Care of a patient with Heart Failure

1. Heart Failure
S Makonde

3. • The basic function of the heart is to pump blood.
• The heart’s ability to pump is measured by cardiac
output (CO), the amount of blood pumped in 1
minute.
• CO is determined by measuring the heart rate (HR)
and multiplying it by the stroke volume (SV), which is
the amount of blood pumped out of the ventricle
with each contraction.

4. • CO usually is calculated using the equation CO = HR ×
SV.
• One of the factors controlling HR is the autonomic
nervous system.
• When SV falls, the nervous system is stimulated to
increase HR and thereby maintain adequate CO.
• SV depends on three factors: preload, afterload, and
contractility.

5. Preload
• is the amount of myocardial stretch just before
systole caused by the pressure created by the volume
of blood within the ventricle.
• Like a rubber band, the ventricular muscle fibres
need to be stretched (by the blood) to produce
optimal ejection of blood.

6. • Too little or too much muscle fibre stretch decreases
the volume of blood ejected.
• The major factor that determines preload is venous
return, the volume of blood that enters the ventricle
during diastole

7. • Another factor that determines preload is ventricular
compliance, which is the elasticity or amount of
“give” when blood enters the ventricle.
• Elasticity is decreased when the muscle thickens, as
in hypertrophic cardiomyopathy or when there is
increased fibrotic tissue within the ventricle.

8. • Fibrotic tissue replaces dead cells, such as after a
myocardial infarction .
• Fibrotic tissue has little compliance, making the
ventricle stiff.
• Given the same volume of blood, a noncompliant
ventricle has a higher intraventricular pressure than a
compliant one.
• The higher pressure increases the workload of the
heart and can lead to heart failure (HF).

9. Afterload
• refers to the amount of resistance to the ejection of
blood from the ventricle.
• To eject blood, the ventricle must overcome this
resistance.
• Afterload is inversely related to SV.
• The major factors that determine afterload are the
diameter and distensibility of the great vessels (aorta and
pulmonary artery) and the opening and competence of
the semilunar valves (pulmonic and aortic valves).

10. • The more open the valves, the lower the resistance.
• If the patient has significant vasoconstriction,
hypertension, or a narrowed opening from a stenotic
valve, resistance (afterload) increases.
• When afterload increases, the workload of the heart
must increase to overcome the resistance and eject
blood.

11. Contractility
• which refers to the force of contraction, is related to
the number and status of myocardial cells.
• Catecholamines, released by sympathetic stimulation
such as exercise or from administration of positive
inotropic medications, can increase contractility and
stroke volume.

12. • MI causes necrosis of some myocardial cells, shifting
the workload to the remaining cells.
• Significant loss of myocardial cells can decrease
contractility and cause HF.
• Afterload must be reduced by stress reduction
techniques or medications to match the lower
contractility

13. Definitions
• HF, often referred to as congestive heart failure (CHF), is
the inability of the heart to pump sufficient blood to
meet the needs of the tissues for oxygen and nutrients
• Heart failure is a clinical syndrome that results from the
progressive process of remodeling, in which mechanical
and biochemical forces alter the size, shape, and function
of the ventricle’s ability to fill with or pump enough
oxygenated blood to meet the metabolic demands of the
body.

14. • HF as a clinical syndrome characterized by signs and
symptoms of fluid overload or of inadequate tissue
perfusion
• These signs and symptoms result when the heart is
unable to generate a CO sufficient to meet the body’s
demands

15. Aetiology
• Risk factors include:
• Hypertension.
• Hyperlipidemia.
• Diabetes.
• CAD.
• Family history.
• Smoking.
• Alcohol consumption.
• Use of cardiotoxic drugs.
• Ventricular dysrhythmias.
• Atrial dysrhythmias.

16. • Myocardial dysfunction is most often caused by
coronary artery disease, cardiomyopathy,
hypertension, or valvular disorders.
• Atherosclerosis of the coronary arteries is the
primary cause of HF.
• Coronary artery disease is found in more than 60% of
the patients with HF (Braunwald et al., 2001).

17. • Ischemia causes myocardial dysfunction because of
resulting hypoxia and acidosis from the accumulation of
lactic acid.
• Myocardial infarction causes focal heart muscle necrosis,
the death of heart muscle cells, and a loss of contractility;
the extent of the infarction correlates with the severity of
HF.
• Revascularization of the coronary artery by a
percutaneous coronary intervention or by coronary
artery bypass surgery may correct the underlying cause
so that HF is resolved

18. • Systemic or pulmonary hypertension increases
afterload (resistance to ejection), which increases the
workload of the heart and leads to hypertrophy of
myocardial muscle fibres; this can be considered a
compensatory mechanism because it increases
contractility.
• However, the hypertrophy may impair the heart’s
ability to fill properly during diastole.

19. • Valvular heart disease is also a cause of HF. The
valves ensure that blood flows in one direction.
• With valvular dysfunction, blood has increasing
difficulty moving forward, increasing pressure within
the heart and increasing cardiac workload, leading to
diastolic HF

20. Types
• There are two types of HF, which are identified by assessment
of left ventricular functioning: an alteration in ventricular
filling (diastolic heart failure)
– stiff myocardium, which impairs the ability of the left
ventricle to fill up with blood. This causes an increase in
pressure in the left atrium and pulmonary
vasculature,causing the pulmonary signs of heart failure
• An alteration in ventricular contractionsystolic heart failure).
• poor contractility of the myocardium results in
decreased CO and an elevated SVR

21. Pathophysiology
• HF results from a variety of cardiovascular diseases
but leads to some common heart abnormalities that
result in decreased contraction (systole), decreased
filling (diastole), or both.
• Significant myocardial dysfunction most often occurs
before the patient experiences signs and symptoms
of HF.

22. • Systolic HF decreases the amount of blood ejected
from the ventricle, which stimulates the sympathetic
nervous system to release epinephrine and
norepinephrine.
• The purpose of this initial response is to support the
failing myocardium, but the continued response
causes loss of beta1-adrenergic receptor sites (down
regulation) and further damage to the heart muscle
cells.

23. • The sympathetic stimulation and the decrease in
renal perfusion by the failing heart cause the release
of renin by the kidney. Renin promotes the formation
of angiotensin I, a benign, inactive substance.
• Angiotensin-converting enzyme (ACE) in the lumen of
blood vessels converts angiotensin I to angiotensin II,
a vasoconstrictor that also causes the release of
aldosterone.

24. • Aldosterone promotes sodium and fluid retention and
stimulates the thirst centre. Aldosterone causes
additional detrimental effects to the myocardium and
exacerbates myocardial fibrosis (Pitt et al., 1999; Weber,
2001).
• Angiotensin, aldosterone, and other neurohormones
(e.g., atrial natriuretic factor, endothelin, and
prostacyclin) lead to an increase in preload and afterload,
which increases stress on the ventricular wall, causing an
increase in the workload of the heart.

25. • As the heart’s workload increases, contractility of the
myofibrils decreases.
• Decreased contractility results in an increase in end-
diastolic blood volume in the ventricle, stretching the
myofibers and increasing the size of the ventricle
(ventricular dilation).

26. • The increased size of the ventricle further increases
the stress on the ventricular wall, adding to the
workload of the heart.
• One way the heart compensates for the increased
workload is to increase the thickness of the heart
muscle (ventricular hypertrophy).

27. • However, the hypertrophy is not accompanied by an
adequate increase in capillary blood supply, resulting in
myocardial ischemia.
• The sympathetic-induced coronary artery
vasoconstriction, increased ventricular wall stress, and
decreased mitochondrial energy production also lead to
myocardial ischemia.
• Eventually, the myocardial ischemia causes myofibril
death, even in patients without coronary artery disease.

28. • The compensatory mechanisms of HF have been called
the “vicious cycle of HF” because the heart does not
pump sufficient blood to the body, which causes the
body to stimulate the heart to work harder; the heart is
unable to respond and failure becomes worse.
• Diastolic HF develops because of continued increased
workload on the heart, which responds by increasing the
number and size of myocardial cells (i.e., ventricular
hypertrophy and altered myocellular functioning).

29. • These responses cause resistance to ventricular
filling, which increases ventricular filling pressures
despite a normal or reduced blood volume. Less
blood in the ventricles causes decreased CO.
• The low CO and high ventricular filling pressures
cause the same neurohormonal responses as
described for systolic HF.

30. Clinical Manifestations
• The signs and symptoms of HF are most often
described in terms of the effect on the ventricles.
• Left-sided heart failure (left ventricular failure)
causes different manifestations than right-sided
heart failure (right ventricular failure).

31. • Chronic HF produces signs and symptoms of failure
of both ventricles.
• Although dysrhythmias (especially tachycardias,
ventricular ectopic beats, or atrioventricular [AV] and
ventricular conduction defects) are common in HF,
they may also be a result of treatments used in HF
(e.g., side effect of digitalis).

32. • Initially, there may be isolated left-sided heart failure,
but eventually the right ventricle fails because of the
additional workload.
• Combined left- and right-sided heart failure is
common

33. Left-Sided Heart Failure
• Pulmonary congestion occurs when the left ventricle
cannot pump the blood out of the ventricle to the
body.
• The increased left ventricular end-diastolic blood
volume increases the left ventricular end-diastolic
pressure, which decreases blood flow from the left
atrium into the left ventricle during diastole.

34. • The blood volume and pressure in the left atrium
increases, which decreases blood flow from the
pulmonary vessels.
• Pulmonary venous blood volume and pressure rise,
forcing fluid from the pulmonary capillaries into the
pulmonary tissues and alveoli, which impairs gas
exchange.

35. • These effects of left ventricular failure have been
referred to as backward failure.
• The clinical manifestations of pulmonary venous
congestion include

36. • dyspnoea, cough, pulmonary crackles, and lower-
than-normal oxygen saturation levels. An extra heart
sound, S3, may be detected on auscultation.
• Dyspnoea, or shortness of breath, may be
precipitated by minimal to moderate activity
(dyspnoea on exertion [DOE]); dyspnoea also can
occur at rest.

37. • The patient may report orthopnoea, difficulty in
breathing when lying flat.
• Patients with orthopnoea usually prefer not to lie
flat.

38. • They may need pillows to prop themselves up in bed,
or they may sit in a chair and even sleep sitting up.
• Some patients have sudden attacks of orthopnoea at
night, a condition known as paroxysmal nocturnal
dyspnoea (PND).

39. • Fluid that accumulated in the dependent extremities
during the day begins to be reabsorbed into the
circulating blood volume when the person lies down.
• Because the impaired left ventricle cannot eject the
increased circulating blood volume, the pressure in the
pulmonary circulation increases, causing further shifting
of fluid into the alveoli.
• The fluid filled alveoli cannot exchange oxygen and
carbon dioxide.

40. • Without sufficient oxygen, the patient experiences
dyspnoea and has difficulty getting an adequate
amount of sleep.
• The cough associated with left ventricular failure is
initially dry and non-productive.

41. • Most often, patients complain of a dry hacking cough
that may be mislabelled as asthma or chronic
obstructive pulmonary disease (COPD).
• The cough may become moist. Large quantities of
frothy sputum, which is sometimes pink (blood
tinged), may be produced, usually indicating severe
pulmonary congestion (pulmonary enema

42. • Adventitious breath sounds may be heard in various
lobes of the lungs.
• Usually, bi-basilar crackles that do not clear with
coughing are detected in the early phase of left
ventricular failure.
• As the failure worsens and pulmonary congestion
increases, crackles may be auscultated throughout all
lung fields.

43. • At this point, a decrease in oxygen saturation may
occur.
• In addition to increased pulmonary pressures that
cause decreased oxygenation, the amount of blood
ejected from the left ventricle may decrease,
sometimes called forward failure.
• The dominant feature in HF is inadequate tissue
perfusion.

44. • The diminished CO has widespread manifestations
because not enough blood reaches all the tissues and
organs (low perfusion) to provide the necessary
oxygen.
• The decrease in SV can also lead to stimulation of the
sympathetic nervous system, which further impedes
perfusion to many organs.

45. • Blood flow to the kidneys decreases, causing
decreased perfusion and reduced urine output
(oliguria).
• Renal perfusion pressure falls, which results in the
release of renin from the kidney.

46. • Release of renin leads to aldosterone secretion.
• Aldosterone secretion causes sodium and fluid
retention, which further increases intravascular
volume.

47. • However, when the patient is sleeping, the cardiac
workload is decreased, improving renal perfusion,
which then leads to frequent urination at night
(nocturia).
• Decreased CO causes other symptoms.
• Decreased gastrointestinal perfusion causes altered
digestion.

48. • Decreased brain perfusion causes dizziness, light-
headedness, confusion, restlessness, and anxiety due to
decreased oxygenation and blood flow.
• As anxiety increases, so does dyspnoea, enhancing
anxiety and creating a vicious cycle.
• Stimulation of the sympathetic system also causes the
peripheral blood vessels to constrict, so the skin appears
pale or ashen and feels cool and clammy.

49. • The decrease in the ejected ventricular volume
causes the sympathetic nervous system to increase
the heart rate (tachycardia), often causing the
patient to complain of palpitations.
• The pulses become weak and thready.

50. • Without adequate CO, the body cannot respond to
increased energy demands, and the patient is easily
fatigued and has decreased activity tolerance.
• Fatigue also results from the increased energy
expended in breathing and the insomnia that results
from respiratory distress, coughing, and nocturia.

51. Right-Sided Heart Failure
• When the right ventricle fails, congestion of the
viscera and the peripheral tissues predominates.
• This occurs because the right side of the heart
cannot eject blood and cannot accommodate all the
blood that normally returns to it from the venous
circulation.

52. • The increase in venous pressure leads to jugular vein
distention (JVD).
• The clinical manifestations that ensue include oedema of
the lower extremities (dependent oedema),
hepatomegaly (enlargement of the liver), distended
jugular veins, ascites (accumulation of fluid in the
peritoneal cavity), weakness, anorexia and nausea, and
paradoxically, weight gain due to retention of fluid

53. • Oedema usually affects the feet and ankles,
worsening when the patient stands or dangles the
legs.
• The swelling decreases when the patient elevates the
legs.
• The oedema can gradually progress up the legs and
thighs and eventually into the external genitalia and
lower trunk.

54. • Oedema in the abdomen, as evidenced by increased
abdominal girth, may be the only oedema present.
• Sacral oedema is not uncommon for patients who are on
bed rest, because the sacral area is dependent.
• Pitting oedema, in which indentations in the skin remain
after even slight compression with the fingertips is
obvious only after retention of at least 4.5 kg of fluid (4.5
litres).

55. • Hepatomegaly and tenderness in the right upper
quadrant of the abdomen result from venous
engorgement of the liver.
• The increased pressure may interfere with the liver’s
ability to perform (secondary liver dysfunction).
• As hepatic dysfunction progresses, pressure within the
portal vessels may rise enough to force fluid into the
abdominal cavity, a condition known as ascites.

56. • This collection of fluid in the abdominal cavity may
increase pressure on the stomach and intestines and
cause gastrointestinal distress.
• Hepatomegaly may also increase pressure on the
diaphragm, causing respiratory distress.

57. • Anorexia (loss of appetite) and nausea or abdominal
pain results from the venous engorgement and
venous stasis within the abdominal organs.
• The weakness that accompanies right-sided
• HF results from reduced CO, impaired circulation,
and inadequate removal of catabolic waste products
from the tissues.

58. Cardiovascular Findings in Both Types
• Cardiomegaly (enlargement of the heart)—detected
by physical examination and chest x-ray.
• Ventricular gallop—evident on auscultation.
• Rapid heart rate.
• Development of pulsus alternans (alternation in
strength of beat).

59. Diagnostic Evaluation
• 1. Echocardiography-two-dimensional with Doppler
flow studies—may show ventricular hypertrophy,
dilation of chambers, and abnormal wall motion.
• 2. ECG (resting and exercise)—may show ventricular
hypertrophy and ischemia.
• 3. Chest x-ray may show cardiomegaly, pleural
effusion, and vascular congestion.

60. • 4. Cardiac catheterization—(left heart catheterization to
rule out CAD).
– a. Right-sided heart catheterization—to measure
pulmonary pressure and left ventricular function.
• 5. ABG studies may show hypoxemia due to pulmonary
vascular congestion.
• 6. Bloodwork: CBC, electrolytes, Ca, Mg, renal function,
glycohemoglobin, lipid profile, thyroid function, and liver
function studies to fully assess patient condition that may
impact heart failure.

61. • 7. Human B-type natriuretic peptide (BNP, triage BNP, N- terminal
prohormone brain NP, or proBNP).
– a. As volume and pressure in the cardiac chambers rise, cardiac
cells produce and release more BNP. This test aids in the
differentiation of heart failure from other pulmonary diseases
(ie, chronic obstructive pulmonary disease) and establish acute
exacerbation of HF.
– b. A level greater than 100/mL is diagnostic for heart failure. In
addition, the higher the BNP, the more severe the heart failure.
– c. BNP is used in emergency departments to quickly diagnose
and start treatment.
• 8. Radionuclide ventriculogram.
• 9. Thallium scan to rule out underlying causes.

62. Management
• Stage A—focuses on eliminating risk factors by
initiating therapeutic lifestyle changes, such as
smoking cessation, increasing physical activity, and
decreasing alcohol consumption.
• This stage also focuses on controlling chronic
diseases, such as hypertension, high cholesterol, and
diabetes.
– Beta adrenergic blockers, ACE inhibitors, and
diuretics are useful in treating this stage.

63. • Stage B—treatment similar to Stage A, with emphasis on
use of ACE inhibitors and beta-adrenergic blockers.
• Stage C—same as A and B, but with closer surveillance
and follow-up.
– Digoxin is typically added to the treatment plan in this
stage.
– Use of diuretic, hydralazine, nitrate, aldosterone
antagonist, as indicated.
– Drug classes to be avoided due to worsening of heart
failure symptoms include anti-arrhythmic agents,
calcium channel blockers, and NSAIDs.

64. • Stage D—may need mechanical circulatory support,
continuous inotropic therapy, cardiac
transplantation, or palliative care.
– Treatment aimed at decreasing excess body fluid.
– May not tolerate other classes of drugs used in
previous stages.

65. Nursing Diagnoses
• Decreased Cardiac Output related to impaired
contractility and increased preload and afterload.
• Impaired Gas Exchange related to alveolar oedema due
to elevated ventricular pressures.
• Excess Fluid Volume related to sodium and water
retention.
• Activity Intolerance related to oxygen supply and demand
imbalance.
• Deficient Knowledge related to lack of previous exposure
to information.

66. Maintaining Adequate Cardiac Output
• Place patient at physical and emotional rest to reduce
work of heart.
• Provide rest in semi-recumbent position or in armchair in
air-conditioned environment—reduces work of heart,
increases heart reserve, reduces BP, decreases work of
respiratory muscles and oxygen utilization, improves
efficiency of heart contraction; recumbency promotes
diuresis by improving renal perfusion.
• Provide bedside commode—to reduce work of getting to
bathroom and for defecation.

67. • Provide for psychological rest—emotional stress
produces vasoconstriction, elevates arterial pressure,
and speeds the heart.
– i. Promote physical comfort.
– ii. Avoid situations that tend to promote anxiety
and agitation.
– iii. Offer careful explanations and answers to the
patient’s questions.

68. • Evaluate frequently for progression of left-sided
heart failure.
• Take frequent blood pressure readings.
– a. Watch for decreasing mean arterial pressure.
– b. Note narrowing of pulse pressure.
– c. Note alternating strong and weak pulsations
(pulsus alternans).

69. • Auscultate heart sounds frequently and monitor
cardiac rhythm.
– a. Note presence of S3 or S4 gallop (S3 gallop is a
significant indicator of heart failure).
– b. Monitor for premature ventricular beats.
– c. Assess chest pain.
– d. Measure CVP.

70. • Observe for signs and symptoms of reduced peripheral
tissue perfusion: cool temperature of skin, facial pallor,
poor capillary refill of nailbeds.
• Administer pharmacotherapy as directed.
– a. Monitor for adverse effects and effect of drug
therapy.
• Monitor clinical response of patient with respect to relief
of symptoms (lessening dyspnoea and orthopnoea,
decrease in crackles, relief of peripheral oedema).

71. Improving Oxygenation
• Raise head of bed 8 to 10 inches (20 to 25 cm)—
reduces venous return to heart and lungs; alleviates
pulmonary congestion.
• Support lower arms with pillows—eliminates pull of
patient’s weight on shoulder muscles.
• Sit orthopneic patient on side of bed with feet
supported by a chair, head and arms resting on an
over-the-bed table, and lumbosacral area supported
with pillows.

72. • Auscultate lung fields at least every 4 hours for
crackles and wheezes in dependent lung fields (fluid
accumulates in areas affected by gravity).
• Mark with indelible ink the level on the patient’s
back where adventitious breath sounds are heard.

73. • Use markings for comparative assessment over time
and among different care providers.
• Observe for increased rate of respirations (could be
indicative of falling arterial pH).

74. • Observe for Cheyne-Stokes respirations (may occur in
older patients because of a decrease in cerebral
perfusion stimulating a neurogenic response).
• Reposition the patient every 2 hours (or encourage
the patient to change position frequently)—to help
prevent atelectasis and pneumonia.

75. • Encourage deep-breathing exercises every 1 to 2
hours—to avoid atelectasis.
• Offer small, frequent feedings—to avoid excessive
gastric filling and abdominal distention with
subsequent elevation of diaphragm that causes
decrease in lung capacity.
• Administer oxygen, as directed.

76. Restoring Fluid Balance
• Administer prescribed diuretic, as ordered.
• Give diuretic early in the morning—nighttime
diuresis disturbs sleep.
• Keep input and output record—patient may lose
large volume of fluid after a single dose of diuretic.
Watch fluid intake.
• Weigh patient daily—to determine if oedema is being
controlled; weight loss should not exceed 0.5 to 1 kg/
day.

77. • Assess for signs of hypovolaemia caused by diuretic
therapy— thirst; decreased urine output; orthostatic
hypotension; weak, thready pulse; increased serum
osmolality; and increased urine specific gravity.

78. • Be alert for signs of hypokalaemia, which may cause
weakening of cardiac contractions and may
precipitate digoxin toxicity in the form of
dysrhythmias, anorexia, nausea, vomiting, abdominal
distention, paralytic ileus, paresthesias, muscle
weakness and cramps, confusion.
• Check electrolytes frequently.

79. • Give potassium supplements, as prescribed.
• Be aware of disorders that may be worsened by
diuretic therapy, including hyperuricaemia, gout,
volume depletion, hypernatremia, magnesium
depletion, hyperglycaemia, and diabetes mellitus.
• There is no evidence to support that patients who
are allergic to sulpha drugs are also allergic to
thiazide diuretics.

80. • Watch for signs of bladder distention in older male
patients with prostatic hyperplasia.
• Administer IV fluids carefully through an intermittent
access device to prevent fluid overload.

81. • Monitor for pitting oedema of lower extremities and
sacral area. Use convoluted foam mattress and
sheepskin to prevent pressure ulcers (poor blood
flow and oedema increase susceptibility).
• Observe for the complications of bed rest—pressure
ulcers (especially in oedematous patients),
phlebothrombosis, pulmonary embolism.

82. • Be alert to complaints of right upper quadrant
abdominal pain, poor appetite, nausea, and
abdominal distention (may indicate hepatic and
visceral engorgement).
• Monitor patient’s diet. Diet may be limited in
sodium—to prevent, control, or eliminate oedema;
may also be limited in calories.
• Caution patients to avoid adding salt to food and
foods with high sodium content.

83. Improving Activity Tolerance
• Increase patient’s activities gradually. Alter or modify
patient’s activities to keep within the limits of his or
her cardiac reserve.
• Assist patient with self-care activities early in the
day(fatigue sets in as day progresses).
• Be alert to complaints of chest pain or skeletal pain
during or after activities.

84. • Observe the pulse, symptoms, and behavioural
response toincreased activity.
• Monitor patient’s heart rate during self-care
activities.

85. • Allow heart rate to decrease to preactivity level
before initiating a new activity.
– Note time lapse between cessation of activity and
decrease in heart rate (decreased stroke volume
causes immediate rise in heart rate).
– Document time lapse and revise patient care plan
as appropriate (progressive increase in time lapse
may be indicative of increased left-sided heart
failure).

86. • Relieve night time anxiety and provide for rest and
sleep— patients with heart failure have a tendency
to be restless at night because of cerebral hypoxia
with superimposed nitrogen retention. Give
appropriate sedation to relieve insomnia and
restlessness.

87. Improving Knowledge
• Explain the disease process, note that the term
“failure” may be terrifying.
– a. Explain the pumping action of the heart: to
move blood through the body to provide nutrients
and aid in the removal of waste.
– b. Explain the difference between heart failure
and heart attack.

88. • Teach about the signs and symptoms of recurrence.
– Watch for weight gain and report a gain or loss of
more than 1 to 1.4 kg in a few days.
– Weigh patient at same time daily to detect any
tendency toward fluid retention: swelling of
ankles, feet, abdomen; persistent cough;
tiredness; loss of appetite; frequent urination at
night.

89. • Review medication regimen.
– Medications recommended for patients with
ejection fraction less than 40% include preload
reductors, such as diuretics, and afterload
reductors, such as ACE inhibitors.
– Medications to control heart rate include digoxin
or beta adrenergic blockers.
– Anticoagulation, if indicated.