Download Chronic HF

(Relates to Chapter 35,
“Nursing Management: Heart Failure,”
in the textbook)
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
 An
abnormal condition involving
impaired cardiac pumping/filling
 Heart is unable to produce an
adequate cardiac output (CO) to meet
metabolic needs.
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2
 Characterized
by
• Ventricular dysfunction
• Reduced exercise tolerance
• Diminished quality of life
• Shortened life expectancy
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3
 Heart
failure (HF) is not a disease
but a “syndrome”
 Associated with long-standing
hypertension, coronary artery
disease (CAD), and myocardial
infarction (MI)
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 Affects
about 5 million people in
the United States
 The most common reason for
hospitalization in adults >65
years old
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 Primary
risk factors
• CAD
• Advancing age
 Contributing
risk factors
• Hypertension
• Diabetes
• Tobacco use
• Obesity
• High serum cholesterol
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 Causes
of HF may be divided into two
subgroups:
• Primary
• Precipitating
 HF
is classified as systolic or diastolic
failure (or dysfunction).
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 Systolic
failure
• Hallmark finding: Decrease in the left
ventricular ejection fraction (EF)
 Caused by
 Impaired contractile function (e.g., MI)
 Increased afterload (e.g., hypertension)
 Cardiomyopathy
 Mechanical abnormalities (e.g., valve
disease)
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 Diastolic failure
• Impaired ability of the ventricles to relax
and fill during diastole, resulting in
decreased stroke volume and CO
• Diagnosis based on the presence of
pulmonary congestion, pulmonary
hypertension, ventricular hypertrophy,
and normal EF
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 Diastolic failure
(cont’d)
• Caused by
 Left ventricular hypertrophy from
chronic hypertension
 Aortic stenosis
 Hypertrophic cardiomyopathy
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 Mixed
systolic and diastolic failure
• Seen in disease states such as dilated
cardiomyopathy (DCM)
• Poor EFs (<35%)
• High pulmonary pressures
• Biventricular failure
 Both ventricles may be dilated and have
poor filling and emptying capacity.
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11
 Compensatory
mechanisms are
activated to maintain adequate CO.
• Sympathetic nervous system (SNS)
activation: First and least effective
mechanism
 Release of catecholamines (epinephrine and
norepinephrine)
 Increased heart rate (HR)
 Increased myocardial contractility
 Peripheral vasoconstriction
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 Compensatory
mechanisms (cont’d)
• Sympathetic nervous system (SNS)
activation
 Over a period of time these mechanisms
are detrimental as they increase the
workload of the failing myocardium and
the need for O2.
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses: Kidneys
release renin
 Renin converts angiotensinogen to
angiotensin I.
 Angiotensin I is converted to
angiotensin II by a converting enzyme
made in the lungs.
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses (cont’d)
 Angiotensin II causes
 Adrenal cortex to release aldosterone
(sodium and water retention)
 Increased peripheral vasoconstriction
(increases BP)
 Response is known as the reninangiotensin-aldosterone system (RAAS).
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses (cont’d)
 Low CO causes a decrease in cerebral
perfusion pressure.
 Antidiuretic hormone (ADH) is secreted
and causes
 Increased water reabsorption in the
renal tubules, leading to water
retention and increased blood volume
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses (cont’d)
 Endothelin is stimulated by ADH,
catecholamines, and angiotensin II,
causing
 Arterial vasoconstriction
 Increase in cardiac contractility
 Hypertrophy
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses (cont’d)
 Proinflammatory cytokines (e.g., tumor
necrosis factor): Released by cardiac
myocytes in response to cardiac injury
 Depress cardiac function by causing
cardiac hypertrophy, contractile
dysfunction, and death of myocytes
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 Compensatory
mechanisms (cont’d)
• Neurohormonal responses (cont’d)
 Over time, a systemic inflammatory
response is mounted and results in
 Cardiac wasting
 Muscle myopathy
 Fatigue
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 Consequences
of compensatory
mechanisms
• Dilation
 Enlargement of the chambers of the
heart that occurs when pressure in the
left ventricle is elevated
 Initially an adaptive mechanism
 Eventually this mechanism becomes
inadequate, and CO decreases.
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Fig. 35-1. A, Dilated heart chambers. B, Hypertrophied heart chambers.
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 Consequences
of compensatory
mechanisms
• Hypertrophy
 Increase in muscle mass and cardiac wall
thickness in response to chronic dilation,
resulting in
 Poor contractility
 Higher O2 needs
 Poor coronary artery circulation
 Risk for ventricular dysrhythmias
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 Counter
regulatory processes
• Natriuretic peptides: Atrial natriuretic
peptide (ANP), b-type natriuretic peptide
(BNP)
 Released in response to increase in atrial
volume and ventricular pressure
 Promote venous and arterial vasodilation,
reducing preload and afterload
 Chronic HF leads to a depletion of these
factors
.
23
 Counter
regulatory processes (cont’d)
• Natriuretic peptides are endothelin and
aldosterone antagonists.
 Enhance diuresis
 Block effects of the RAAS
• Natriuretic peptides inhibit the
development of cardiac hypertrophy and
may have antiinflammatory effects.
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 Counter
regulatory processes (cont’d)
• Nitric oxide (NO)
 Released from the vascular endothelium
in response to compensatory
mechanisms
 NO relaxes arterial smooth muscle,
resulting in vasodilation and decreased
afterload.
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 Left-sided
HF (most common) from left
ventricular dysfunction (e.g., MI
hypertension, CAD, cardiomyopathy)
• Backup of blood into the left atrium and
pulmonary veins
 Pulmonary congestion
 Pulmonary edema
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Fig. 35-2. Pathophysiology of heart failure. Elevated systemic vascular resistance results in left-sided
heart failure that leads to right-sided heart failure. Systemic vascular resistance and preload are
exacerbated by the renin-angiotensin-aldosterone system. ADH, Antidiuretic hormone; LA, left atrium;
LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; RV, right ventricle.
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 Right-sided
HF from left-sided HF, cor
pulmonale, right ventricular MI
• Backup of blood into the right atrium and
venous systemic circulation
 Jugular venous distention
 Hepatomegaly, splenomegaly
 Vascular congestion of GI tract
 Peripheral edema
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 Pulmonary
edema, often lifethreatening
• Early
 Increase in the respiratory rate
 Decrease in PaO2
• Later
 Tachypnea
 Respiratory acidemia
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Fig. 35-3. As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the
alveolar-capillary interface. A, Normal relationship. B, Increased pulmonary capillary hydrostatic pressure
causes fluid to move from the vascular space into the pulmonary interstitial space. C, Lymphatic flow
increases in an attempt to pull fluid back into the vascular or lymphatic space. D, Failure of lymphatic flow
and worsening of left heart failure result in further movement of fluid into the interstitial space and into
the alveoli.
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 Physical
findings
• Orthopnea
• Dyspnea, tachypnea
• Use of accessory muscles
• Cyanosis
• Cool and clammy skin
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 Physical
findings
• Cough with frothy, blood-tinged sputum
• Breath sounds: Crackles, wheezes,
rhonchi
• Tachycardia
• Hypotension or hypertension
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.
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 Fatigue
 Dyspnea,
orthopnea, paroxysmal
nocturnal dyspnea
 Persistent, dry cough, unrelieved with
position change or over-the-counter
cough suppressants
 Tachycardia
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 Dependent
edema
• Edema may be pitting in nature
• Sudden weight gain of >3 lb (1.4 kg) in 2
days may indicate an exacerbation of HF.
35
 Nocturia
 Skin
• Dusky, cool, damp to touch
• Lower extremities: Shiny and swollen,
diminished or absent hair growth,
pigment changes
36
 Restlessness,
confusion, decreased
memory
 Chest
pain (angina)
 Weight changes
• Anorexia, nausea
• Fluid retention
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 Pleural
effusion
 Atrial fibrillation (most common
dysrhythmia)
• Promotes thrombus/embolus formation,
increasing risk for stroke
• Treatment can include rate control,
cardioversion, antidysrhythmics, and/or
systemic anticoagulation.
.
38
 High
risk of fatal dysrhythmias (e.g.,
sudden cardiac death, ventricular
tachycardia) with HF and an EF <35%
 HF can lead to severe hepatomegaly,
especially with RV failure.
• Fibrosis and cirrhosis can develop over
time.
 Renal
insufficiency or failure
.
39
 Primary
goal: Determine and treat
underlying cause
• History and physical examination
• Chest x-ray
• ECG
• Lab studies (e.g., cardiac enzymes, BNP)
40
 Primary
goal: Determine and treat
underlying cause
• Hemodynamic assessment (pressures
within the heart)
• Echocardiogram
• Stress testing
• Cardiac catheterization
• Ejection fraction
41
 New York
Heart Association Functional
Classification of HF
• Classes I to IV
 ACC/AHA Stages
of HF
• Stages A to D
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 Overall
goals of therapy for ADHF and
Chronic HF
• Decrease patient symptoms.
• Improve LV function.
• Reverse ventricular remodeling.
• Improve quality of life.
• Decrease mortality and morbidity.
43
 High Fowler’s
position
 Supplemental oxygen
 Continuous ECG monitoring
 Ultrafiltration: Option for patients
with volume overload
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 Circulatory
assist devices are used
to treat patients with deteriorating
HF.
 Coexisting psychologic disorders
should be addressed.
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 Decrease
intravascular volume
• Reduces venous return and preload
 Loop diuretics (e.g., furosemide [Lasix])
 Ultrafiltration or aquapheresis
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 Decrease
venous return (preload)
• Reduces the amount of volume returned
to the LV during diastole
 High-Fowler’s position
 IV nitroglycerin
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 Decrease
afterload
• Improves CO and decreases pulmonary
congestion
 IV sodium nitroprusside (Nipride)
 Morphine sulfate
 Nesiritide (Natrecor)
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 Improve gas
exchange and
oxygenation
• Supplemental oxygen
• Morphine sulfate
• Noninvasive ventilatory support (BiPAP)
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 Improve cardiac
function
• For patients who do not respond to
conventional pharmacotherapy (e.g.,
diuretics, vasodilators, morphine sulfate)
 Inotropic therapy
 Digitalis
 -Adrenergic agonists (e.g., dopamine)
 Phosphodiesterase inhibitors (e.g.,
milrinone)
 Hemodynamic monitoring
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 Reduce
anxiety
• Distraction, imagery
• Sedative medications (e.g., morphine
sulfate, benzodiazepines)
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 Main
treatment goals
• Treat the underlying cause and
contributing factors
• Maximize CO
• Provide treatment to alleviate symptoms
• Improve ventricular function
• Improve quality of life
• Preserve target organ function
• Improve mortality and morbidity
.
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 Oxygen
administration
 Physical and emotional rest
 Non-pharmacologic therapies
• Cardiac resynchronization therapy (CRT)
or biventricular pacing
• Cardiac transplantation
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 Nonpharmacologic therapies
(cont’d)
• Intraaortic balloon pump (IABP) therapy
• Ventricular assist devices (VADs)
• Destination therapy—Permanent,
implantable VAD
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 Therapeutic
goals for drug therapy
• Identification of type of HF and causes
• Correction of sodium and water retention
and volume overload
• Reduction of cardiac workload
• Improvement of myocardial contractility
• Control of precipitating and complicating
factors
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 Drug
therapy
• Diuretics
 Thiazide
 Loop
 Spironolactone
.
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 Drug
therapy (cont’d)
• ACE inhibitors
• Angiotensin II receptor blockers
• Aldosterone antagonists
• Nitrates
• -Adrenergic blockers
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 Drug
therapy (cont’d)
• Positive inotropic (contractility)agents
 Digitalis
 Calcium sensitizers
• BiDil (combination drug containing
isosorbide dinitrate and hydralazine)
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 Nutritional
therapy
• Diet and weight reduction: Individualize
recommendations and consider cultural
background
• Recommend Dietary Approaches to Stop
Hypertension (DASH) diet.
• Sodium is usually restricted to 2.5 g per
day.
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 Nutritional
therapy
• Fluid restriction not generally required
• Daily weights are important
 Same time, same clothing each day
• Weight gain of 3 lb (1.4 kg) over 2 days or
a 3- to 5-lb (2.3 kg) gain over a week
should be reported to health care
provider.
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 Assessment
• Subjective data
 Past health history
 Functional health patterns
 Medications
• Objective data
 Physical examination
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 Nursing
diagnoses
• Activity intolerance
• Fluid volume excess
• Impaired gas exchange
• Anxiety
• Deficient knowledge
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 Planning: Overall
goals
• Decrease in symptoms (e.g., shortness of
breath, fatigue)
• Decrease in peripheral edema
• Increase in exercise tolerance
• Compliance with the medical regimen
• No complications related to HF
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 Health
promotion
• Treatment or control of underlying heart
disease key to preventing HF and episodes
of ADHF (e.g., valve replacement, control
of hypertension, coronary
revasculariztion)
• Early detection of worsening HF may
prevent future hospitalizations.
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 Health
promotion
• Patient/caregiver teaching: Medications,
diet, and exercise regimens
 Exercise training (e.g., cardiac
rehabilitation) improves symptoms but
is often underprescribed.
• Home nursing care may be required for
follow-up and to monitor patient’s
response to treatment.
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 Acute
intervention
• HF is a progressive disease—Treatment
plans are established with quality-of-life
goals.
• Symptom management is controlled with
the use of self-management tools (e.g.,
daily weights).
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 Acute
intervention
• Salt must be restricted.
• Energy must be conserved.
• Support systems are essential to the
success of the entire treatment plan.
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 Ambulatory
and home care
• Explain to patient and caregiver
physiologic changes that have occurred.
• Assist patient to adapt to both the
physiologic and psychologic changes.
• Integrate patient and caregiver(s) or
support system into the overall care plan.
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 Implementation: Patient
education
• Medications (lifelong)
• Taking pulse rate
 Know when drugs (e.g., digitalis, adrenergic blockers) should be withheld
and reported to health care provider.
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 Implementation: Patient
and caregiver
education
• Home BP monitoring
• Signs of hypokalemia and hyperkalemia if
taking diuretics that deplete or spare
potassium
• Instruct patient in energy-conserving and
energy-efficient behaviors.
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 Evaluation
• Respiratory status
• Fluid balance
• Activity tolerance
• Anxiety control
• Knowledge of disease process
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 Treatment
of choice for patients with
refractory end-stage HF, inoperable
CAD, and cardiomyopathy
• Goal of the transplant evaluation process
is to identify patients who would most
benefit from a new heart.
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 Transplant
candidates are placed on a
list.
• Stable patients wait at home and receive
ongoing medical care.
• Unstable patients may require
hospitalization for more intensive
therapy.
• Overall waiting period for a heart is long;
many patients die during this time.
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 Bridge
to transplantation devices
 Surgery involves removing the
recipient’s heart, except for the
posterior right and left atrial walls and
their venous connections.
 Recipient’s heart is replaced with the
donor heart.
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 Donor
sinoatrial (SA) node is preserved
so that a sinus rhythm may be
achieved postoperatively.
 Immunosuppressive therapy usually
begins in the operating room.
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 Infection
is the primary complication,
followed by acute rejection, in the first
year after transplantation.
 Malignancy (especially lymphoma) and
coronary artery vasculopathy are
major causes of death after the first
year.
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 Endomyocardial
biopsies are
obtained from the right ventricle
weekly for the first month, monthly
for the following 6 months, and
yearly thereafter to detect rejection.
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 Nursing
care focuses on
• Promoting patient adaptation to the
transplant process
• Monitoring cardiac function
• Managing lifestyle changes
• Providing relevant teaching
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 68-year-old
woman is admitted to
the hospital for shortness of breath.
 She
was diagnosed 4 years ago with
HF after failing to follow the
recommended medical regimen for
an MI she suffered 6 years ago.
79
 States
she was taking a diuretic but
ran out 4 days ago; has not been able
to refill her prescription
 States
she noticed some swelling in
her feet that seemed worse than usual
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 Physical
examination
• Alert and oriented to person, place,
and time
• Fine crackles bilateral lower lobes
• Shortness of breath on minimal
exertion
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 Physical
examination (cont’d)
• O2 saturation 89%, room air
• S1 and S2 without murmur or extra
heart sounds
• Capillary refill sluggish in lower
extremities, normal in upper
extremities
• 2+ edema bilateral lower extremities
82
1.
What is the priority of care for her?
2.
How would you evaluate whether
your nursing actions were successful?
3.
What teaching measures would you
use to prevent a reoccurrence of
ADHF?
83