Transcript Interventions for Clients with Cardiac Problems

Interventions for Clients with
Cardiac Problems
Heart Failure
Also called pump failure, general
term for the inadequacy of the heart
to pump blood throughout the body;
causes insufficient perfusion of body
tissue with vital nutrients and
oxygen
 Left-sided heart failure
 Right-sided heart failure
 High-output failure
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Compensatory Mechanisms
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Increased heart rate
Because cardiac output is the product of heart rate and stroke volume,
an increase in heart rate results in an immediate increase in cardiac
output. An increase in heart rate is limited in its ability to compensate
for decreased cardiac output. If heart rate becomes too rapid, diastolic
filling time is limited and cardiac output may start to fall. An increase in
heart rate also significantly increases oxygen demand by the
myocardium. If the heart is poorly perfused because of arteriosclerosis,
heart failure may worsen
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Improved stroke volume
Stroke volume is also improved by sympathetic stimulation.
Sympathetic stimulation increases venous return to the heart, which
further stretches the myocardial fibers. This increased stretch is
referred to as preload. In accordance with Starling's law of the heart,
increased myocardial stretch results in more forceful contraction, which
increases stroke volume and cardiac output. After a critical point is
reached, further volume and stretch reduce the force of contraction and
cardiac output
Compensatory Mechanisms
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Arterial vasoconstriction
Sympathetic stimulation also results in arterial vasoconstriction.
Constriction of the arteries has the benefit of maintaining blood
pressure and improving tissue perfusion in low-output states.
However, constriction of the arteries increases afterload, the
resistance against which the heart must pump. Afterload is the
major determinant of myocardial oxygen requirements. As afterload
increases, the left ventricle requires more energy to eject its
contents, and stroke volume may decline
Sodium and water retention
Reduced blood flow to the kidneys, a common occurrence in lowoutput states, results in the activation of the renin-angiotensinaldosterone mechanism. Vasoconstriction becomes more
pronounced in response to angiotensin, and aldosterone secretion
causes sodium and water retention. The volume of blood returning
to the left ventricle is further increased by activation of this
mechanism
Compensatory Mechanisms
Myocardial hypertrophy
 Myocardial hypertrophy, with or without
chamber dilation, is the final compensatory
mechanism. The walls of the heart thicken to
provide more muscle mass. This results in more
forceful contractions, further increasing cardiac
output. However, cardiac muscle may
hypertrophy more rapidly than collateral
circulation can provide adequate blood supply to
the muscle. Often, a hypertrophied heart is
slightly oxygen deprived
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Etiology
Heart failure is caused by systemic
hypertension in 75% of cases.
 About one third of clients
experiencing myocardial infarction
also develop heart failure.
 Structural heart changes, such as
valvular dysfunction, cause pressure
or volume overload on the heart.
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Left-Sided Heart Failure
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Manifestations include:
– Weakness
– Fatigue
– Dizziness
– Confusion
– Pulmonary congestion
– Shortness of breath
(Continued)
Left-Sided Heart Failure
(Continued)
– Oliguria
– Organ failure, especially renal failure
– Death
Assessment
 Palpation the precordium - increased heart size is common, with a
displacement of the apical impulse to the left.
 On auscultation, the nurse may hear a third heart sound (S3) gallop, an
early diastolic filling sound indicating an increase in left ventricular pressure.
A fourth heart sound (S4) can also occur; it is not a sign of failure but is a
reflection of decreased ventricular compliance.
 Crackles and wheezes may be present on auscultation of the lungs. Late
inspiratory crackles and fine profuse crackles that repeat themselves from
breath to breath and do not diminish with coughing indicate heart failure.
Crackles usually develop in the bases and spread upward as the condition
worsens. Wheezes indicate a narrowing of the bronchial lumen caused by
engorged pulmonary vessels
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Right-Sided Heart Failure
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Manifestations include:
– Distended neck veins, increased
abdominal girth
– Hepatomegaly (liver engorgement)
– Hepatojugular reflux
– Ascites
– Dependent edema
– Weight: the most reliable indicator of
fluid gain or loss
Assessments
Laboratory assessment
Radiographic assessment
Electrocardiography – may demonstrate
ventricular hypertrophy, dysrhythmias, and any
degree of myocardial ischemia, injury, or
infarction
 Echocardiography - is useful in diagnosing
cardiac valvular changes, pericardial effusion,
chamber enlargement, and ventricular
hypertrophy
 Pulmonary artery catheters
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Impaired Gas Exchange
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Interventions include:
– Ventilation assistance (promotion of the
optimal spontaneous breathing pattern that
maximizes oxygen and carbon dioxide
exchange in the lungs)
– Hemodynamic regulation (optimization of
heart rate, preload, afterload, and
contractility)
– Energy management, diet therapy, drug
therapy
Decreased Cardiac Output
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Interventions include:
– Optimization of cardiac output: stroke
volume (determined by preload,
afterload, and contractility) and heart
rate
(Continued)
Decreased Cardiac Output
(Continued)
– Drug therapy including:
 Angiotensin-converting enzyme inhibitors (
afterload)
 Diuretics ( preload)
 Human B-type natriuretic peptides (
afterload)
 Nitrates
 Inotropics
 Beta-adrenergic blockers ( preload)
Hemodynamic Regulation
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Interventions include:
– Reduce afterload.
– Reduce preload.
– Improve cardiac muscle contractility.
– Administer drugs as prescribed.
– Monitor for therapeutic and adverse
effects.
– Teach client and family drug therapy.
Drugs That Reduce
Afterload
Angiotensin-converting enzyme
(ACE) inhibitors
 Human B-type natriuretic peptides
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Interventions That Reduce
Preload
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Diet therapy
– Fluid, sodium restrictions
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Drug therapy
– Diuretics
– Venous vasodilators
Drugs That Enhance
Contractility
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Digitalis
– Digitalis toxicity includes anorexia,
fatigue, changes in mental status.
– Monitor heart rate and electrolytes.
Other inotropic drugs including
dobutamine, milrinone, and
levosimendan
 Beta-adrenergic blockers
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Other Nonsurgical Options
Continuous positive airway pressure
 Cardiac resynchronization therapy
 Investigative gene therapy
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Surgical Management
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Newer surgical therapies include the
following:
– Partial left ventriculectomy
– Endoventricular circular patch
– Acorn cardiac support device
– Myosplint
Activity Intolerance
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Interventions include:
– Ventilation assistance
– Hemodynamic regulation
– Energy management
– Interdisciplinary interventions, which
regulate energy to prevent fatigue and
optimize function
Potential for Pulmonary
Edema
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Interventions include:
– Assess for early signs, such as crackles
in the lung bases, dyspnea at rest,
disorientation, and confusion.
– Rapid-acting diuretics are prescribed,
such as Lasix or Bumex.
– Oxygen is always used.
– Strictly monitor fluid intake and output.
Valvular Heart Disease
Mitral stenosis
 Mitral regurgitation (insufficiency)
 Mitral valve prolapse
 Aortic stenosis
 Aortic regurgitation (insufficiency)
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Assessment
Client may become suddenly ill or
slowly develop symptoms over many
years.
 Question client about attacks of
rheumatic fever, infective
endocarditis, and possibility of IV
drug abuse.
 Obtain chest x-ray, echocardiogram,
and exercise tolerance test.
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Common Nursing Diagnoses
Decreased Cardiac Output related to
altered stroke volume
 Impaired Gas Exchange related to
ventilation perfusion imbalance
 Activity Intolerance related to
inability of the heart to meet
metabolic demands during activity
 Acute Pain related to physiologic
injury agent (hypoxia)
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Nonsurgical Management
Drug therapy, including diuretics,
beta blockers, digoxin, oxygen, and
sometimes nitrates
 Prophylactic antibiotic
 Management of atrial fibrillation,
cardioversion
 Anticoagulant
 Rest with limited activity
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Surgical Management
Reparative procedures
 Balloon valvuloplasty
 Direct, or open, commissurotomy
 Mitral valve annuloplasty
 Replacement procedures
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Infective Endocarditis
Microbial infection involving the
endocardium
 Occurs primarily with IV drug abuse,
valvular replacements, systemic
infections, or structural cardiac
defects
 Possible ports of entry: mouth, skin
rash, lesion, abscess, infections,
surgery, or invasive procedures
including IV line placement
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Manifestations
Clinical manifestations usually occur within
2 weeks of a bacteremia.
 Assessment usually reveals a recurrent
fever.
 Most clients have temperatures from 37.2°
to 39.4° C.
 Many older adults remain afebrile.
 The severity of symptoms may depend on
the virulence of the infecting organism
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Manifestations
Manifestations
Fever associated with chills, night sweats,
malaise and fatigue
 Anorexia and weight loss
 Cardiac murmur (newly developed or change in
existing)
 Development of heart failure
 Evidence of systemic embolization
 Petechiae
 Splinter hemorrhages
 Osier's nodes
 Janeway's lesions
 Splenic infarction
 Neurologic changes
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Janeway's lesions on the sole of the foot
Splinter hemorrhage lesions in
endocarditis
Interventions
Antimicrobials
 Rest, balanced with activity
 Supportive therapy for heart failure
 Anticoagulants
 Surgical management
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Pericarditis
Inflammation or alteration of the
pericardium, the membranous sac
that encloses the heart
 Dressler’s syndrome
 Postpericardiotomy syndrome
 Chronic constrictive pericarditis
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Assessment
Substernal precordial pain radiating
to left side of the neck, shoulder, or
back
 Grating, oppressive pain, aggravated
by breathing, coughing, swallowing
 Pain worsened by the supine
position; relieved when the client sits
up and leans forward
 Pericardial friction rub
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Interventions
Hospitalization for diagnostic
evaluation, observation for
complications, and symptom relief
 Nonsteroidal anti-inflammatory
drugs
 Corticosteroid therapy
 Comfortable position, usually sitting
 Pericardial drainage
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(Continued)
Interventions (Continued)
Chronic pericarditis: radiation or
chemotherapy
 Uremic pericarditis: dialysis
 Pericardiectomy
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Emergency Care of Cardiac Tamponade
Cardiac tamponade — an extreme
emergency
 Increased fluid volume
 Hemodynamic monitoring
 Pericardiocentesis
 Pericardial window
 Pericardiectomy
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Rheumatic Carditis
Sensitivity response that develops
following an upper respiratory tract
infection with group A betahemolytic streptococci
 Inflammation in all layers of the
heart
 Impaired contractile function of the
myocardium, thickening of the
pericardium, and valvular damage
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Clinical Manifestations
Tachycardia
 Cardiomegaly
 New or changed murmur
 Pericardial friction rub
 Precordial pain
 Changes in electrocardiogram
 Indications of heart failure
 Existing streptococcal infection
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Cardiomyopathy
Subacute or chronic disease of
cardiac muscle
 Dilated cardiomyopathy
 Hypertrophic cardiomyopathy
 Restrictive cardiomyopathy
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Interventions
Nonsurgical management
 Surgical management
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– Cardiomyoplasty
– Heart transplantation