Download Portfolio I – Heart Failure Nursing 307P Portfolio I – Heart Failure

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Portfolio I – Heart Failure
Nursing 307P
Portfolio I – Heart Failure
Sara Voigtritter
Jennifer Lillibridge
June 24, 2011
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Portfolio I – Heart Failure
Heart Failure
Pathophysiology
Heart failure arises from myocardial dysfunction caused by factors such as
ischemic heart disease, hyperthyroidism, myocardial infarction, valvular disease,
hypertension, drug use, or alcohol abuse (Smeltzer, Bare, Hinkle, & Cheever, 2008, p.
949). The myocardial dysfunction causes decreased cardiac output, a resultant
decrease in systemic blood pressure, and a decrease in perfusion to the kidneys that
ultimately leads to vasoconstriction and activation of the renin-angiotensin-aldosterone
system (Smeltzer et al., 2008, p. 949). Vasoconstriction increases afterload, blood
pressure, and heart rate resulting in ventricular remodeling and further weakening of the
heart (Smeltzer et al., 2008, p. 949).
Vasoconstriction occurs when a decrease in cardiac output activates
baroreceptors in the left ventricle, aortic arch and carotid sinus (Smeltzer et al., 2008, p.
949). The activation of the baroreceptors stimulates vasomotor regulatory centers in the
medulla, and activates the sympathetic nervous system (SNS) (Smeltzer et al., 2008, p.
949). The SNS releases catecholamines called norepinephrine and epinephrine, which
cause vasoconstriction (Smeltzer, Bare, Hinkle, & Cheever, 2008, p. 949).
At the same time vasoconstriction is occurring, activation of the reninangiotensin-aldosterone system results from decreased perfusion to the kidneys
(Smeltzer et al., 2008, p. 949). The ill-perfused kidneys release renin, which combines
with angiotensinogen from the liver and becomes angiotensin I (Smeltzer et al., 2008, p.
949). Angiotensin I is converted to angiotensin II in the lungs (Smeltzer et al., 2008, p.
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949). Angiotensin II causes vasoconstriction, and triggers the release of aldosterone by
the adrenal cortex (Smeltzer et al., 2008, p. 949).
The increase in aldosterone increases sodium and water retention, which
increases ventricular remodeling (Smeltzer et al., 2008, p. 949). Aldosterone increases
further heart failure by causing the release of vasopressin and endothelin that increase
vasoconstriction and cytokines that cause increased ventricular remodeling (Smeltzer et
al., 2008, p. 949).
Related Nursing Care.
The general presentation of a heart failure patient is of “pale, cyanotic skin,
dependent edema, decreased activity tolerance and altered mental status or confusion”
(Smeltzer et al., 2008, p. 950). Cardiovascular symptoms include: an enlarged heart,
“third heart sound (S3), murmurs, tachycardia and JVD” (Smeltzer et al., 2008, p. 950).
Cerebrovascular symptoms include “lightheadedness, dizziness, and confusion”
(Smeltzer et al., 2008, p. 950). Gastrointestinal symptoms may include: “nausea,
anorexia, enlarged liver, and ascites” (Smeltzer et al., 2008, p. 950). Renal symptoms
include: “decreased urinary frequency during the day and nocturia” (Smeltzer et al.,
2008, p. 950). Lastly, respiratory symptoms include: “dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea, bilateral crackles that do not clear with cough, and
cough on exertion or when supine” (Smeltzer et al., 2008, p. 949).
Proper administration of medications and assessment of the heart failure
patient’s response to pharmacologic therapy is very important for heart failure patients
(Smeltzer et al., 2008, p. 957). Medications may cause side effects such as
hypotension, bradycardia, hypokalemia, cough, or toxicity (Smeltzer et al., 2008, p.
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957). Careful nursing monitoring of response is therefore critical (Smeltzer et al., 2008,
p. 957).
Fluid status monitoring is very important in heart failure patients as shifts in fluid
status can indicate that the patient’s heart failure is worsening (Smeltzer et al., 2008, p.
957). Careful assessment of patient response can prevent further harm to the patient.
Strict intake and output measurements are an essential tool for nurse in optimizing the
patient’s fluid volume balance (Smeltzer et al., 2008, p. 957). Daily weights, at the
same time of day, post voiding, monitoring for 2-3 pound differences in a day or 5 pound
differences in a week can reveal fluid status changes (Smeltzer et al., 2008, p. 957).
Proper assessment of lung sounds for crackles can reveal fluid build-up or decrease in
the lungs (Smeltzer et al., 2008, p. 957). Other ways to monitor fluid status are:
determining the degree of jugular venous distention, identifying the severity of
dependent edema, monitoring pulse rate and blood pressure, checking for postural
hypotension, and examining skin turgor and mucous membranes (Smeltzer et al., 2008,
p. 957).
Scientific Principles and Concepts Underlying Nursing Interventions
“Administering medications and assessing the patient’s response to the
pharmacologic intervention” is important as many of the medications used to treat heart
failure can cause harm to patients if not properly monitored (Smeltzer et al., 2008, p.
957). Some of the medications that are frequently used to treat heart failure and can
cause dangerous side effects include: diuretics, digitalis, beta-blockers and angiotensin
II converting enzyme inhibitors (ACE inhibitors) (Smeltzer et al., 2008, p. 952).
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Loop and thiazide diuretics, which are often used to treat heart failure, can cause
hypokalemia (Smeltzer et al., 2008, p. 957). Symptoms of hypokalemia include
“dysrhythmias, hypotension, muscle weakness, diminished deep tendon reflexes, and
generalized weakness” (Smeltzer et al., 2008, p. 957). Digitalis allows the heart to
pump more effectively and causes stronger contractions, but it also can slow heart rate
to dangerous levels and can cause toxicity (Smeltzer et al., 2008, p. 954). Symptoms of
digitalis toxicity include: “anorexia, nausea, vomiting, fatigue, depression, malaise,
changes in heart rate or rhythm, onset of irregular rhythm, and ECG changes” (Smeltzer
et al., 2008, p. 956). In addition, digitalis toxicity combined with hypokalemia can
increase the risk of dangerous dysrhythmias, so heart failure patients on potassium
depleting diuretics and digitalis are very much at risk (Smeltzer et al., 2008, p. 957).
ACE inhibitors, angiotensin II receptor blockers (ARBs), and spirolactone can cause
hyperkalemia (Smeltzer et al., 2008, p. 958). Hyponatremia can also be caused by longterm diuretic use and is characterized by “disorientation, apprehension, weakness,
fatigue, malaise, and muscle cramps” (Smeltzer et al., 2008, p. 958). Medications may
also have to be changed several times before the right regimen for the patient is
determined (Smeltzer et al., 2008, p. 957).
Physical examination of heart failure patients can reveal changes in the patient’s
fluid volume status. Crackles in the lungs indicate that the small airways and alveoli are
being stuck together with fluid, an indication of fluid overload (Smeltzer et al., 2008, p.
958). A S3 heart sound indicates that the ventricle is being overfilled each beat and is an
indication of heart failure (Smeltzer et al., 2008, p. 958). Jugular venous distention
(JVD) “greater than 3 cm above the sternal angle… is an estimate… of central venous
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pressure” (Smeltzer et al., 2008, p. 958). Manual pressure over the right upper quadrant
of the abdomen will cause neck vein distention greater than one centimeter, or positive
hepatojugular reflex, another indication of increased central venous pressure (Smeltzer
et al., 2008, p. 958).
Other indications of fluid volume status are level of consciousness and
dependent edema. The patient’s level of consciousness can reveal the amount of blood
reaching the brain, and therefore an indication of the heart’s function (Smeltzer et al.,
2008, p. 958). Dependent edema is a sign that fluid is leaking out of the vascular space
and into the interstitial spaces (Smeltzer et al., 2008, p. 958). Fluid shifts downward with
gravity. “If the patient is sitting upright, the feet and lower legs are examined for edema;
if the patient is supine in bed, the sacrum and back are also assessed for edema”
(Smeltzer et al., 2008, p. 958).
Careful intake and output measurements and daily weights are important for
inpatients, and daily weights are a crucial skill to be taught for outpatient management
of heart failure (Smeltzer et al., 2008, p. 958-960). Patients should be taught to take
diuretics in the morning so that the patient’s sleep is not interrupted by nighttime trips to
diurese (Smeltzer et al., 2008, p. 960). Intravenous fluids should be minimized in these
patients to prevent fluid overload (Smeltzer et al., 2008, p. 960). Fluid restrictions should
be followed to minimize cardiac workload (Smeltzer et al., 2008, p. 960).
Physiological, Psychological and Cultural/Spiritual Factors
Activity intolerance is a physiological factor that can make heart failure difficult to
live with (Smeltzer et al., 2008, p. 959). Bed rest is often recommended for these
patients when they have exacerbations of heart failure, but this can decondition the
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patient and put them at risk for skin breakdown, especially in conjunction with
dependent edema (Smeltzer et al., 2008, p. 959). To avoid deconditioning, thirty to
forty-five minutes of physical activity daily should be recommended and encouraged
inside and outside of the hospital (Smeltzer et al., 2008, p. 959). Severely debilitated
patients can break up this activity into 3-4 minute segments to allow for periods of rest
(Smeltzer et al., 2008, p. 959).
One major psychological issue for patients with heart failure is anxiety (Smeltzer
et al., 2008, p. 961). Due to the act that these patients have problems with oxygenation,
they are at a greater risk for feeling overwhelmed or breathless, especially at night
(Smeltzer et al., 2008, p. 961). As they become stressed, the sympathetic nervous
system is activated, increasing vasoconstriction, increasing arterial pressure, increasing
heart rate and increasing the heart’s workload (Smeltzer et al., 2008, p. 961). These
patients can receive oxygen to decrease cardiac workload as they become anxious
(Smeltzer et al., 2008, p. 961). The nurse can then teach the patient to control or avoid
their anxiety, while promoting physical and psychological comfort (Smeltzer et al., 2008,
p. 961). Some factors that may increase anxiety are: sleep deprivation, being
uninformed, and decreased nutritional status (Smeltzer et al., 2008, p. 961). Restraints
are to be avoided with these patients as they may increase cardiac workload and further
increase anxiety (Smeltzer et al., 2008, p. 961). Screening for depression is
recommended as there is a high incidence of depression in heart failure patients
(Smeltzer et al., 2008, p. 961).
Heart failure patients often feel powerless over their diagnosis (Smeltzer et al.,
2008, p. 962). Teaching about low-sodium diets, monitoring daily weights at home, and
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ensuring fluid restrictions are explained in a way that makes sense to the patient can
help them adhere to the regimens and take control of their own health (Smeltzer et al.,
2008, p. 962). Active listening and engaging the patient in taking control over their own
activity pacing can help the patients to feel supported and empowered (Smeltzer et al.,
2008, p. 962).
Patient X Case Study
Patient X was directly admitted to a telemetry floor in San Diego, after he had
visited his primary care provider and been found to have moderate dependent edema in
his lower extremities, hypotension, bradycardia, and shortness of breath. Upon physical
examination, the telemetry nurse found the patient’s heart rate was 42, blood pressure
was 84/45, lung sounds revealed crackles bilaterally that did not clear with coughing,
moderate dependent edema to the lower extremities, bounding pulses, and an S 3 heart
sound was ascultated. The nurse placed an intravenous saline lock and verified the
patient’s home medications.
Written orders for the patient included Lasix 40 milligrams intravenous push
immediately followed by potassium chloride once. The nurse gave the Lasix, which is a
loop diuretic, and explained that giving the potassium would help prevent low potassium
that can occur from use of the diuretic (Smeltzer et al., 2008, p. 953). The patient stated
he had stopped taking Lasix at home because he felt it made him go to the bathroom all
night, but it was alright, because he was eating a lot of cucumbers, cilantro and celery
that would help him diurese naturally. The nurse replied that it was great that he was
eating those foods, but that his Lasix is very important to help move fluid out of the
patient’s blood where it was causing his heart to work hard and out of his kidneys
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(Smeltzer et al., 2008, p. 953). She told him that she recommends patients take Lasix
first thing in the morning so that they can diurese all day and not lose sleep (Smeltzer et
al., 2008, p. 960).
The nurse also found out that the patient was on high doses of ACE inhibitors
and beta-blockers at home. She explained that ACE inhibitors can cause patients to
have what is called hypotension or low blood pressure and that beta-blockers can lower
patient’s heart rates and blood pressure, so it is important for him to monitor himself
outside of his doctor visits (Smeltzer et al., 2008, p. 953). She taught the patient how to
monitor his own heart rate and instructed him on locations have his blood pressure
taken or that he could buy a home blood pressure machine to monitor his blood
pressure. Because the patient did not seem ready to self-monitor by discharge, the
nurse had case management arrange home health to check on the patient (Smeltzer et
al., 2008, p. 962-963).
While patient X was in the hospital, strict intake and output measurements were
taken. Though he was on bed rest, activity was encouraged throughout the day to total
thirty to forty-five minutes. His legs were elevated to promote drainage. His lung sounds
and heart sounds were carefully monitored. His crackles and S3 heart sound dissipated.
He was educated about his medications and home health followed him for a couple of
weeks to ensure he experienced no further exacerbations. Studies have shown that
heart failure clinic referrals and telehealth management can result in fewer
exacerbations and hospitalizations (Smeltzer et al., 2008, p. 962-963).
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References
Smeltzer, S.C., Bare, B.G., Hinkle, J.L., & Cheever, K.H. (2008). Brunner and
suddarth's textbook of medical-surgical nursing (11th ed.). Philadelphia: Lippincott
Williams & Wilkins.