LeMone & Burke’s Medical-Surgical Nursing:

Clinical Reasoning in Patient Care

Seventh Edition

Chapter 32

Nursing Care of Patients with

Vascular and Lymphatic Disorders

Hypertension

Copyright © 2020, 2015, 2011 Pearson Education, Inc. All Rights Reserved
Learning Outcomes (1 of 2)

• Describe the pathophysiology , risk factors , causes, diagnostic

examinations and manifestations related to :
• Myocardial Infarction
• Angina Pectoris
• Heart Failure

• outline the interprofessional care and nursing care of patients with

this disorder.
LeMone & Burke’s Medical-Surgical Nursing:
Clinical Reasoning in Patient Care
Seventh Edition

Chapter 30

Nursing Care of Patients with

Coronary Heart Disease

Myocardial Infarction
Angina Pectoris

Copyright © 2020, 2015, 2011 Pearson Education, Inc. All Rights Reserved
The Patient with Coronary Heart Disease

• Affects 16.3 million people in the U.S.

• Can lead to:
• Angina pectoris
• Acute coronary syndrome
• Myocardial infarction
• Dysrhythmias
• Heart failure
• Sudden death
Incidence and Prevalence
Saudi Arabia:
Cardiovascular diseases account for 37 per cent of
all deaths in Saudi Arabia according to Saudi
Health Ministry statistics local media reported.

A recent statistic, obtained by Al Watan

newspaper, also showed that 15 per cent of Saudi
Arabia’s population suffer from hypertension, a
risk factor that contributes significantly to
cardiovascular diseases.

World Gulf News, Sept 2020

https://www.cdc.gov/
Physiology Review
• Left main coronary artery
• Anterior descending artery
• Circumflex artery
• Right coronary artery
• Supplies the right ventricle
• Posterior descending artery
• Coronary arteries
• Blood flow regulated by aortic
pressure
• Collateral channels
• Develop between small
arteries
• Providing alternative routes for
blood flow
Coronary heart disease

• Categories of coronary heart disease

• Chronic ischemic heart disease

• Stable and vasospastic angina
• Silent myocardial ischemia

• Acute coronary syndrome

• From unstable angina to myocardial infarction

• Ischemia - results from inadequate oxygen supply to the

heart muscle
 Risk Factors
Nonmodifiable Modifiable
Pathophysiologic Lifestyle
Age Hyperlipidemia Cigarette smoking
Men ≥ 45 years Elevated LDL cholesterol Obesity
Women ≥ 55 years Elevated triglycerides Physical inactivity
Low HDL cholesterol Atherogenic diet

Gender Hypertension Women only: Use of oral

contraceptives, hormone replacement
therapy

Heredity Diabetes mellitus

Behavioral Chronic stress
Social isolation
Anxiety and depression
Emerging risk factors:
Elevated homocysteine levels
Thrombogenic factors
Inflammatory factors
Impaired fasting glucose
 Risk Factor Management of Coronary
Heart Disease
• Smoking
• Cessation • Exercise
• Diet – At least 30 minutes 5-
• Reduced saturated fat, 6 days each week
cholesterol – Hypertension
• Increased soluble, ▪ Cannot be
insoluble fiber prevented or
• Sodium : Less than cured, but can be
2300 mg/day and up controlled
to 1500 mg for those
ages 51 and older or – Diabetes
those who have ▪ Weight loss
hypertension, diabetes,
▪ Reduced fat intake
or chronic kidney disease
or are African American ▪ Increased exercise
Diagnosis of Coronary Heart
Disease
• Total serum cholesterol: is elevated in hyperlipidemia. A lipid
profile includes triglyceride, HDL, and LDL levels and enables
calculation of the ratio of HDL to total cholesterol.. Elevated lipid
levels are associated with an increased risk of atherosclerosis.
• C-reactive protein:is a serum protein associated with
inflammatory processes. Recent evidence suggests that elevated
blood levels of this protein may be predictive of CHD.
• Ankle-brachial blood pressure index (A B I):is an
inexpensive, noninvasive test for peripheral vascular disease that
may be predictive of CHD. Doppler is used to measure the
systolic blood pressure in the brachial, posterior tibial, and
dorsalis pedis arteries. An ABI of < 0.9 in either leg indicates the
presence of peripheral arterial disease and a significant risk for
CHD.
Diagnosis of Coronary Heart
Disease
• Exercise E C G testing: assesses the cardiac response to
increased workload induced by exercise. The test is
considered positive for CHD if myocardial ischemia is
detected on the ECG (depression of the ST segment by > 3
mm

• Electron beam computed tomography (E B C T):creates

a three-dimensional image of the heart and coronary arteries
that can reveal coronary artery calcification and other
abnormalities.

• Myocardial perfusion imaging: to evaluates myocardial

blood flow and perfusion, both at rest and during stress
testing (exercise or mental stress
Nursing Care of the Patient with Coronary
Heart Disease
• Nursing Diagnoses
• Imbalanced Nutrition: More than Body
Requirements
• Ineffective Health Maintenance

• Continuity of care
• Cardiac rehabilitation program
• Teaching, support for patient management
Pharmacological Treatment
• Diet and exercise programs
• Supplemental vitamins
• Behavioral therapies

Complementary Therapies
• Drug therapy to lower total serum cholesterol and
LDL levels, raise HDL levels
• High-risk MI patients
• Prophylactic low-dose aspirin therapy
 2. Angina Pectoris
• Chest pain resulting from reduced
coronary blood flow
• Pathophysiology
• Imbalance between myocardial blood
supply and demand
• Myocardial ischemia
 Pectoris
Types of CHARACTERISTICS / OCCURRENCE
angina
Stable • the most common and • occurs with a predictable amount of relieved
angina: predictable form of activity or stress by rest
angina. • occurs when the work of the heart is and
• A common increased by physical exertion, nitrates
manifestation of CHD. exposure to cold, or stress. .

Prinzmetal • caused by coronary • occurs unpredictably (unrelated to

(variant) artery spasm with or activity) and often at night.
angina: without an
atherosclerotic lesion
Unstable • Patients with unstable • occurs with increasing frequency,
angina: angina are at risk for severity, and duration.
myocardial infarction • Pain is unpredictable and occurs with
decreasing levels of activity or stress
• may occur at rest.
Silent • is thought to be • may occur with either activity or with
myocardial common in people with mental stress
ischemia: CHD.
 Manifestations of Angina Pectoris
• The cardinal manifestation of angina is chest pain.

• The pain is typically precipitated by an identifiable event, such as

physical activity, strong emotion, stress, eating a heavy meal, or
exposure to cold.

• The classic sequence of angina is activity–pain, rest–relief.

• The patient may describe the pain as a tight, squeezing, heavy

pressure or a constricting sensation.

• It characteristically begins beneath the sternum and may

radiate to the jaw, neck, shoulder, or arm.

• Less characteristically, the pain may be felt in the jaw, epigastric

region, or back.
Manifestations of Angina Pectoris
• Anginal pain usually occurs in a crescendo–
decrescendo pattern (increasing to a peak, then
gradually decreasing), typically lasting 2 to 5 minutes; it
is generally relieved by rest.

• Additional manifestations of angina include

dyspnea, pallor, tachycardia, and great anxiety and
fear.

• Women frequently present with atypical symptoms of

angina, including fatigue, indigestion or nausea and
vomiting, and upper back pain.
Figure 30.1

ECG changes during an episode of angina. Note characteristic T-

wave inversion and ST-segment depression of myocardial
ischemia.
Diagnosis of Angina Pectoris
1. Medical history and family history
2. Comprehensive description of chest pain
3. Physical assessment findings
4. Electrocardiography (Resting E C G)
5. Stress electrocardiography (Exercise stress test)
6. Radionuclide testing - May be combined with pharmacologic stress testing
7. Echocardiography - Transesophageal echocardiography (T E E)
8. Coronary angiography- Gold standard for evaluating coronary arteries
Nursing Care of the Patient with Angina
Pectoris
• Health assessment & physical assessment

• Priorities of care
• Reduce myocardial oxygen demand and improve
oxygen supply

• Nursing Diagnoses
• Ineffective Tissue Perfusion: Cardiac
• Risk for Ineffective Therapeutic Regimen Management
Nursing Diagnosis:
Ineffective Cardiac Tissue Perfusion
NURSING INTERVENTIONS:
• Keep prescribed nitroglycerin tablets at the patient’s side so one can be taken at
the onset of pain.
• Start oxygen at 4 to 6 L/min per nasal cannula or as prescribed. Supplemental
oxygen reduces myocardial hypoxia.
• Pace activities to allow rest between them.
• Teach about prescribed medications
• Instruct to take sublingual nitroglycerin before engaging in activities that
precipitate angina
• Encourage to implement and maintain a progressive exercise program
• Refer to a smoking cessation program as indicated.
Pharmacological Treatment of Angina
Pectoris
• Reduce oxygen demand, increase oxygen supply

1. Nitrates: nitroglycerin and longer-acting nitrate preparations, are used

to treat acute anginal attacks and prevent angina.; It may also improve
myocardial oxygen supply by dilating collateral blood vessels and
reducing stenosis.
• Sublingual nitroglycerin is the drug of choice to treat acute
angina.
• It acts within 1 to 2 minutes, decreasing myocardial work and
oxygen demand through venous and arterial dilation, which in turn
reduce preload and afterload.
• 2. Beta-blockers
• 3. Calcium channel blockers
• 4. Low-dose aspirin
2. Acute Myocardial Infarction

• Death/irreversible damage of
myocardial cells due to blood
flow being blocked from
cardiac muscle
• May lead to cardiogenic
shock and death
• Risk factors same as for
coronary heart disease
Pathophysiology of Acute Myocardial
Infarction
• Stable or unstable lesions form from atherosclerotic
plaque.
• Non-Q wave infarction or Q-wave infarction
• Described by damaged area of the heart
• Cocaine-induced MI
• Increased SNS activity
• Releases catecholamines
• Interferes with reuptake of catecholamines
Pathophysiology of Acute Myocardial
Infarction
• necrosis (death) of myocardial cells ; a life-threatening event.
• If circulation to the affected myocardium is not promptly restored, loss
of functional myocardium affects the heart’s ability to maintain an
effective cardiac output. This may ultimately lead to cardiogenic shock
and death.
• Myocardial infarction rarely occurs without preexisting coronary
heart disease.

Risk factors for MI: are those for coronary heart disease:
• Age, gender (Women and older adults often experience atypical chest
pain.)
• heredity, race, smoking,
• obesity, hyperlipidemia, hypertension, diabetes,
• sedentary lifestyle, diet, and others.
Manifestations of Acute Myocardial
Infarction
• Chest pain
• More severe than anginal pain
• Distinguished by duration and continuous nature
• Vital Signs: Tachycardia, Tachypnea
• Integumentary: Diaphoresis, Cool, mottled skin;
• Cardiovascular: Hypotension or hypertension ,Palpitations,
dysrhythmias, diminished peripheral pulses, Signs of left heart failure,
Vasoconstriction
• Neurological: Anxiety , Decreased level of consciousness
• Lab Exams: Elevated W B C count and Elevated temperature
Diagnostic Lab Tests Diagnostic Tests
• Creatine kinase
• CK-MB • Electrocardiogram
• Cardiac-specific troponin T • Echocardiography
• Cardiac-specific troponin I • Radionuclide imaging
• Myoglobin • Hemodynamic
monitoring
• CBC
• ABGs
Nursing Care of the Patient with Myocardial
Infarction
• Nursing Diagnoses Immediate treatment
goals :
• Acute Pain
• Ineffective Tissue Perfusion • Rapid assessment and early
diagnosis are important in
• Ineffective Coping
treating AMI.
• Fear
• “Time is muscle” is a medical
truism for the patient with AM
• Continuity of care • Relieve chest pain
• Assess readiness to learn • Reduce the extent of
• Follow up by telephone myocardial damage
• Provide resources • Maintain cardiovascular
stability
• Decrease cardiac workload
• Prevent complications
Pharmacological Treatment of Acute
Myocardial Infarction (1 of 2)
• Aspirin considered an essential • Other medications
part of treating A M I
• Beta blockers
• Analgesics
• Angiotensin-converting
• Nitroglycerin
enzyme (A C E) inhibitors
• Morphine sulfate
• Anticoagulants and
• Fibrinolytic therapy
antiplatelet medications
• Dissolves, breaks up blood clots
• Standard or low-molecular-
• Antidysrhythmics
weight heparin
• Class I or II
preparations
• Vasopressors
• Antilipemic agents
 Nonpharmacologi
Surgical Treatment
cal Treatment
• Revascularization procedures
• Bed rest, constant • Angioplasty
monitoring • Stent placement
• Liquid diet for first 4-12 • CABG surgery
hours • Other invasive procedures
• Dietary restrictions • Intra-aortic balloon pump (I AB
P)
• After cardiac surgery
• Cardiogenic shock following
AMI
• Ventricular assist device (VAD)
 Figure 30.6a

The intra-aortic balloon pump. When

inflated during diastole, the balloon
supports cerebral, renal, and
coronary artery perfusion.
Complications of Acute Myocardial Infarction
• Dysrhythmias • Structural defects
• Disturbances or irregularities of – Ventricular aneurysm
heart rhythm; arrhythmogenic
tissue – Regurgitation
• Pump failure
• Cardiogenic shock • Pericarditis
• Impaired tissue perfusion – Pericardial friction rub
• Infarct extension – Dressler syndrome
• Reinfarction in the area of original
infarction
 Comparing Stable Angina, and Acute
Myocardial Infarction
Stable Angina Acute Myocardial Infarction
Pathophysiolo • Myocardial ischemia occurs with • Obstruction of a coronary artery by
gy increased workload (e.g., during a thrombus blocks blood supply to a
exercise) due to stable portion of the myocardium,
atherosclerotic plaque narrowing resulting in necrosis.
coronary arteries.
Chest pain • Stable and predictable, occurring • Begins abruptly, unrelated to rest or
with exertion or emotion exercise

• Crescendo–decrescendo pattern • Severe, “crushing”

May radiate to neck, shoulder,
arms • Unrelieved by rest or nitroglycerin

• Usually lasts 5–10 min, relieved by • Radiates to arms, neck, jaw

rest
Comparing Stable Angina, and Acute
Myocardial Infarction
Stable Angina Acute Myocardial Infarction
Other • Indigestion, nausea • Epigastric pain, nausea
manifestations Possible shortness of breath Dyspnea

• Anxiety • Pallor, diaphoresis

• Tachycardia or bradycardia,
hyper- or hypotension

Diagnosis • ECG: T-wave inversion during • ECG: ST-segment elevation

anginal episodes possible Q wave

• Cardiac markers: Within normal • Cardiac markers: Elevated

range
LeMone & Burke’s Medical-Surgical Nursing:
Clinical Reasoning in Patient Care
Seventh Edition

Chapter 31

Nursing Care of the Patients with

Cardiac Disorders

Heart Failure

Copyright © 2020, 2015, 2011 Pearson Education, Inc. All Rights Reserved
 Blood
Circulat
ion
 Physiology Review of the Heart
• Heart rate : the volume of blood ejected with each mint
• Stroke volume: the volume of blood ejected with each heartbeat
• Cardiac output (CO): Is a product of heart rate and stroke volume.
Heart rate affects cardiac output by controlling the number of ventricular
contractions per minute.
• Preload is the initial stretching of the cardiac myocytes (muscle cells)
prior to contraction. It is related to ventricular filling.
• Preload: Think about a new rubber band. As you stretch the rubber band
and then release it, it snaps back into shape with great force.
• Afterload is the force or load against which the heart has to contract to
eject the blood. ... Afterload is the 'load' to which the heart must pump
against.
• Afterload: When a hose is crimped or plugged, more force is required to
eject a stream of water out its end.
 Physiology Review of the Heart

• Contractility: is the natural ability of cardiac muscle fibers to

shorten during systole.

• Ejection fraction (E F):refers to how well your left ventricle

(or right ventricle) pumps blood with each heart beat. Most
times, EF refers to the amount of blood being pumped out of
the left ventricle each time it contracts. The left ventricle is
the heart's main pumping chamber.50:70%
Pathophysiology of Heart Failure
• Primary compensatory mechanisms
• Frank-Starling mechanism
• Neuroendocrine responses
• Ventricular remodeling: occurs as the heart chambers
and myocardium adapt to fluid volume and pressure increases.
Which leads to ventricular hypertrophy
 3. Heart Failure
• Is a complex syndrome resulting Causes
from cardiac disorders that impair • Impaired myocardial
the ventricles’ ability to fill with contraction
and effectively pump blood. • Structural cardiac
disorders
• In heart failure, the heart is • Acute excess demands
unable to pump enough blood to placed on the
meet the metabolic demands of myocardium
the body. • Hypertension
• Disorder of cardiac function • Coronary heart disease
 Causes of HF
Impaired Myocardial Increased Cardiac Acute Noncardiac
Function Workload Conditions
•Coronary heart disease •Hypertension •Volume overload
•Cardiomyopathies •Valve disorders •Hyperthyroidism
•Rheumatic fever •Anemias •Fever, infection
•Infective endocarditis •Congenital heart •Massive pulmonary
defects embolus
Risk Factors for Heart Failure

• Incidence, prevalence, and risk factors

• More than 6.6 million people in United States
• Rapid rise in prevalence after age 65
• Mortality rate higher in African Americans than
Whites
• Ischemic heart disease leading risk factor
 Compensatory Mechanisms Activated in Heart
Failure
Mechanism Physiology Effect on Body Complications
Systems
Frank- • The greater •Increased •Increased
Starling the stretch of contractile myocardial
mechanism cardiac muscle force leading oxygen demand
fibers, the to increased •Limited by
greater the CO overstretching
force of
contraction.

Ventricular • Increased •Increased •Increased

hypertroph cardiac contractile myocardial
y workload force to oxygen demand
causes maintain CO •Cellular
myocardial enlargement
muscle to
hypertrophy
 Compensatory Mechanisms Activated in Heart
Failure
Mechanis Physiology Effect on Body Complications
m Systems
Neuro • Decreased CO • Increased HR, BP, • Tachycardia with
endocrin stimulates the and contractility decreased filling
e sympathetic • Increased vascular time and decreased
response nervous system resistance CO
and • Increased venous • Increased vascular
catecholamine return resistance
release. • Increased myocardial
workload and oxygen
demand

• Decreased CO • Vasoconstriction • Increased myocardial

and decreased and increased BP workload
renal perfusion • Renal
stimulate renin– vasoconstriction and
angiotensin decreased renal
system. perfusion

• Angiotensin • Salt and water • Increased preload

 Compensatory Mechanisms Activated in Heart
Failure

Mechani Physiology Effect on Body Complications

sm Systems
Neuro • ADH is released • Water excretion • Fluid retention
endocrine from posterior inhibited and increased
response pituitary. Atrial • Increased sodium preload and
natriuretic excretion afterload
factor is • Diuresis
released.

• Blood flow is • Decreased • Renal failure

redistributed to perfusion of other • Anaerobic
vital organs organ systems metabolism and
(heart and • Decreased lactic acidosis
brain). perfusion of skin
and muscles
American Heart Association Heart
Failure Stages
Stages Defining Physiology, Characteristics

A At high risk for HF but without structural heart

disease or symptoms of HF
B Structural heart disease but without signs or
symptoms of HF
C Structural heart disease with prior or current
symptoms of HF
D Refractory HF
 Classifications and Manifestations of Heart
Failure
• Systolic versus diastolic failure Acute Vs. Chronic HF
• Systolic when ventricle fails to Acute failure
eject a sufficient blood volume • is the abrupt onset of a myocardial injury
into arterial system (such as a massive MI) resulting in suddenly
• Diastolic when heart cannot decreased cardiac function and signs of
completely relax in diastole decreased cardiac output.

Chronic failure
• Left-sided versus right-sided failure • is a progressive deterioration of the heart
• Coronary heart disease, hypertension muscle due to cardiomyopathies, valvular
common causes of left-sided disease, or coronary heart disease (CHD).
• Orthopnea
• Conditions that restrict blood flow to
lungs often cause of right-sided
• Pulmonary disease
 Systolic versus Diastolic Failure
Systolic failure Diastolic failure

OCCURENCE occurs when the ventricle fails to contract Results when the heart cannot completely relax in
adequately to eject a sufficient blood diastole, disrupting normal filling. Passive diastolic
volume into the arterial system. filling decreases, increasing the importance of atrial
contraction to preload.

Effect Systolic function is affected by loss of Diastolic dysfunction results from decreased
myocardial cells due to ischemia and ventricular compliance due to hypertrophic and cellular
infarction, cardiomyopathy, or inflammation. changes and impaired relaxation of the heart muscle.

Manifestations decreased cardiac output: Weakness, result from increased pressure and congestion behind
: fatigue, and decreased exercise tolerance. the ventricle: Shortness of breath, tachypnea, and
. respiratory crackles if the left ventricle is affected;
distended neck veins, liver enlargement, anorexia,
and nausea if the right ventricle is affected.

• Many patients have components of both systolic and diastolic failure.

 Left-Sided versus Right-Sided
Failure
• Depending on the pathophysiology involved, either the left or the right ventricle may be
primarily affected.
• In chronic heart failure, however, both ventricles are typically impaired to some degree.

Left-sided heart failure

Right-sided heart failure
• Coronary heart disease and hypertension are common
causes of left-sided heart failure • often caused by conditions that restrict
blood flow to the lungs, such as acute or
• can also lead to right-sided failure as pressures in the
chronic pulmonary disease.
pulmonary vascular system increase with congestion
behind the failing left ventricle. •
 Left-Sided versus Right-Sided Failure
• As left-ventricular function fails, cardiac
output falls.
• Pressures in the left ventricle and atrium
increase as the amount of blood remaining
in the ventricle after systole increases.
• These increased pressures impair filling,
causing congestion and increased pressures
in the pulmonary vascular system.
• Increased pressures in this normally low-
pressure system increase fluid movement
from the blood vessels into interstitial
tissues and the alveoli
Figure 31.1 The hemodynamic Figure 31.2 The hemodynamic
effects of Right-sided heart failure. effects of left - sided heart failure.
Manifestations :
Right-sided heart failure
Left-sided heart failure
• result from pulmonary congestion (backward effects)
• increased pressures in the pulmonary and decreased cardiac output (forward effects).
vasculature or right-ventricular muscle • Fatigue and activity intolerance (common early
damage impair the right ventricle’s ability manifestations).
to pump blood into the pulmonary
circulation. • Dizziness and syncope also may result from decreased
cardiac output.
• The right ventricle and atrium become
distended, and blood accumulates in the • Pulmonary congestion causes dyspnea, shortness of
systemic venous system. breath, and a cough.
• Increased venous pressures cause • orthopnea
abdominal organs to become congested • Cyanosis from impaired gas exchange
and peripheral tissue edema to develop.
• On auscultation of the lungs, inspiratory crackles
(rales) and wheezes may be heard in lung bases.
• An S3 gallop may be present, reflecting the heart’s
attempts to fill an already distended ventricle.
Diagnosis of Heart Failure
• Atrial natriuretic factor (A N F) and Brain natriuretic peptide
(B N P)
• Serum electrolytes
• Urinalysis
• Liver function tests
• Thyroid function tests
• Arterial blood gases (A B G s)
• Chest x-ray
• Electrocardiography
• Echocardiography with Doppler flow studies
• Radionuclide imaging
 Interprofessional Care of the Patient with Heart
Failure

Hemodynamic monitoring

• Is the study of forces involved in blood circulation.

• used to assess cardiovascular function in patients who are critically ill or
unstable.
• Main goals: to evaluate cardiac and circulatory function and the response to
interventions.
• Intra-arterial pressure monitoring: commonly used in intensive and
coronary care units.
• Venous pressure monitoring: Central venous pressure (CVP) and right
atrial pressure (RAP) are measures of blood volume and venous return.
They also reflect right heart filling pressures.
• Pulmonary artery pressure monitoring: The PA catheter is used to
evaluate left-ventricular and overall cardiac function
 • Hemodynamic
Figure 31.3 parameters
• Heart rate
• Arterial blood
pressure
• Central venous
or right atrial
pressure
• Pulmonary
pressure
• Cardiac output

A hemodynamic monitoring setup.

 Figure 31.4

Inflation of the balloon on the flow-directed catheter allows it to be carried through the
pulmonic valve into the pulmonary artery.
Nursing Care of the Patient with Heart
Failure
• Diagnoses, outcomes, and interventions
• Decreased Cardiac Output
• Excess Fluid Volume
• Activity Intolerance
• Deficient Knowledge: Low-Sodium Diet
 Interprofessional Care-
Medications

• Medications
• A C E inhibitors
• Angiotensin receptor blockers
• Beta blockers
• Diuretics
• Inotropic medications: Digitalis improves myocardial contractility by
interfering with ATPase in the myocardial cell membrane and
increasing the amount of calcium available for contraction.
• Direct vasodilators
• Antidysrhythmic drugs
Interprofessional Care-Treatment
• Nutrition and activity
• Sodium-restricted diet
• Exercise to reduce intolerance
• Continuity of care
• Active participation by patient, family
• Provide referrals
• Other treatments
• Circulatory assistance
• Cardiac transplantation
• Other procedures
• Cardiomyoplasty
• Ventricular reduction surgery
Nursing Care: Monitoring Cardiac Output

• Monitor vital signs and oxygen saturation as indicated.

• Auscultate heart and breath sounds regularly
• Administer : supplemental oxygen as needed and prescribed medications as
ordered.
• Encourage rest, explaining the rationale.
• Elevate the head of the bed to reduce the work of breathing.
• Provide a bedside commode, and assist with ADLs. Instruct to avoid the
Valsalva maneuver. These measures reduce cardiac workload.

• SAFETY ALERT:
• Report manifestations of decreased cardiac output and tissue perfusion: Changes in
mentation; decreased urine output; cool, clammy skin; diminished pulses; pallor or
cyanosis; or dysrhythmias. These are manifestations of decreased tissue perfusion to organ
systems.
Nursing Care: Monitoring
Fluid volume

• Assess respiratory status and auscultate lung sounds at least every 4

hours. Notify the physician of significant changes in condition.
Declining respiratory status indicates worsening left heart failure.
• Monitor intake and output. Notify the physician if urine output is <
30 mL/h. Weigh daily.
• Record abdominal girth every shift. Note complaints of a loss of
appetite, abdominal discomfort, or nausea. Venous congestion can
lead to ascites
• Restrict fluids as ordered.
 Nursing Care: Promoting Low-
Sodium Diet.
• Discuss the rationale for sodium restrictions. Understanding fosters compliance
with the prescribed diet.
• Consult with dietitian to plan and teach a low-sodium and, if necessary for weight
control, low-kilocalorie diet. Provide a list of high-sodium, high-fat, high-cholesterol
foods to avoid.
• Teach how to read food labels for nutritional information.
• Assist the patient to construct a 2-day meal plan choosing foods low in sodium. This
allows for learning assessment, clarification of misunderstandings, and
reinforcement of teaching.
• Encourage small, frequent meals rather than three heavy meals per day. Small,
frequent meals provide continuing energy resources and decrease the work
required to digest a large meal.
 Nursing Care: Promoting Balance Activity and
Rest
• Organize nursing care to allow rest periods. Grouping activities together allows
adequate time to rest and recharge.
• Assist with ADLs as needed. Assisting with ADLs helps ensure that care needs
are met while reducing cardiac workload
• Encourage independence within prescribed limits.. Involving the patient
promotes a sense of control and reduces helplessness.
• Plan and implement progressive activities. Progressive activity slowly increases
exercise capacity by strengthening and improving cardiac function without
strain. . Activity also helps prevent skeletal muscle atrophy.
 Balance Activity and Rest (cont..)
• Use passive and active ROM exercises as appropriate. ROM exercises
prevent complications of immobility in severely compromised patients.
• Consult with physical therapist on activity plan
• Provide written and verbal information about activity after discharge.
Written information provides a reference for important information. Verbal
information allows for clarification and validation of the material.
Complications of Heart Failure
• Congestive hepatomegaly
• Splenomegaly
• Impaired liver function
• Myocardial distention
• Cardiogenic shock
• Acute pulmonary edema

End-of-life care
• Honest discussion with family about anticipated course of
disease
• Discuss advance directives
• Severe dyspnea common