exercise training and relaxation
cytokines in heart failure: double-edged swords. Heart Fail Rev. 2010; therapy. Gerontology. 2007;53(2):74-81.
15(6):543-562. 107. Radzewitz A, Miche E, Herrmann G, et al. Exercise and muscle strength
85. Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. training and their effects on quality of life in patients with chronic heart
Cytokines and cytokine receptors in advanced heart failure: an analysis failure. Eur J Heart Fail. 2002;4(5):627-634.
of the cytokine database from the Vesnarinone trial (VEST). Circulation. 108. Keteyian SJ, Leifer ES, Houston-Miller N, et al; HF-ACTION Investigators.
2001;103(16):2055-2059. Relation between volume of exercise and clinical outcomes in patients
86. Rauchhaus M, Doehner W, Francis DP, et al. Plasma cytokine parame- with heart failure. J Am Coll Cardiol. 2012;60(19):1899-1905.
ters and mortality in patients with chronic heart failure. Circulation. 109. Blumenthal JA, Sherwood A, Babyak MA, et al. Exercise and pharmaco-
2000;102(25):3060-3067. logical treatment of depressive symptoms in patients with coronary
87. Torre-Amione G, Kapadia S, Benedict C, Oral H, Young JB, Mann DL. heart disease: results from the UPBEAT (Understanding the Prognostic
Proinflammatory cytokine levels in patients with depressed left ventric- Benefits of Exercise and Antidepressant Therapy) study. J Am Coll Cardiol.
ular ejection fraction: a report from the Studies of Left Ventricular Dys- 2012;60(12):1053-1063.
function (SOLVD). J Am Coll Cardiol. 1996;27(5):1201-1206. 110. Eyre HA, Papps E, Baune BT. Treating depression and depression-like
88. Guinjoan SM, Vigo DE, Castro MN, et al. Mood, Th-1/Th-2 cytokine behavior with physical activity: an immune perspective. Front Psychiatry.
profile, and autonomic activity in older adults with acute/decompen- 2013;4:3. doi:10.3389/fpsyt.2013.00003. eCollection 2013.
sated heart failure: preliminary observations. World J Biol Psychiatry. 111. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for
2009;10(4 pt 3):913-918. the management of heart failure: executive summary: a report of the
89. Ferketich AK, Ferguson JP, Binkley PF. Depressive symptoms and American College of Cardiology Foundation/American Heart Associa-
inflammation among heart failure patients. Am Heart J. 2005;150(1): tion Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):
132-136. 1495-1539. doi:10.1016/j.jacc.2013.05.020.
90. Anand IS, Latini R, Florea VG, et al; Val-HeFT Investigators. C-reactive 112. Schwarz KA, Mion LC, Hudock D, Litman G. Telemonitoring of heart
protein in heart failure: prognostic value and the effect of valsartan. failure patients and their caregivers: a pilot randomized controlled trial.
Circulation. 2005;112(10):1428-1434. Prog Cardiovasc Nurs. 2008;23(1):18-26.
91. Watkins LR, Maier SF, Goehler LE. Cytokine-to-brain communication: 113. Powell LH, Calvin JE Jr, Richardson D, et al; HART Investigators. Self-
a review and analysis of alternative mechanisms. Life Sci. 1995;57(11): management counseling in patients with heart failure: the Heart Failure
1011-1026. Adherence and Retention randomized behavioral trial. JAMA. 2010;
92. Empana JP, Jouven X, Canoui-Poitrine F, et al. C-reactive protein, 304(12):1331-1338.
interleukin 6, fibrinogen and risk of sudden death in European middle- 114. Riegel B, Carlson B, Glaser D, Romero T. Randomized controlled trial of
aged men: the PRIME study. Arterioscler Thromb Vasc Biol. 2010;30(10): telephone case management in Hispanics of Mexican origin with heart
2047-2052. failure. J Card Fail. 2006;12(3):211-219.
93. Milo-Cotter O, Cotter-Davison B, Lombardi C, et al. Neurohormonal 115. Mårtensson J, Strömberg A, Dahlström U, Karlsson JE, Fridlund B.
activation in acute heart failure: results from VERITAS. Cardiology. 2011; Patients with heart failure in primary health care: effects of a nurse-led
119(2):96-105. intervention on health-related quality of life and depression. Eur J Heart
94. Gegenava T, Gegenava M, Kavtaradze G. C-reactive protein level corre- Fail. 2005;7(3):393-403.
lation with depression and anxiety among patients with coronary artery 116. Dunagan WC, Littenberg B, Ewald GA, et al. Randomized trial of a nurse-
disease. Georgian Med News. May 2011;(194):34-37. administered, telephone-based disease management program for patients
95. Angiolillo DJ, Ueno M, Goto S. Basic principles of platelet biology and with heart failure. J Card Fail. 2005;11(5):358-365.
clinical implications. Eur Heart J. 2010;74(4):597-607. 117. Azad N, Molnar F, Byszewski A. Lessons learned from a multidisciplinary
96. Woltz PC, Chapa DW, Friedmann E, Son H, Akintade B, Thomas SA. heart failure clinic for older women: a randomised controlled trial. Age
Effects of interventions on depression in heart failure: a systematic review. Ageing. 2008;37(3):282-287.
Heart Lung. 2012;41(5):469-483. doi:10.1016/j.hrtlng.2012.06.002. 118. Andryukhin A, Frolova E, Vaes B, Degryse J. The impact of a nurse-led
97. O’Connor CM, Jiang W, Kuchibhatla M, et al; SADHART-CHF Investi- care programme on events and physical and psychosocial parameters in
gators. Safety and efficacy of sertraline for depression in patients with patients with heart failure with preserved ejection fraction: a randomized
heart failure: results of the SADHART-CHF (Sertraline Against Depres- clinical trial in primary care in Russia. Eur J Gen Pract. 2010;16(4):205-214.
sion and Heart Disease in Chronic Heart Failure) trial. J Am Coll Cardiol. 119. Rumsfeld JS, Alexander KP, Goff DC Jr, et al; American Heart Association
2010;56(9):692-699. Council on Quality of Care and Outcomes Research, Council on Cardio-
98. Gottlieb SS, Kop WJ, Thomas SA, et al. A double-blind placebo-controlled vascular and Stroke Nursing, Council on Epidemiology and Prevention,
pilot study of controlled-release paroxetine on depression and quality Council on Peripheral Vascular Disease, and Stroke Council. Cardiovas-
of life in chronic heart failure. Am Heart J. 2007;153(5):868-873. cular health: the importance of measuring patient-reported health status:
99. Lekakis J, Ikonomidis I, Papoutsi Z, et al. Selective serotonin re-uptake a scientific statement from the American Heart Association. Circulation.
inhibitors decrease the cytokine-induced endothelial adhesion molecule 2013;127(22):2233-2249.
expression, the endothelial adhesiveness to monocytes and the circulating
levels of vascular adhesion molecules. Int J Cardiol. 2010;139(2):150-158.
100. Fraguas R, da Silva Telles RM, Alves TC, et al. A double-blind, placebo-
controlled treatment trial of citalopram for major depressive disorder
in older patients with heart failure: the relevance of the placebo effect
and psychological symptoms. Contemp Clin Trials. 2009;30(3):205-211.
101. Miche E, Roelleke E, Zoller B, et al. A longitudinal study of quality of
life in patients with chronic heart failure following an exercise training
program. Eur J Cardiovasc Nurs. 2009;8(4):281-287.
102. Dracup K, Evangelista LS, Hamilton MA, et al. Effects of a home-based
exercise program on clinical outcomes in heart failure. Am Heart J. 2007;
154(5):877-883.

24 CriticalCareNurse Vol 34, No. 2, APRIL 2014 www.ccnonline.org


CNE Test Test ID C142: Pathophysiological Relationships Between Heart Failure and Depression and Anxiety
Learning objectives: 1. Describe the biopsychosocial holistic model for cardiovascular health 2. Identify 2 neurohormonal pathways and their impact in
heart failure 3. Identify nursing implications for heart failure, depression, and anxiety

1. Which of the following are the neurohormones involved in heart failure (HF)? 7. Which of the following statements best describes the role of the cytokine cascade in HF?
a. Glucagon, acetylcholine, aldosterone, and cortisol a. TNF-α is a pro-inflammatory cytokine that leads to left ventricular dysfunction.
b. Aldosterone, growth-hormone releasing factor, oxytocin, and TNF-α b. Decreased interleukin-6 in HF patients is a predictor of mortality.
c. Angiotensin II, cortisol, somatostatin, and glucagon c. Pro-inflammatory cytokines are not implicated in toxic effects on heart muscle.
d. Norepinephrine, angiotensin II, aldosterone, and TNF-α d. The cytokine cascade is mediated by C-reactive protein in depressed patients.

2. Which of the following statements best reflects the biopsychosocial holistic model of 8. Nursing management of HF patients with depression and anxiety includes which of the
cardiovascular health? following?
a. Depression and anxiety are usually only increased in HF patients with a lower socioeconomic a. Frequent vital signs, visitor restrictions, and medication education
status. b. Enrollment in out-patient disease management program
b. Neurohormonal dysfunction from HF is the primary cause of depression and anxiety. c. Fluid restriction, a psychiatric consult, and frequent vital signs
c. The interaction of physiologic and psychological factors affects HF patients and may lead to d. Education regarding treatment options for depression including selective serotonin reuptake
increased depression and anxiety. inhibitors and exercise.
d. The holistic model of depression/anxiety/HF indicates that pet therapy always alleviates anxiety.
9. Which of the following statements summarizes the pathophysiologic processes of depres-
3. Which of the following statements best describes activation of the hypothalamic- sion, anxiety, and HF?
pituitary-adrenal (HPA) axis in cardiovascular function? a. Neurohormonal dysregulation in depressed and anxious patients causes worsening HF.
a. Neurohormonal functioning in HF decreases the incidences of depression and anxiety b. Increased sodium and water retention and increased catecholamine levels lead to increased
through decreased activation of the HPA axis. anxiety.
b. Mental and physical stress leads to a release of cortisol and aldosterone, which leads to c. Activation of the HPA axis, cytokine and platelet cascade, and autonomic dysfunction in
increased inflammation and hypertension and cardiac remodeling. depressed and anxious patients affects cardiovascular function in HF patients.
c. The HPA axis is only activated by a failing ventricle, which increases aldosterone production. d. Aldosterone production and cytokine cascade are the primary connection of HF to depression
d. Hypoactivity of the HPA axis increases the production of circulating levels of norepinephrine and anxiety.
and epinephrine, which leads to decompensated HF.
10. Which of the following statements reflects the role of norepinephrine in depression and HF?
4. Which of the following statements best reflects the effects of psychological status on a. Mental focus and attention are regulated in depressed patients by norepinephrine.
HF patients? b. Patients with depression and HF have increased circulating norepinephrine.
a. Depression in HF patients is less prevalent than in the general population. c. Hyperactivity of the parasympathetic nervous system is mediated by norepinephrine in HF.
b. HF patients with depression symptoms have higher mortality rates. d. High circulating norepinephrine levels are associated with improved prognosis in HF.
c. Anxiety in HF patients causes increased platelet activation.
d. Psychological effects from neurohormonal dysregulation cause HF through inhibition of 11. Which of the following statements best reflects research regarding the patients with HF,
serotonin secretion. depression, and anxiety?
a. Current evidence indicates the most effective treatments for patients with HF and depression
5. Which of the following statements uses the biopsychosocial holistic model to address are based on biologic factors.
cardiovascular health? b. The progression of HF is not linked to anxiety.
a. Medication management in HF prevents the progression of disease. c. The similar pathophysiologic changes for HF, depression, and anxiety would benefit from
b. Psychological therapy as a single modality decreases anxiety in HF patients. nursing research to determine treatment guidelines.
c. Decreased readmission rates for HF patients can be related to social support and medication d. Qualitative research on quality of life for the depressed and anxious HF patient is robust.
management.
d. Neurohormonal dysfunction in HF is often a short-term problem. 12. Which of the following statements is true regarding the RAAS?
a. The parasympathetic nervous system regulates the release of renin.
6. Which of the following statements best reflects the effect of autonomic dysregulation b. Angiotensin II and aldosterone promotes release of inflammatory cytokines.
and HF? c. The RAAS is inhibited in patients with depression and anxiety.
a. Heart rate variability is caused by the release of pro-inflammatory cytokines. d. The activation of angiotensin II in HF causes the release of norepinephrine.
b. PR intervals are used to measure heart rate variability in HF patients.
c. Depressed patients experience heart rate variability due to sympathetic and parasympathetic
tone imbalances.
d. The renin-angiotensin-aldosterone system (RAAS) increases cardiac arrhythmias leading to
sudden cardiac death.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. q a 2. q a 3. q a 4. q a 5. q a 6. q a 7. q a 8. q a 9. q a 10. q a 11. q a 12. q a
qb qb qb qb qb qb qb qb qb qb qb qb
qc qc qc qc qc qc qc qc qc qc qc qc
qd qd qd qd qd qd qd qd qd qd qd qd
Test ID: C142 Form expires: April 1, 2017 Contact hours: 1.0 Pharma hours: 0.25 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%)
Synergy CERP Category B Test writer: Cheri Blevins, MSN, RN, CCRN, CCNS

Program evaluation Name Member #


Yes No
Address
Objective 1 was met q q
Objective 2 was met q q City State ZIP
Objective 3 was met q q
Content was relevant to my Country Phone
For faster processing, take nursing practice q q
E-mail
this CNE test online at My expectations were met q q
This method of CNE is effective RN Lic. 1/St RN Lic. 2/St
www.ccnonline.org for this content q q
or mail this entire page to: The level of difficulty of this test was: Payment by: q Visa q M/C q AMEX q Discover q Check
AACN, 101 Columbia q easy q medium q difficult
To complete this program, Card # Expiration Date
Aliso Viejo, CA 92656.
it took me hours/minutes. Signature
The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.
AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN
programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

Вам также может понравиться