Diagnosis: Decreased cardiac output r/t altered contractility aeb SOB, edema and MR.

Long Term Goal: Patient will increase cardiac output.

Outcome Criteria Interventions Scientific Rationale Evaluation

1. Patients vital signs will 1. Assess VS 1. Patient is an 85 yo female admitted with acute on 1. Unmet:
remain within normal q4h. chronic diastolic congestive heart failure with +2 Patients BP
limits, BP 90/60- mitral regurgitation and mild acute pulmonary was 152/63,
130/80mmHg, P 60-100 edema. She has a past medical history of and O2 98% 2
bpm, T <100.4 F and O2 sat hypertension, hyperlipidemia, diastolic dysfunction L/min via NC.
>95% RA q4h. of left ventricle, and left atrial dilation. At baseline
this patient is hypertensive, but has a regular NSR.
She has remained afebrile during hospitalization
also. Her vital signs should be monitored frequently
because of the indicators of decrease in cardiac
function with her history of cardiac issues. This
patient is at risk for an MI related to her PMH.
Initially the BP rises, but as the condition
deteriorates, BP may actually decrease because the
heart has been working too hard trying to
compensate. The temperature may increase within
the first 24 hours and may last as long as 1 week r/t
systemic inflammatory process caused by
myocardial cell death. Also with decreased cardiac
output oxygen saturation levels will decrease
because of the hearts inability to pump effectively.
Further decline in cardiac output may be proven by
compensatory tachycardia, as the heart attempts to
make up for decreased cardiac output by pumping
more frequently. The patients heart rate is rapid
and BP may elevate or decrease depending on the
severity of the heart failure.
Lewis pg. 710
2. Patient will maintain 2+ 2. Assess 2. Patient is an 85 yo female admitted with acute on 2. Unmet:
peripheral pulses q shift. peripheral chronic diastolic congestive heart failure with +2 Patient had
pulses q shift. mitral regurgitation and mild acute pulmonary weak 2+
edema. She has a past medical history of pulses
hypertension, hyperlipidemia, and a transient bilaterally.
ischemic attack. If there is a decreased cardiac
output, blood may not adequately flow threw the
peripheral arteries. Heart failure can cause
diminished peripheral pulses because the heart is
not adequately pumping enough blood throughout
the body to reach the lower extremities. Class
notes.
3. Patients lung sounds will 3. Assess lung 3. Patient is an 85 yo female admitted with acute on 3. Unmet:
become clear by discharge. sounds q4 chronic diastolic congestive heart failure with +2 Patient had
hours. mitral regurgitation and mild acute pulmonary crackles
edema. She has a past medical history of a murmur, present
diastolic dysfunction of left ventricle, and left atrial bilaterally at
dilation. Normally air flows through the airways in bases of lungs.
an unobstructed pattern. Upon auscultation lung
sounds bilaterally had adventurous sounds of
crackles present in bilaterally at the bases of lungs.
Abnormal sounds result from air passing through
moisture, mucous, or narrowed airways.
Recognizing the sounds created by normal airflow
allows the nurse to detect sounds caused by airway
obstruction. Crackles would indicate fluid in the lung
tissue. A decreased cardiac output causes fluid
volume excess related to heart failure due to the
heart inability to properly pump effectively. In heart
failure, an increase in the pulmonary venous
pressure is caused by failure of the left ventricle.
This results in engorgement of the pulmonary
vascular system. As a result, the lungs become less
compliant and there is increased resistance in the
 small airways. In addition, the lymphatic system
increases its flow to help maintain a constant
volume of the pulmonary extravascular fluid. This
early stage is clinically associated with a mild
increase in the RR and a decrease in partial
pressure of oxygen in arterial blood. If pulmonary
venous pressure continues to increase, the increase
in intravascular pressure causes more fluid to move
into the interstitial space than the lymphatics can
remove. Intestinal edema occurs at this point.
Tachypnea develops and the patient becomes
symptomatic. If pulmonary venous pressure
increases further, the alveoli lining cells are
disrupted and fluid moves into the alveoli. As the
disruption becomes worse from further increases in
the pulmonary venous pressure, the alveoli and
airways are flooded with fluid resulting in crackles
being heard in the lungs upon auscultation.
P&P pg. 457-458
4. Patients edema will be 4. Assess for 4. Patient is an 85 yo female admitted with acute on 4. Unmet:
< 1+ pitting edema by edema q4h. chronic diastolic congestive heart failure with +2 Patients had
discharge. mitral regurgitation and mild acute pulmonary 2+ pitting
edema. She has a past medical history of a murmur, edema
diastolic dysfunction of left ventricle, and left atrial bilaterally in
dilation. Skin that is edematous may feel cool lower
because of fluid accumulation and a decrease in extremities.
blood flow secondary to the pressure of the excess
fluid. The fluid may also stretch the skin, causing it
to feel taut and hard. A decreased cardiac output
causes fluid retention leading to edema. When the
heart doesnt pump effectively the fluid in the
vascular system doesnt get excreted through the
kidneys because the kidneys need a large amount
of blood per minute to adequately function. This
 patients diastolic dysfunction of left ventricle
because the heart is able to maintain an ejection
fraction of 65% or greater, but the inability of the
ventricles to relax and fill during diastole. Heart
failure is an abnormal clinical syndrome that
involves inadequate pumping and/or filling of the
heart. Decreased filling of the ventricles results in
decreased stroke volume and CO. This patient has
diastolic HF, which is characterized by filling
pressures because of stiff ventricles. This results in
venous engorgement in both the pulmonary and
systemic vascular systems. Edema in the
extremities can be caused by gravity, interruption
of venous return or right-sided heart failure.
pg. 767-770
5. Patient will have a 5. Monitor 5. Patient is an 85 yo female admitted with acute on 5. Met:
greater output then intake intake and chronic diastolic congestive heart failure with +2 Patients
qshift. output q shift. mitral regurgitation and mild acute pulmonary output: 1,600
edema. . She has a past medical history of a mL and intake:
murmur, diastolic dysfunction of left ventricle, and 390 mL
left atrial dilation. Blood flow to the kidneys is
approximately 1,200 mL/min, accounts for 20-25%
of the cardiac output. Therefore, urine cannot be
made if proper blood flow to the kidneys isnt
adequate. Decreased cardiac output would
decrease the blood flow to the kidneys. The use of
monitoring I&O is to give information regarding fluid
and electrolyte problems. A decreased cardiac
output cause fluid retention, which would be seen
because the intake would be significantly greater
than the output. This patient has edema in her feet,
ankle and calves bilaterally with complaints of pain
to the touch. She also has crackles bilaterally
present in the bases of her lungs. These are both
 signs of fluid retention. Keeping tract of I&O allows
us to see if she is still retaining fluid or excreting
what was already retained. P&P pg. 292 Lewis pg.
1047
6. Patient wont have JVD 6. Assess JVD 6. Patient is an 85 yo female admitted with acute on 6. Met: Patient
q2h. q2h chronic diastolic congestive heart failure with +2 did not have
mitral regurgitation and mild acute pulmonary JVD.
edema. She has a past medical history of a murmur,
diastolic dysfunction of left ventricle, and left atrial
dilation. Jugular vein distention is a sign of fluid
retention because there is more volume in the
vascular space. The primary cause of right-sided HF
is left sided HF. In this situation, left-sided HF results
in pulmonary congestion and increased pressure in
the blood vessels of the lung. Eventually, chronic
pulmonary hypertension results in right-sided
hypertrophy and HF. Right-sided HF causes a back
up of blood into the right atrium and venous
circulation. Venous congestion in the circulation
results in jugular venous distention. A decreased
cardiac output causes fluid retention leading to an
increase in weight. When the heart doesnt pump
adequately the fluid in the vascular system doesnt
get excreted through the kidneys related to the
large amount of blood per minute they require for
proper function. To assess for JVD position the
patient at a 45-degree angle and turn their head
away from you. Assess the jugular vein for
distention/bulging. Class notes
7. Patients edema will 7. Administer 7. Patient is an 85 yo female admitted with acute on 7. Unmet:
decrease to 1+ pitting Furosemide 40 chronic diastolic congestive heart failure with +2 Patient had 2+
edema by the end of the mg tab PO mitral regurgitation and mild acute pulmonary pitting edema.
day. twice daily. edema. She has a past medical history of a murmur,
diastolic dysfunction of left ventricle, and left atrial
 dilation. Diuretics are the mainstay of treatment in
patients with volume overload. Diuretics act to
decrease sodium reabsorption at varies sites within
the nephrons, thereby enhancing sodium and water
loss. Decreasing intravascular volume with the use
of diuretics reduces venous return and subsequently
the volume returning to the LV. This allows the LV to
contract more efficiently. Cardiac output is
increased, pulmonary vascular pressures are
decreased, and gas exchange is improved. Lewis
pg. 773-774
8. Patients BP will 8. Administer 8. Patient is an 85 yo female admitted with acute on 8. Unmet:
decrease between 90/60- Losartan 50 chronic diastolic congestive heart failure with +2 Patient was
130/80 mmHg by end of mg tab PO mitral regurgitation and mild acute pulmonary discharged
shift. once daily @ edema. She has a past medical history of before onset of
0900. hypertension, a murmur, diastolic dysfunction of left drug took
ventricle, and left atrial dilation. Angiotensin II place.
receptor antagonists are used alone or with other
agents in the management of hypertension.
Losartan blocks the vasoconstrictor and
aldosterone-secreting effects of angiotensin II at
various receptor sites, including vascular smooth
muscle and the adrenal glands. Because cardiac
output is dependent on afterload in chronic HF, the
reduction in SVR seen with the use of ARBs causes a
significant increase in cardiac output. Nursing
central, Lewis pg. 776
9. Patients edema in 9. Administer 9. Patient is an 85 yo female admitted with acute on 9. Unmet:
bilateral extremities will be Metolazone 2.5 chronic diastolic congestive heart failure with +2 Patients
1+ pitting to no pitting mg tab every mitral regurgitation and mild acute pulmonary edema
edema by discharge. other day. edema. She has a past medical history of bilaterally in
hypertension, diastolic dysfunction of left ventricle, lower
and left atrial dilation. Metolazone is used to treat extremities
mild to moderate hypertension and edema was 1-2+
 associated with HF or the nephrotic syndrome. This pitting edema.
medication increases excretion of sodium and water
by inhibiting sodium reabsorption in the distal
tubule, promotes excretion of chloride, potassium,
magnesium, and bicarbonate, and may produce
arteriolar dilation. With the decrease in fluid,
cardiac output increases because the heart doesnt
have to work against as much pressure, allowing for
adequate blood flow. Nursing Central
10. Patients BP will remain 10. Administer 10. Patient is an 85 yo female admitted with acute 10. Unmet:
between 118-130/45-63, Carvediol 12.5 on chronic diastolic congestive heart failure with +2 Patients initial
pulse 60-100 bmp, and mg PO twice mitral regurgitation and mild acute pulmonary BP was 152/63,
deny presence of chest daily with food. edema. She has a past medical history of a murmur, but pt was
pain q4h. diastolic dysfunction of left ventricle, and left atrial discharged
dilation. Patients who have left ventricular before onset of
dysfunction, have elevated BP, or have had an MI drug.
should start and continue BB indefinitely. Carvediol
is an antihypertensive Beta Blocker (BB). BB blocks
stimulation of beta-adrenergic receptor sites
selective for myocardial receptors. These drugs
decrease myocardial contractility, HR, SVR, and BP,
all of which reduce the myocardial oxygen demand.
If SVR is decreased, the heart doesnt have to pump
against as much pressure, thus its workload
decreases, increasing cardiac output. As this patient
has an extensive PMH of cardiac issues it is vital
that she remain on BB therapy to lessen the
likelihood of future cardiac events. Lewis pg. 745,
Nursing Central
11. Patients BUN level will 11. Monitor 11. Patient is an 85 yo female admitted with acute 11. Met:
decrease to 40 by BUN q day on chronic diastolic congestive heart failure with +2 Patients BUN
discharge. mitral regurgitation and mild acute pulmonary level was 57,
edema. She has a past medical history of a murmur, but decreased
diastolic dysfunction of left ventricle, and left atrial to 50. This is
 dilation. Blood flow to the kidneys is approximately not WNL (7-
1,200 mL/min, accounts for 20-25% of the cardiac 21), but
output. Blood urea nitrogen level is used to evaluate heading back
renal function. In the kidneys, almost all urea is in the correct
filtered out of the blood by glomerular function. direction.
Some urea is reabsorbed with water in the renal
tubules, but most is removed from the body in
urine. The amount of urea excreted is dependent on
the state of hydration and renal perfusion. This
patient has CHF, which causes decreased cardiac
output because the myocardium isnt adequately
pumping. If cardiac output is decreased the kidneys
are not going to be perfused, which is going to
cause an increase in the BUN level. Lewis pg.
1057,1108
12. Patients BNP levels will 12. Monitor 12. Patient is an 85 yo female admitted with acute 12. Unmet:
decrease between 600-900 BNP levels q on chronic diastolic congestive heart failure with +2 Patients BNP
by discharge. day. mitral regurgitation and mild acute pulmonary level was
edema. She has a past medical history of a murmur, 1,449.
diastolic dysfunction of left ventricle, and left atrial
dilation. The bodys attempts to maintain balance
are demonstrated by several counter regulatory
processes. Natriuretic peptides (b-NP) are hormones
produced by the muscle. BNP is released from the
ventricles in response to increased blood volume in
the heart. The natriuretic peptides have
cardiovascular effects including vasodilation and
decreased BP. When leaves are elevated, the heart
is working harder because of the excess blood in
the heart and the inability to pump it out. When
levels are increased it is a clear indicator of HF and
decreased cardiac output. This patients BNP level
was 1,449 indicating severe HF. Lewis pg. 768
13. Patients Hgb >9.1, Hct 13. Obtain 13. Patient is an 85 yo female admitted with acute 13. Unmet:
>27 and trend towards repeat order on chronic diastolic congestive heart failure with +2 Patients Hgb
normal range by discharge. for H&H daily. mitral regurgitation and mild acute pulmonary elevated to
edema. She has a past medical history of a murmur, 9.1, and Hct
diastolic dysfunction of left ventricle, left atrial 26.7, but still
dilation, and a history of GI bleeding. With the not WNL.
patients extensive cardiac and GI bleed history her
RBC and Hbg levels run low. The primary functions
of RBCs include transport of gases and assistance in
maintaining acid-base balance. If the levels are low,
then sufficient oxygen amounts are not getting into
the blood causing muscle to be unable to contract
decreasing the workload it can do, decreasing
cardiac output. Lewis pg. 615
14. Patient will have normal 14. Monitor 14. Patient is an 85 yo female admitted with acute 14. Met:
sinus rhythm as assessed telemetry q4h on chronic diastolic congestive heart failure with +2 Patient
q4h. and prn. mitral regurgitation and mild acute pulmonary remained in
edema. She has a past medical history of a murmur, NSR.
diastolic dysfunction of left ventricle, and left atrial
dilation. Telemetry monitoring is the observation of
a patients HR and rhythm at a site distant from the
patient. The use of this technology can help rapidly
diagnose dysrhythmias, ischemia, or infarction.
Chronic HF causes enlargement of the chamber of
the heart. This enlargement can cause changes in
the normal electrical pathways. Dysrhythmias result
from disorders of impulse formation, conduction of
impulses, or both. Decreased CO could lead to
hypoxemia and patient could become hypoxic if
untreated. Tissue damage occurs within minutes.
Any damage to the myocardium can disrupt
conductivity and cause ischemic injury or
arrhythmias.Lewis pg. 735
15. Patient will verbalize 15. Teach daily 15. Patient is an 85 yo female admitted with 15. Unmet:
importance of daily weights weight acute on chronic diastolic congestive heart failure Patient was
by discharge and that 2 importance by with +2 mitral regurgitation and mild acute anxious about
pounds in two days is too discharge. pulmonary edema. She has a past medical history discharge to
much. of a murmur, diastolic dysfunction of left FLCL and
ventricle, and left atrial dilation. Accurate daily unable to
weights provide the easiest measurement of verbalize back
volume status. An increase of two pounds (1 kg) importance.
is equal to 1000 mL of fluid retention, providing
the patient has maintained usual dietary intake or
hasnt been NPO). However, weight changes must
be obtained under standardized conditions. Teach
the pt that accurate weight requires the patient
to be weighed at the same time everyday,
wearing the same garments and on the same
calibrated scale. If the patient notices a weight
change greater than 2 pounds in 2 days the need
to notify the MD. If the patient is retaining fluid it
is going to decrease cardiac output.
Lewis pg. 771