4. Pneumothorax, COPD, CVDs.pdf cardiovascular system

Introduction
 Pneumothorax is an accumulation of air in the
pleural cavity that leads to partial or complete lung
collapse.
 The air buildup puts pressure on the lung(s),
preventing its normal expansion.
 The amount of air trapped in the intrapleural space
determines the degree of lung collapse.
 It occurs when the parietal or visceral pleura is
breached and the pleural space is exposed to
positive atmospheric pressure.

Introduction
 In some cases, venous return to the heart is
impeded causing a life-threatening condition called
tension pneumothorax.
 A spontaneous pneumothorax occurs with the
rupture of a bleb.
 An open pneumothorax occurs when an
opening through the chest wall allows the entrance
of positive atmospheric pressure into the pleural
space.

Classification
 Pneumothorax can be classified as traumatic or
spontaneous and tension.
 Spontaneous/simple pneumothorax occurs
when air enters the pleural space through
a breach of either the parietal or visceral pleura.
 Traumatic pneumothorax occurs when air
escapes from a laceration in the lung itself and
enters the pleural space or from a wound in the
chest wall.
 Traumatic pneumothorax may be further classified
as open or closed.

Classification
 Tension pneumothorax occurs when air is
drawn into the pleural space from a lacerated
lung or through a small opening or wound in
the chest wall.

Etiology
 Traumatic pneumothorax may be open
or closed.
 Causes of open pneumothorax include:
◦ Penetrating chest injury (stab or gunshot
wound)
◦ Insertion of a central venous catheter
◦ Thoracentesis or closed pleural biopsy
◦ Transbronchial biopsy
◦ Chest surgery.
6

Etiology
 Causes of closed traumatic pneumothorax include:
◦ Blunt chest trauma
◦ Interstitial lung disease such as eosinophilic
granuloma
◦ Tubercular or cancerous lesions that erode into
the pleural space
◦ Air leakage from ruptured blebs
◦ Rupture resulting from barotrauma caused by
high intrathoracic pressures during mechanical
ventilation.
7

Etiology
 Spontaneous pneumothorax is usually caused by
the rupture of a subpleural bleb (a small cystic
space) at the surface of a lung.
 Risk factors for spontaneous pneumothorax
include cigarette smoking, familial history, mitral
valve disease and changes in atmospheric
pressure.
8

Etiology
 Causes of tension pneumothorax include:
◦ Penetrating chest wound treated with an
airtight dressing
◦ Fractured ribs
◦ Mechanical ventilation
◦ Chest tube occlusion or malfunction
◦ High-level PEEP that causes alveolar blebs
to rupture.
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Pathophysiology
Traumatic pneumothorax
 Open pneumothorax results from atmospheric
air flowing directly into the pleural cavity (under
negative pressure) due to a breach in the chest
wall.
 As the air pressure in the pleural cavity becomes
positive, the lung on the affected side collapses,
causing decreased total lung capacity.
 As a result, the patient develops aV/Q imbalance
that leads to hypoxia.

Pathophysiology
Traumatic pneumothorax
 Closed pneumothorax results when an opening is
created between the intrapleural space and the
parenchyma of the lung.
 Could be from laceration of the lung tissue
 Air enters the pleural space from within the lung,
causing increased pleural pressure and preventing
lung expansion during inspiration.
 The affected lung collapses leading to a decreased
total lung capacity.
 The patient develops a ventilation-perfusion
mismatch leading to hypoxia.

Pathophysiology
Spontaneous pneumothorax
 The rupture of a subpleural bleb
causes air leakage into the pleural
spaces, which causes the lung to
collapse.
 Hypoxia results from decreased total
lung capacity, vital capacity and lung
compliance.
12

Pathophysiology
Tension pneumothorax
 It results when air in the pleural space is under
higher pressure than air in the adjacent lung.
 Air enters the pleural space from the site of
pleural rupture, which acts as a one-way valve.
 Thus, air enters the pleural space on inspiration
but can’t escape as the rupture site closes on
expiration.
 More air enters with each inspiration and air
pressure begins to exceed barometric pressure.
13

Pathophysiology
Tension pneumothorax
 The air pushes against the recoiled lung, causing
compression atelectasis and pushes against the
mediastinum, compressing and displacing the
heart and great vessels.
 The mediastinum eventually shifts away from the
affected side, affecting venous return and putting
ever greater pressure on the heart, great vessels,
trachea, and contralateral lung.
 Without immediate treatment, this emergency
can rapidly become fatal. 14

Clinical Manifestations
 Presence of sudden, sharp, unilateral
pleuritic chest pain.
 Chest movement, breathing and coughing
exacerbate the pain.
 Shortness of breath.
 Decreased chest expansion
 The skin may be cool, clammy and cyanotic.
 Crackling beneath the skin of the chest wall
(subcutaneous emphysema) and decreased
vocal fremitus.

 Hyperresonance on percussion of the
affected side.
 Decreased or absent breath sounds on the
affected side.
 Respiratory distress
 Tension pneumothorax also causes:
distended jugular veins; mediastinal shift
and increased cardiovascular pressure;
hypotension and tachycardia due to
decreased CO; tracheal deviation to the
opposite side (a late sign).

Diagnostic Evaluation
 Chest X-rays reveal air in the pleural
space and a mediastinal shift of
structures, which confirm
pneumothorax.
 Thoracic CT Scan is more sensitive than
x-ray in detecting thoracic injuries, lung
contusion, hemothorax, and
pneumothorax
 ABG analysis PaCO2 is elevated;
PaO2 may be normal or decreased;
oxygen saturation are decreased.

 Thoracentesis reveal presence of
blood/serosanguineous fluid indicates
hemothorax.
 Hemoglobin maybe decreased, indicating
blood loss
 Electrocardiogram-ECG changes expected.

Medical management
 A small chest tube is inserted near the
second intercostal space to drain the fluid and
air.
 It helps to achieve lung re-expansion.
 Maintain a closed chest drainage system.
 Antibiotics for prophylaxis against infections
from contamination.
 Oxygen therapy – those with possible tension
pneumothorax should immediately be given a
high concentration of supplemental oxygen to
treat the hypoxemia.

Surgical Management
 If more than 1500 ml of blood is aspirated
initially by thoracentesis, the rule is to open
the chest wall surgically.
 Thoracotomy.The chest wall is opened
surgically to remove the blood or air trapped
in the pleural space.

Nursing Management
Nursing Assessment
 Tracheal alignment.
 Expansion of the chest.
 Breath sounds.
 Percussion of the chest.

Nursing Diagnosis
 Ineffective breathing pattern related to
respiratory distress.
 Ineffective peripheral tissue perfusion
related to severe hypoxemia.
 Acute pain related to the positive pressure
in the pleural space.
 Anxiety related to difficulty in breathing.

Nursing Care Planning
The goals for the patient include:
 Relief of pain
 Adherence to the prescribed pharmacological
regimen.
 Establishment of a normal, effective
respiratory pattern as evidenced by the
absence of cyanosis.
 Demonstration of increase in perfusion.
 Be relaxed and report reduced anxiety

Nursing Interventions
 Re-expansion – instruct the patient to inhale
and strain against a closed glottis to
reexpand the lung and eject the air from the
thorax.
 Trauma site/opening is plugged by sealing it
with sterile gauze
 Maintain bed rest in high Fowler position.
 Monitor oxygen saturation levels closely for
changes; obtain ABG analysis as ordered.
 Administer O2 to maintain saturations
at >93%

 Reassurance—chest pain and breathlessness
can be very frightening.
 Assess the patient’s respiratory status,
including auscultation of bilateral breath
sounds.
 Assist with chest tube insertion (care of a
patient with chest tube insertion and under
water seal drainage system).
 Cardiac monitoring since hypoxemia can
predispose the patient to arrhythmias.

 Monitor for complications signaled by pallor,
gasping respirations and sudden chest pain.
 Monitor vital signs at least every hour for
indications of shock, increasing respiratory
distress or mediastinal shift.
 Prepare for ET intubation and mechanical
ventilation if the respiratory status
deteriorates

Nursing Evaluation
Expected patient outcomes include:
 Pain is relieved.
 Adhered to prescribed pharmacological
regimen.
 Established a normal, effective respiratory
pattern as evidenced by absence of cyanosis.
 Demonstrated increase in perfusion.
 Patient is relaxed and reported anxiety is
reduced to a manageable level.

Chronic Obstructive Pulmonary
Disease (COPD)
 It is a condition of chronic dyspnea with
expiratory airflow limitation.
 The Global Initiative for Chronic Obstructive
Lung Disease defines it as “a preventable and
treatable disease with some significant extra-
pulmonary effects that may contribute to the
severity in individual patients. It is
characterized by airflow limitation that is not
fully reversible.

Introduction
 The airflow limitation is usually progressive
and associated with an abnormal
inflammatory response of the lung to noxious
particles or gases”
 There are two classifications of COPD:
chronic bronchitis and emphysema.

Chronic Bronchitis
 Chronic bronchitis is a disease of the airways
and is defined as the presence of cough
and sputum production for at least 3
months in each of 2 consecutive years.
 Pollutants or allergens irritate the airways
and leads to the production of sputum by the
mucus-secreting glands and goblet cells.
 A wide range of viral, bacterial, and
mycoplasmal infections can produce acute
episodes of bronchitis.

Emphysema
 Pulmonary Emphysema is the abnormal
distention of airspaces beyond the
terminal bronchioles and destruction of the
walls of the alveoli.
 There is impaired carbon dioxide and oxygen
exchange resulting from the destruction of the
walls of overdistended alveoli.
 There are two main types of emphysema:
panlobular and centrilobular.
◦ In panlobular, there is destruction of the respiratory
bronchiole, alveolar duct, and alveolus.
◦ In centrilobular, the pathologic changes occur in the
lobule, whereas the peripheral portions of the acinus
are preserved

Causes
 Smoking depresses the activity of scavenger cells
and affects the respiratory tract’s ciliary cleansing
mechanism.
 Prolonged and intense exposure to occupational
dust and chemicals, indoor air pollution, and
outdoor air pollution all contribute to the
development of COPD.
 The genetic risk factor is a deficiency of alpha1-
antitrypsin, an enzyme inhibitor that protects the
lung parenchyma from injury

Pathophysiology
 In COPD, the airflow limitation is both progressive
and associated with an abnormal inflammatory
response of the lungs to noxious gases or particles.
 An inflammatory response occurs throughout the
proximal and peripheral airways, lung parenchyma,
and pulmonary vasculature.
 Due to the chronic inflammation, changes and
narrowing occur in the airways.
 There is an increase in the number of goblet cells
and enlarged submucosal glands leading to
hypersecretion of mucus.

Pathophysiology
 Over a period of time, the ongoing injury-and-repair
process causes scar tissue formation and narrowing
of the airway lumen.
 Inflammatory and structural changes also occur in
the lung parenchyma.
 Alveolar wall destruction leads to loss of alveolar
attachments and a decrease in elastic recoil.
 The chronic inflammatory process affects the
pulmonary vasculature and causes thickening of the
lining of the vessel and hypertrophy of smooth
muscle, which may lead to pulmonary hypertension.

 Chronic cough is one of the primary symptoms of
COPD.
 There is a hyperstimulation of the goblet cells and
the mucus-secreting gland leading to
overproduction of sputum.
 Dyspnea on exertion is usually progressive,
persistent, and worsens with exercise.
 As COPD progress, dyspnea at rest may occur.
 Weight loss as dyspnea interferes with eating and
the work of breathing is energy depleting.
 Barrel chest.

Prevention
 Smoking cessation is the single most cost-
effective intervention to reduce the risk of
developing COPD and to stop its progression.
 Healthcare providers should promote cessation by
explaining the risks of smoking and personalizing the
“at-risk” message to the patient.

Complications
 Respiratory failure - the acuity and the onset of
respiratory failure depend on baseline pulmonary
function, pulse oximetry or arterial blood gas
values, comorbid conditions, and the severity of
other complications of COPD.
 Respiratory insufficiency can be acute or chronic,
and may necessitate ventilator support until other
acute complications can be treated.

Assessment and Diagnostic
Findings
 Health history – the nurse should obtain a
thorough health history from patients with
known or potential COPD.
 Pulmonary function studies are used to help
confirm the diagnosis of COPD, determine
disease severity, and monitor disease
progression.
 Spirometry is used to evaluate airway
obstruction, which is determined by the ratio
of FEV1 to forced vital capacity.
 Arterial blood gas measurement is used to
assess baseline oxygenation and gas exchange
and is especially important in advanced COPD.

Findings
 Chest x-ray: May reveal hyperinflation of
lungs, flattened diaphragm, increased
retrosternal air space, decreased vascular
markings/bullae (emphysema), increased
bronchovascular markings (bronchitis)
 Sputum culture identifies pathogen.
 Electrocardiogram in case of arrhythmias
 Exercise ECG, stress test to assess the
degree of pulmonary dysfunction, evaluating
effectiveness of bronchodilator therapy,
planning/evaluating exercise program.

Findings
 Bronchogram: Can show cylindrical dilation of
bronchi on inspiration; bronchial collapse on
forced expiration (emphysema); enlarged
mucous ducts (bronchitis).
 Complete blood count and
differential: Increased hemoglobin (advanced
emphysema).
 Blood chemistry to screen for alpha1-
antitrypsin is measured to verify deficiency
and diagnosis of primary emphysema in
patients younger than 45 years old and for
those with a strong family history of COPD

Medical Management
PharmacologicTherapy
 Bronchodilators to relieve bronchospasm by
altering the smooth muscle tone and reduce
airway obstruction by allowing increased oxygen
distribution throughout the lungs and improving
alveolar ventilation through inhalers & nebulizers
 Corticosteroids - a short trial course of oral
corticosteroids to improve pulmonary function
improves and decrease symptoms.
 Other medications include alpha1-antitrypsin
augmentation therapy, antibiotic agents, mucolytic
agents, antitussive agents, vasodilators.

Medical Management
 Hospitalization for acute exacerbation of
COPD include severe dyspnea that does not
respond to initial therapy, confusion or
lethargy, respiratory muscle fatigue, paradoxical
chest wall movement, and peripheral edema.
 Supplemental oxygen therapy is administered
and rapid assessment is performed to
determine if the exacerbation is life-
threatening.
 Antibiotics have benefited patients with
increased dyspnea, increased sputum
production, and increased sputum purulence.

Surgical Management
 Bullectomy for patients with bullous
emphysema and can help reduce dyspnea and
improve lung function.
 Lung transplantation is a viable option for
definitive surgical treatment of end-stage
emphysema.

Nursing Assessment
 Assessment of the respiratory system should
be done rapidly yet accurately.
 Assess patient’s exposure to risk factors.
 Assess the patient’s past and present medical
history.
 Assess the signs and symptoms of COPD and
their severity.
 Assess the patient’s knowledge of the disease.
 Assess the patient’s vital signs.
 Assess breath sounds and pattern.

Nursing Diagnosis
 Impaired gaseous exchange due to chronic
inhalation of toxins.
 Ineffective airway clearance related to
bronchoconstriction, increased mucus
production, ineffective cough, and other
complications.
 Ineffective breathing pattern related to
shortness of breath, mucus,
bronchoconstriction, and airway irritants.
 Self-care deficit related to fatigue.
 Decreased activity tolerance related to
hypoxemia

Nursing Planning & Goals
Goals to achieve in patients with COPD include:
 Improvement in gas exchange.
 Achievement of airway clearance.
 Improvement in breathing pattern.
 Independence in self-care activities.
 Improvement in activity tolerance
 Ventilation/oxygenation adequate to meet self-
care needs.
 Nutritional intake meeting caloric needs.
 Infection treated/prevented.
 Disease process/prognosis and therapeutic
regimen understood.

Nursing Priorities
 Maintain airway patency.
 Assist with measures to facilitate gas
exchange.
 Enhance nutritional intake.
 Prevent complications, slow progression of
condition.
 Provide information about disease
process/prognosis and treatment regimen.

 Patient and family teaching is an important nursing
intervention to enhance self-management in
patients with any chronic pulmonary disorder.
 Reassurance of patient and family
 Nurse the patient in an upright position.
 Administer bronchodilators through nebulization
(may need to be continuous) and IV theophylline
(for patients who do not respond to nebulizers)
 Administer corticosteroids as prescribed and
become alert for potential side effects.
 The nurse instructs the patient on direct or
controlled coughing, which is more effective and
reduces fatigue associated with undirected forceful
coughing.

 Instruct patient on inspiratory muscle training to help improve
the breathing pattern.
 Instruct patient on diaphragmatic breathing reduces respiratory
rate, increases alveolar ventilation, and sometimes helps expel
as much air as possible during expiration.
 Instruct patient on pursed lip breathing helps slow expiration,
prevents collapse of small airways, and control the rate and
depth of respiration.
 Schedule daily activities to allow for rest periods throughout
the day and support devices can be also used to decrease
energy expenditure.
 Exercise training can help strengthen muscles of the upper and
lower extremities and improve exercise tolerance and
endurance.
 Use of walking aids may be recommended to improve activity
levels and ambulation

 Mouth care
 IV fluids administration if the patient is dehydrated.
 Administer analgesics as prescribed
 The nurse should monitor for cognitive changes
such as personality and behavior changes
and memory impairment.
 Pulse oximetry values are used to assess the
patient’s need for oxygen and administer
supplemental O2 therapy to keep saturations in the
range of 88–92%
 The nurse should encourage the patient to be
immunized against influenza and S. pneumonia
because the patient at risk for respiratory infection.

Nursing Evaluation
The patient:
 Identifies the hazards of cigarette smoking.
 Identifies resources for smoking cessation.
 Enrolls in smoking cessation program.
 Minimizes or eliminates exposures.
 Verbalizes the need for fluids.
 Is free of infection.
 Practices breathing techniques.
 Performs activities with less shortness of
breath.

Introduction
 Review anatomy and physiology of the
heart and heart layers; pericardium;
heart chambers; heart valves;
atrioventricular node; the bundle of
His; purkinje fibers; sinoatrial node;
coronary arteries; heart sounds; heart
rate and autonomic nervous system
 Blood pressure control
 The vascular system

Introduction
 The WHO estimates that CVDs are the
number one cause of death globally.
 In Kenya, it is estimated that 25% of
hospital admissions are due to CVD and
13% of autopsies revealed CVDs as cause
of death
 The CVDs are costly to diagnose and
manage leading to premature death
among the most productive individuals in
the household and the society.

Introduction
 Majority of CVDs are preventable with
control of risk factors, early detection and
prompt management.
 Hypertension is the single most important
risk factor for CVDs.
 A small proportion of the population are
born with conditions that predispose them
to CVDs, while the majority who develop
them do so because of a combination of
modifiable and non-modifiable risk factors

Modifiable risk factors
 Tobacco use and exposure to tobacco
smoke
 Unhealthy diet
 Overweight/ obesity
 Physical inactivity
 Harmful use of alcohol
 Hypertension
 Diabetes and hyperlipidemia
 Infections e.g. Rheumatic fever/heart
disease

Non-modifiable risk factors
 Gender
 Age
 Race,
 Family history

Prevention
 Early detection, appropriate screening and
surveillance, vaccination.
 Lifestyle modification e.g. cessation of
tobacco and alcohol use, consumption of
healthy diet low in saturated fat, salt and
refined sugars and high in fruits and
vegetables
 Providing appropriate treatment and care,
support groups, medication adherence

Prevention
 Rehabilitation and palliative care at the
various stages of the disease pathway.
Revascularization i.e. coronary bypass
surgery

Cardiovascular conditions
 Cardiovascular conditions are a common
presentation in health facilities and the
number of deaths from heart disease
remains high.
 Any patient presenting with chest pain that
appears to have a cardiac origin should have
an ECG recorded without delay to ensure
that a cardiac cause is either identified in a
timely way or ruled out.

 Typically, patients with chest pain of cardiac
origin present with anterior wall pressure/
discomfort, which can radiate to the left or
right arm and shoulder/neck and be
associated with nausea and vomiting.
 Patients can also complain of epigastric pain
and pain between the shoulder blades.
 Nurses need to be mindful that patients
who are having a cardiac event may also
present with atypical symptoms.

 The atypical symptoms include nausea and
vomiting, shortness of breath or generally
feeling unwell.
 Equally, patients presenting with a cardiac
event may complain of pain in the left side of
the neck, jaw, shoulder, or arm but no chest
pain.
 Failure to recognize a cardiac cause may
result in possible treatment delay.

 Cardiac problems are very frightening for
the patient and family with a high mortality.
 Nurses need to demonstrate not only
competence and speed, but also empathy
and understanding, when caring for this
group.

Assessment of the cardiovascular
system
Use a systematic approach— follow ABCDE.
 A. Ensure a patent airway. If at risk, call for
help immediately.
 B. Record the respiratory rate, rhythm, and
depth. Note the use of accessory muscles
and abnormal noises. Record SpO2, and
administer O2 therapy as indicated— aim at
achieving SaO2 >94% or 88– 92% if the
patient has COPD.

Assessment of cardiovascular
system
 C. Record the BP; attach to a cardiac
monitor and manually record the pulse.
Obtain a 12- lead ECG promptly.
 D.Assess the conscious status— consider
GCS. Note any limb weakness or altered
sensation.
 E.Assess any exposures and ensure the
patient is undressed to enable a full
assessment (remember to keep the patient
warm).
Record the temperature.

system
 Do not forget to record the blood sugar and
correct any abnormality.
 Obtain an ‘AMPLE’ at the same time as
assessing the patient:
 Allergies; Medications - prescribed/over- the-
counter/ herbal/ supplements
 Past (relevant) medical history; Last meal
 Events leading up to admission; duration of
pain.

system
 Assess pain using ‘PQRST’.
 Provokes - what causes the pain/makes it
better or worse?
 Quality - what does it feel like e.g. sharp/
dull?
 Radiates - does it radiate/ is it only in one
place/ did it start in one place and then
move location?

system
 Severity - how severe on a scale of 0 (no
pain) to 10 (worst pain ever)?
 Time - onset and how long did it last/ when
was it at its worst?

Coronary Artery Disease (CAD)
 Ischaemic heart disease (IHD), also known as
coronary heart disease/coronary artery
disease.
 It is a progressive myocardial dysfunction
characterized by occlusion of one or more
coronary arteries by cholesterol plaque that
decreases blood flow to the heart muscle.
 CAD results from atherosclerosis.
 Atherosclerosis is an accumulation of fatty
plaques (made of cholesterol) and lipids on the
inside walls of the arteries

Coronary artery disease
 Restriction of blood flow deprives the heart
muscle of oxygen and nutrients causing tissue
damage
 Chest pain occurs when the demand for
oxygen by the heart muscle is greater than can
be delivered by the blood vessels.
 CAD can present itself as angina pectoris or as
myocardial infarction (MI).
 CAD leads to hypertension, angina,
dysrhythmias, MI, heart failure and death

Coronary artery disease
 Symptoms occur when the coronary artery is
occluded to the point that inadequate blood
supply to the muscle occurs, causing ischemia.
 Coronary artery narrowing is significant if the
lumen diameter of the left main artery is reduced
at least 50% or if any major branch is reduced at
least 75%
 The goal of treatment is to alter the
atherosclerotic progression

Risk factors of atherosclerosis
 Family history
 Gender and age: males aged 35-55, females >50
or postmenopausal
 Hyperlipidemia
 Hypertension
 Diabetes
 Cigarette smoking
 Personality traits e.g. anger, aggression,
competitiveness
 In premenopausal females: severe hypertension,
use of estrogen oral contraceptives, smoking
history

Clinical manifestations
 Possibly normal findings during
asymptomatic periods
 Chest pain
 Palpitations
 Dyspnoea
 Syncope
 Cough or hemoptysis
 Excessive fatigue

 Electrocardiogram – will show a depressed
ST segment orT wave when blood flow is
reduced and ischemia occurs
 In patients with chest pain the ECG should
be performed within 10 minutes of
presentation.
 Blood for cardiac troponin should be drawn
immediately after the ECG. A rise in
troponin suggests a coronary cause of chest
pain.

Medical management
 Pain should be managed with morphine or
morphine derivatives e.g. fentanyl. Dosage
Morphine – 2.5-5mg IV or SC; Fentanyl 25mcg -
100mcg IV
 For patients with respiratory distress, these
drugs can cause respiratory failure and airway
support should be available
 Nitrates to dilate the coronary arteries
 Calcium channel blockers to dilate the coronary
arteries and reduce vasospasms
 Cholesterol-lowering medications to reduce the
development of atherosclerotic plaques

Surgical management
 Percutaneous transluminal coronary angioplasty
(PTCA) to compress the plaque against the walls
of the artery and dilate the vessel
 Laser angioplasty to vaporize the plaque
 Stenting - vascular stent to prevent the artery
from closing
 Coronary artery bypass graft to improve blood
flow to the myocardial tissue that is at risk for
ischemia or infarction because of occluded
artery.

Nursing management
 Assist the client to identify risk factors that can be
modified to reduce their impact
 Stress the importance of not smoking or using
tobacco products. Nicotine causes heart to work
faster, constrict blood vessels, decrease amount of
oxygen delivered to the heart
 Discuss the role stress plays in increasing CAD.
Needs to deal with feelings of denial, anger and
depresison.
 Discuss benefits of exercises- improves
cardivascular status, decreases HDLipoproteins
which lowers BP, weight loss

Nursing management
 Promote physical activity - 30 minutes of moderate
intensity aerobic exercise atleast 5times/week.
 Dietary advise – promote low calorie, low sodium,
low cholesterol, low fat diet with an increase in
dietary fiber. Restrict table salt and sodium intake.
 Lipids – aim for LDL <2mmol/L
 Control blood pressure control – aim for BP <
130/85mmHg. Use ACEI/ARB and beta blockers
particularly in patients with impaired LV dysfunction.
Other anti-hypertensives may be utilized to optimize
BP.

Nursing management
 Diabetes control – aim for HBA1c<7.1%
 Promote compliance with the medications
 Instruct them on the importance of controlling
weight to normal BMI (18.5-24.9)
 Administer anti-platelets e.g. aspirin for prophylaxis.
Those intolerant to aspirin should be given
clopidogrel
 Patient should be connected to ECG monitors
immediately on arrival to the health facility

Nursing management
 Oxygen therapy should be considered to those
patients with saturation of less than 92% at room.
 Connect them to ECG monitor and vitals assessed
every 15 minutes.
 There should be resuscitation trolley and teams
ready to manage the patients

Angina pectoris
 Angina pectoris or chest pain, caused by myocardial
ischemia is not a separate disease, but rather a
symptom of coronary artery disease (CAD).
 It is caused by a blockage or spasm of a coronary
artery, leading to a diminished myocardial blood
supply.
 The lack of oxygen causes myocardial ischemia, which
is felt as chest discomfort, pressure, or pain.
 Angina may occur anywhere in the chest, neck, arms,
or back, but the most commonly described location is
pain or pressure behind the sternum.
 The pain often radiates to the left arm but can also
radiate down both arms and to the back, shoulder, jaw,
or neck.

Classification
 Stable angina is chest pain that is consistent and
predictable that occurs on exertion. It is relieved by
rest and/or nitroglycerin.This type of angina is
associated with stable plaque build-up in the coronary
arteries.
 Unstable angina is pain that occurs more often and in
unpredictable patterns. It may not be relieved with rest
or nitroglycerin and often causes the client to limit their
activity.
 Variant or Prinzmetal’s angina is a less common form of
angina. It is characterized by episodes of chest pain that
occur at rest.Thought to be caused by coronary artery
vasospasms, which can cause an increase in myocardial
oxygen demand and a transient ST-segment elevation.
 Intractable or refractory angina is severe incapacitating
chest pain.

Causes
 Physical exertion precipitates an attack by
increasing myocardial oxygen demand.
 Exposure to cold can cause vasoconstriction
and elevated BP, with increased oxygen
demand.
 Eating a heavy meal increases the blood flow
to the mesenteric area for digestion, thereby
reducing the blood supply available to the
myocardium.
 Stress causes the release of catecholamines,
which increased blood pressure, HR and
myocardial workload.

Pathophysiology
 Angina is usually caused obstruction of coronary
blood flow because of atherosclerosis, coronary
artery spasm and conditions increasing myocardial
oxygen consumption
 Normally, the myocardium utilizes large amounts of
oxygen from the coronary circulation to meet its
continuous demands.
 When there is an increase in demand e.g. exertion
or emotion, blood flow through the coronary
arteries needs to be increased.
 When there is blockage in a coronary artery, flow
cannot be increased, and myocardial ischemia caused
by inadequate myocardial blood and oxygen supply
results.This leads to necrosis or MI

 Pain
◦ Can develop slowly or quickly
◦ Pain is usually described as mild or moderate
◦ Substernal, crushing, squeezing pain may occur
◦ Pain may radiate to the shoulders, arms, jaw, neck and
back
◦ Pain usually lasts less than 5 minutes, however the pain
can last upto 15-20 minutes
◦ The pain is relieved by nitroglycerine or rest
 Hypertension
 A feeling of numbness in the arms, wrists and hands.
 Shortness of breath due to increase in oxygen demand
 Pallor due to inadequate blood supply to peripheral
tissues
 Others include sweating, palpitations and tachycardia,
dizziness

Complications
 Myocardial infarction is the end result of
angina pectoris if left untreated.
 Cardiac arrest - the heart pumps more and
more blood to compensate the decreased
oxygen supply, and the cardiac muscles
would ultimately fail leading to cardiac
arrest.
 Cardiogenic shock-MI also predisposes the
patient to cardiogenic shock

Findings
 Electrocardiogram – Depression of the ST segment
or T wave inversion signifies ischemia.
 Cardiac enzymes - elevation indicates myocardial
damage.
 Serum lipids - may be elevated (CAD risk factor).
 Cardiac catheterization is the most definitive means
of diagnosis as it will provide information about the
patency of the coronary arteries

Medical management
The goal of treatment is to provide relief of an acute attack,
correct the imbalance between myocardial oxygen supply and
demand, prevent the progression of the disease and further
attacks to reduce the risk of MI.
 Assess the pain
 Pain should be managed with morphine or morphine
derivatives e.g. fentanyl. Dosage Morphine: 2.5-5mg IV or SC;
Fentanyl 25mcg -100mcg IV
 Provide bed rest
 Oxygen therapy is usually initiated at the onset of chest pain
in an attempt to increase the amount of oxygen delivered to
the myocardium and reduce pain.

Medical management
 Nitrates e.g. nitroglycerin reduces the oxygen requirements
of the myocardium and relieve chest pain through
vasodilation within 3 minutes.
 Antiplatelets e.g.Aspirin 300mg orally stat; Clopidogrel
300mg stat to prevent platelet aggregation
 Anticoagulants e.g. Enoxaparin 1mg/kg SC stat to reduce the
risk of clot formation
 Beta blockers to decrease heart rate, BP and force of
contraction of the heart muscle and prevent cardiac
arrhythmias
 Calcium channel blockers e.g. nifedipine to dilate the
coronary arteries and reduce vasospasms, also have negative
inotropic effects.
 Cholesterol-lowering medications to reduce the
development of atherosclerotic plaques

Surgical management
 Percutaneous transluminal coronary
angioplasty (PTCA) to compress the
plaque against the walls of the artery and
dilate the vessel
 Laser angioplasty to vaporize the plaque
 Stenting - vascular stent to prevent the
artery from closing
 Coronary artery bypass graft to improve
blood flow to the myocardial tissue that
is at risk for ischemia or infarction
because of occluded artery.

Nursing Management
Nursing Assessment
Assess for the following subjective and objective data:
 Reports of pain varying in frequency, duration and intensity
(especially as the condition worsens)
 Narrowed focus
 Distraction behaviors (moaning, crying, pacing, restlessness)
 Autonomic responses (e.g., diaphoresis, blood pressure, and
pulse rate changes, pupillary dilation, increased/decreased
respiratory rate)
 Situational crisis and reports of anxiety
Assess for factors related to the cause of chest pain:
 Decreased myocardial blood flow
 Increased cardiac workload and oxygen consumption
 Myocardial tissue ischemia

Nursing Diagnosis
 Acute pain related to myocardial ischemia
 Anxiety related to difficulty in breathing.
 Ineffective cardiac tissue perfusion related
to reduced coronary blood flow.
 Risk for ineffective peripheral tissue
perfusion related to decreased cardiac
output
 Deficient knowledge related to post-angina
self-care

Nursing Care Planning
Goals and expected outcomes should include:
 The client will report decreased anginal episodes in
frequency, duration, and severity.
 The client will demonstrate relief of pain as
evidenced by stable vital signs, absence of muscle
tension, and restlessness.
 The client will verbalize understanding of their
disease process, therapeutic regimen, management
and potential complications.
 The client will initiate necessary lifestyle changes to
prevent potential myocardial complications of chest
pain.

 Assess and document the client’s response to medication.
 Monitor vital signs every five (5) minutes during the initial
anginal attack; monitor heart rate and rhythm.
 Auscultate heart sounds for murmurs
 Elevate the head of the bed to 30 degrees if the client is
short of breath or during nitrates administration.
 Encourage immediate reporting of pain for prompt
administration of medications as indicated.
 Monitor and document effects or adverse responses to
medications, noting BP, heart rate, and rhythm.
 Administer nitrates e.g. sublingual nitroglycerin or
Isosorbide dinitrate as prescribed. Nitrates are not usually
given if the systolic blood pressure is 90 mm Hg or less.

 Administer oxygen at 3L/min by nasal cannula as
prescribed
 Assist the patient identify and avoid physical and
emotional factors that precipitate angina
 Instruct the patient to avoid exercises in extremes of
weather (hot or cold days), after heavy meals, when
emotionally upset.
 Instruct the patient to stop activities and rest whenever
the chest pain occurs and take nitroglycerin as
prescribed. Including sexual activity that should be
avoided when fatigued.

 Instruct the patient to adhere to the prescribed
medications at all times
 Instruct the patient on the need to maintain the
lifestyle changes that have been recommended
 Instruct the patient on self management during
episodes of chest pain: stop activity and rest; take
nitrates as ordered; seek medical attention if pain
persists longer than 20 minutes or diaphoresis and
shortness of breath appears
 Diet : instruct the patient to avoid eating heavy meals
and exercising after eating; explain that caffeine and
heavy alcohol should be avoided

 Note skin color and the presence and quality of pulses.
 Maintain bed or chair rest in a position of comfort during
acute episodes.
 Clients with unstable angina require admission to the
hospital for bed rest with continuous telemetry
monitoring
 Stress the importance of avoiding straining down,
especially during defecation.
 Maintain a calm environment and stay with the client who
is experiencing pain or appears anxious.
 Evaluate the client’s and family member’s level of
understanding of the diagnosis.
 Identify previous coping strengths of the client and family
members and current areas of control and ability.

Nursing Evaluation
 Reported pain is relieved.
 Reported decrease in anxiety.
 Understood ways to avoid complications and
is free of complications.
 Adhered to self-care program.

Myocardial infarction
 Also referred to as heart attack.
 Occurs when the myocardial tissue is
abruptly and severely deprived of oxygen
causing death to the myocardial tissue.
 Ischemia can lead to necrosis of myocardial
tissue if blood flow is not restored
 Not all clients experience the classic
symptoms of a MI
 Women may experience atypical discomfort,
shortness of breath or fatigue

Risk factors of Myocardial infarction
 Atherosclerosis
 Coronary artery disease
 Elevated cholesterol levels
 Smoking
 Hypertension
 Obesity
 Impaired glucose tolerance
 Stress

Pathophysiology
 In cases of MI, there is a profound imbalance exists
between myocardial oxygen supply and demand.
 There is reduced blood flow in a coronary artery,
often due to rupture of an atherosclerotic plaque,
but the artery is not completely occluded.
 As the cells are deprived of oxygen, ischemia
develops, cellular injury occurs, and lack of oxygen
leads to infarction or death of the cells.
 Infarction does not occur instantly but evolves over
several hours

Pathophysiology
 Obvious physical changes do not occur in the heart
until 6 hours after the infarction, when the
infarcted area appears blue and swollen
 After 48 hours the infarct turns gray with yellow
streaks as the neutrophils invade the tissue
 8-10 days after infarction granulation tissue forms
 Over 2-3 months, the necrotic area develops into a
scar, scar tissue permanently changes the size and
shape of the entire left ventricle

Location of Myocardial infarction
 Obstruction of the left anterior descending
artery results in anterior wall or septal MI
or both
 Obstruction of the circumflex artery results
in posterior wall or lateral wall MI
 Obstruction of the right coronary artery
results inferior wall MI

Clinical manifestation
 Chest pain
◦ Squeezing, substernal and crushing pain
◦ Pain may radiate to to the left arm, jaw, neck, or
shoulder blades
◦ Pain may occur with cause, primarily early in the
morning
◦ Pain persists for upto 12 hours or more
◦ The pain is unrelieved by nitroglycerine or rest and
is relieved only by opioids
 Shortness of breath
 Tachycardia and tachypnea
 Indigestion due to stimulation of the
sympathetic nervous system

Clinical manifestation
 Coolness of extremities, restlessness, feelings
of fear and anxiety
 Dysrhythmias

Prevention
 Promote exercising at least thrice a week to lower
cholesterol levels
 Promote smoking cessation as nicotine
causes vasoconstriction which can increase BP and
result in MI.

Assessment and Diagnostic Findings
 Patient history includes the presenting symptoms,
the history of previous cardiac and other illnesses,
and family history of heart diseases.
 Total creatinine kinase levels- they rise within 3
hours after onset of chest pain
 CK-MB isoenzyme-elevates within 4–8 hr, peaks in
12–20 hrs, returns to normal in 48–72 hrs after
onset of chest pain
 Troponin levels-elevated at 4–6 hrs, peak at 14–18
hr, and return to baseline over 6–7 days after onset
of chest pain
 Myoglobin levels-elevation within 2 hrs after an
acute MI, and peak levels occurring in 3–15 hrs.

Assessment and Diagnostic Findings
 LDH levels-elevates within 8–24 hrs, peaks within
72–144 hrs, lasts upto 14 days to return to normal.
An LDH1 greater than LDH2 confirm/diagnose MI
 Electrocardiogram – will show an elevation of ST
segment,T wave inversion and an abnormal Q wave
 White blood cell count – elevated on the second
day after MI and lasts up to a week

Medical Management
 Goal is to :
◦ Minimize myocardial damage, preserve
myocardial function and prevent
complications
◦ Control of hypertension and diabetes
◦ Stress management
◦ Reduction of cholesterol and lipid levels
◦ Weight reduction
◦ Exercise
◦ Smoking cessation

Medical Management
Following an acute episode:
 Obtain a description of the chest discomfort
 Oxygen therapy by nasal cannula as prescribed
 Pain relief measures using morphine and nitroglycerin
 Assess vital signs and cardiovascular status and
maintain cardiac monitoring
 Ensure bedrest and place the patient in semi fowlers
position to enhance comfort and tissue oxygenation
 ACE inhibitors to control BP
 Insert an IV access line
 Obtain an ECG
 Antidysrhythmics for arrhythmias

Medical Management
 Aspirin 300mg orally stat; Clopidogrel 300mg stat;
Enoxaparin 1mg/kg sc stat within 30 minutes of
diagnosis being made
 Monitor signs of bleeding if the patient is receiving
fibrinolytic therapy
 Monitor laboratory values as prescribed.

Surgical Management
Emergent Percutaneous Coronary
Intervention
 The procedure is used to open the occluded
coronary artery and promote reperfusion to
the area that has been deprived of oxygen.
 PCI may also be indicated in patients with
unstable angina and NSTEMI for patients
who are at high risk due to persistent
ischemia.

Nursing Management
Nursing Assessment
 Assess for chest pain not relieved by rest or medications.
 Monitor vital signs, especially the blood pressure and pulse
rate.
 Assess for presence of shortness of breath, dyspnea,
tachypnea, and crackles.
 Assess for nausea and vomiting
 Assess for decreased urinary output.
 Assess for the history of illnesses.
 Perform a precise and complete physical assessment to
detect complications and changes in the patient’s status.
 Assess IV sites frequently.

Nursing Diagnosis
 Acute pain related to myocardial ischemia
 Anxiety related to shortness of breath.
 Ineffective cardiac tissue perfusion related
to reduced coronary blood flow.
 Risk for ineffective peripheral tissue
perfusion related to decreased cardiac
output
 Deficient knowledge related to post-MI self-
care

Nursing planning and goals
 Relief of chest pain or ischemic signs and symptoms.
 Prevention of myocardial damage.
 Absence of respiratory dysfunction.
 Maintenance or attainment of adequate tissue
perfusion.
 Reduced anxiety.
 Heart rate/rhythm sufficient to sustain adequate
cardiac output/tissue perfusion.
 Achievement of activity level sufficient for basic self-
care.
 Disease process, treatment plan and prognosis
understood.

 Encourage bed rest with the back rest elevated to
help decrease chest discomfort and dyspnea.
 Encourage changing of positions frequently to help
keep fluid from pooling in the bases of the lungs
 Check skin temperature and peripheral pulses
frequently to monitor tissue perfusion.
 Provide information in an honest and supportive
manner.
 Monitor the patient closely for changes in cardiac
rate and rhythm, heart sounds, blood pressure,
chest pain, respiratory status, urinary output,
changes in skin color, and laboratory values.

 Administer nitrates e.g. sublingual nitroglycerin or
Isosorbide dinitrate as prescribed. Nitrates are not
usually given if the systolic blood pressure is 90 mm
Hg or less.
 AdministerAspirin 300mg orally stat; Clopidogrel
300mg stat; Enoxaparin 1mg/kg sc stat.
 Administer oxygen at 3L/min by nasal cannula as
prescribed
 Administer fibrinolytics e.g. alteplase within 30
minutes of diagnosis being made for STEMI
 Assist the patient identify and avoid physical and
emotional factors that precipitate angina

Nursing Evaluation
 There is an absence of pain or ischemic signs and
symptoms.
 Myocardial damage is prevented.
 Absence of respiratory dysfunction.
 Adequate tissue perfusion maintained.
 Anxiety is reduced.

Introduction
 Heart failure is the inability of the heart to pump
sufficient blood to meet the needs of the tissues for
oxygen and nutrients.
 It is also referred to as congestive heart failure
which is a clinical syndrome characterized by signs
and symptoms of fluid overload or of inadequate
tissue perfusion.
 Heart failure indicates myocardial disease in which
there is a problem with contraction of the
heart (systolic dysfunction) or filling of the
heart (diastolic dysfunction) that may or may not
cause pulmonary or systemic congestion.

Introduction
 Heart failure is most often a progressive, life-long
condition that is managed with lifestyle changes and
medications to prevent episodes of acute
decompensated heart failure.

Classification
Classified into two types: left-sided and right-sided
heart failure.
Left-Sided Heart Failure
 Left-sided heart failure or left ventricular failure.
 Pulmonary congestion occurs when the left
ventricle cannot effectively pump blood out of the
ventricle into the aorta and the systemic circulation.
 Pulmonary venous blood volume and pressure
increase, forcing fluid from the pulmonary capillaries
into the pulmonary tissues and alveoli,
causing pulmonary interstitial edema and impaired
gaseous exchange.

Classification
Right-Sided Heart Failure
 When the right ventricle fails, congestion in
the peripheral tissues and the viscera
predominates.
 The right side of the heart cannot eject
blood and cannot accommodate all the blood
that normally returns to it from the venous
circulation.
 Increased venous pressure leads to JVD and
increased capillary hydrostatic pressure
throughout the venous system.

Functional classification of heart failure
The NewYork Heart Association (NYHA) Functional
Classification is based on the degree of
limitation of the patient's day-to-day activities of
living and is a strong predictor of hospitalization
and mortality.
 I- No limitations of physical activity. No HF
symptoms
 II- Slight limitations of physical activity.
Comfortable at rest, but ordinary activity results in
HF symptoms

Functional classification of heart failure
 III- Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes HF symptoms
 IV- Unable to carry on any physical activity
without HF symptoms

Causes
 Atherosclerosis of the coronary arteries is the
primary cause of HF, and CAD accounts for more
than 60% of the patients with HF.
 Ischemia – it deprives heart cells of oxygen and
leads to acidosis from the accumulation of lactic
acid (Angina/MI)
 Cardiomyopathy - HF due to cardiomyopathy is
usually chronic and progressive.
 Systemic/pulmonary hypertension - increase in
afterload, which increases the workload of the heart
thus hypertrophy of myocardial muscle fibers.

Causes
 Valvular heart disease - blood has increasing
difficulty moving forward, increasing pressure within
the heart and increasing cardiac workload.
 Congenital heart defects-atrial & ventricular septum
defects, aortic stenosis
 Inflammatory heart disease-autoimmune
myocarditis

Pathophysiology
 Heart failure results from a variety of cardiovascular
conditions, including chronic hypertension, coronary
artery disease and and valvular diseases.
 Systolic dysfunction results when the left ventricle
can’t pump enough blood out to the systemic
circulation leading to a decreased CO
 Diastolic dysfunction results when the ability of the
left ventricle to relax and fill during diastole is
reduced and the stroke volume falls.
 The decreased CO triggers compensatory
mechanisms that improve cardiac output at the
expense of increased ventricular work.

Pathophysiology
 These compensatory mechanisms include:
increased sympathetic activity; activation of the
renin–angiotensin–aldosterone system; ventricular
dilation; ventricular hypertrophy.
 Increased sympathetic NS activity enhances
peripheral vascular resistance, contractility, heart
rate, and venous return.
 Increased sympathetic activity also restricts blood
flow to the kidneys, causing them to secrete renin,
which in turn converts angiotensinogen to
angiotensin I.
 Angiotensin I is converted by ACE to angiotensin
II—a potent vasoconstrictor.

Pathophysiology
 Angiotensin causes the adrenal cortex to release
aldosterone, leading to sodium and water retention
and an increase in circulating blood volume.
 In ventricular dilation, an increase in end-diastolic
ventricular volume (preload) causes increased
stroke work and stroke volume during contraction.
 The increased volume stretches cardiac muscle
fibers so that the ventricle can accept the increased
volume.
 In ventricular hypertrophy, an increase in ventricular
muscle mass allows the heart to pump against
increased resistance to the outflow of blood,
improving cardiac output.

Left-sided HF
 Dyspnea or shortness of breath precipitated by
minimal to moderate activity.
 Orthopnea
 Cough that is initially dry and nonproductive
 Hemoptysis
 Adventitious breath sounds - Pulmonary
congestion, pulmonary crackles
 Weak, thready pulse
 Tachycardia
 Oliguria, nocturia
 Fatigue

Right-sided HF
 Hepatomegaly resulting from venous
engorgement of the liver.
 Ascites
 Edema of the lower extremities
 Weight gain (fluid retention)
 Anorexia and nausea from venous engorgement
and venous stasis within the abdominal organs.
 Distended neck veins
 Congestion of the viscera and peripheral tissues
 Weakness

Prevention
 HF can be delayed or prevented by treating risk
factors for HF early. Control of hypertension will
delay the onset of HF and will prolong life.
 The mainstay of prevention is screening for and
treating the underlying conditions such as cardio-
metabolic conditions (diabetes, hypertension,
dyslipidaemia) and avoiding acute rheumatic fever.
 Combating behavioural risk factors such emotional
stress; healthy diet by avoiding intake of fatty and
salty foods; engaging in cardiovascular
exercises thrice a week; smoking cessation as
nicotine causes vasoconstriction.

Complications
 Hypokalemia from excessive and repeated
dieresis
 Hyperkalemia may occur with the use of ACE
inhibitors,ARBs, or spironolactone.
 Prolonged diuretic therapy might lead to
hyponatremia and result in disorientation, fatigue,
apprehension, weakness and muscle cramps.
 Dehydration and hypotension from volume
depletion from excessive fluid loss

Findings
 Clinical history – History of common risk
factors (HTN, RHD or CAD), family history of
cardiac disease. Exposition to cardiotoxicity
(alcohol, drugs/radiation).Typical symptoms
Shortness of breath on exertion. Good
response to diuretic therapy.
 Physical examination – On auscultation:
Bilateral crackles, third heart sound, murmurs.
Signs of RV failure: Elevated JVP,
hepatomegaly/ascites or bilateral pedal
oedema.

Findings
 Chest radiograph- to show cardiomegaly,
pleural effusions and interstitial oedema.
 Chest x-ray to rule out differential diagnoses
like pneumonia, COPD or pulmonaryTB.
 Electrocardiogram (ECG)- features in HF
include poor R-wave progression, atrial
fibrillation, left or right ventricular
hypertrophy and pathological Q-waves.

Findings
Echocardiography-is the gold standard test for
characterizing cardiac dysfunction in HF as it: -
 Determines systolic LV performance through
determining left ventricular ejection fraction
(LVEF), cardiac output, chamber quantification and
regional wall motion abnormalities.
 Determines end-diastolic LV filling pressures for
assessment of diastolic dysfunction and systolic
pulmonary artery pressure to diagnose pulmonary
hypertension.
 Identifies valvular and pericardial disease.

Findings
Laboratory investigations- to include:-
 Natriuretic peptides are useful for ruling out HF
 Full blood count: HF due to, or aggravated by,
anaemia or infections; HF associated anaemia
which is associated with poorer prognosis.
 Serum urea, electrolytes and creatinine (UECs):
renal dysfunction, a major determinant of disease
progression.
 Serum albumin: rule out oedema secondary to low
serum albumin in nephrotic syndrome

Findings
 Lipid profile, thyroid function tests (TFTs):
reveal potential cardiovascular or thyroid
disease as a cause of HF.
 Urinalysis: proteinuria due to nephropathy
or nephritic syndrome, or red blood
cells/casts due to glomerulonephritis.
 Liver function tests: may indicate liver
dysfunction in liver failure or disease
progression in liver congestion.
 FBS:Type 2 DM is more common in HF.

Findings
 Blood cultures: suspected infectious
endocarditis.
 Serum magnesium and calcium: Low levels
precipitate arrhythmias or poor
contractility.
 TroponinT or I: to rule out ischemic
aetiology.

Medical Management
 Aim is to relieve patient symptoms, improve
functional status and quality of life and to extend
survival.
 ACE inhibitors for patients with left ventricular
dysfunction to reduce production of angiotensin
II, resulting in preload and afterload reduction
 Beta-adrenergic blockers to prevent remodeling
in patients with mild to moderate heart failure
caused by left ventricular systolic dysfunction
 Inotropes for patients with heart failure due to
left ventricular systolic dysfunction to increase
myocardial contractility, improve cardiac output,
reduce the volume of the ventricle, and decrease
ventricular stretch

Medical Management
 Diuretics to reduce fluid volume overload,
venous return, and preload
 Diuretics, nitrates, morphine, and oxygen to
treat pulmonary edema
 Lifestyle modifications, such as weight loss (if
obese), limited sodium (to 2 g per day) and
alcohol intake, reduced fat intake, smoking
cessation, stress reduction, and development of
an exercise program to reduce symptoms
 Treatment of the underlying cause, if known.
 Supplemental oxygen based on the degree of
pulmonary congestion and resulting hypoxia.

Surgical Management
 Coronary artery bypass graft (CABG)
surgery involves creating a new pathway for
blood to flow to the heart by bypassing
blocked or narrowed coronary arteries.
 Heart valve replacement surgery involves
replacing a damaged or diseased heart valve
with a prosthetic valve
 Angioplasty is a minimally invasive procedure
used to open blocked or narrowed blood
vessels, typically arteries supplying the heart

Nursing Assessment
 Health History
 Assess the signs and symptoms such as dyspnea, shortness of
breath, fatigue, and edema.
 Assess for sleep disturbances by shortness of breath.
 Explore the patient’s understanding of HF, self management
strategies, and the ability and willingness to adhere to those
strategies.
 Physical Examination
 Auscultate the lungs for presence of crackles and wheezes.
 Auscultate the heart for the presence of an S3 heart sound.
 Assess JVD for presence of distention.
 Evaluate the sensorium and level of consciousness.
 Assess the dependent parts of the patient’s body for perfusion and
edema.
 Measure the urinary output carefully
 Weigh the patient daily

Nursing Diagnosis
 Decreased Cardiac Output related to
impaired myocardial function
 Risk for Ineffective Health Maintenance
related to lack of knowledge regarding
diagnostic and laboratory procedures
necessary for monitoring heart failure status.
 Impaired Gas Exchange related to fluid
overload and pulmonary congestion
 Excess fluid volume related to compromised
heart function and renal perfusion

Nursing Diagnosis
 Acute pain related to decreased myocardial
oxygenation
 IneffectiveTissue Perfusion (cardiopulmonary)
related to decreased cardiac output
 Imbalanced Nutrition: Less Than Body
Requirements related to dietary restrictions and
fluid management in heart failure
 Decreased activity tolerance related to
imbalance between oxygen supply and demand
 Anxiety related to changes in health status and
uncertainty about the future due to heart failure
diagnosis

 The patient will exhibit optimal cardiac output,
indicated by vital signs within acceptable ranges,
absence/control of dysrhythmias, and absence of
heart failure symptoms.
 The patient will engage in activities that reduce
cardiac workload.
 The patient will actively participate in desired
activities and meet their own self-care needs.
 The patient will maintain stable fluid volume,
with balanced intake and output, clear/clearing
breath sounds, vital signs within acceptable range,
stable weight, and absence of edema.

 The patient will verbalize understanding of
individual dietary and fluid restrictions.
 The patient will prioritize maintaining skin
integrity
 The patient will effectively manage pain.
 The patient will identify strategies to reduce
anxiety.
 The patient will exhibit improved
concentration.
 The patient will actively participate in their
treatment regimen based on their abilities and
situation.

 Enhance heart’s pumping function to ensure
adequate blood flow to organs by
administering IV inotropes e.g. milrinone or
dobutamine
 Monitor blood pressure closely before and
during the administration of milrinone, as it
can cause hypotension.
 Administer diuretics – furosemide, aldactone,
hydrochrolothiazide to reduce congestion
 Nurse the patient in Fowler position to
maximize chest expansion
 Administer supplemental oxygen, as ordered,
to ease breathing.

 Monitor oxygen saturation levels and ABGs as indicated. If
respiratory status deteriorates, anticipate the need for ET
intubation and mechanical ventilation.
 Institute continuous cardiac monitoring and notify the
doctor of changes in rhythm and rate.
 If the patient develops tachycardia, administer beta-
adrenergic blockers as ordered; if atrial fibrillation is
present, administer anticoagulants or antiplatelet agents, as
ordered, to prevent thrombus formation.
 If the patient develops a new arrhythmia, obtain a 12-lead
ECG immediately.
 Monitor hemodynamic status, including cardiac output,
cardiac index, and pulmonary and systemic vascular
pressures, at least hourly, noting trends.

 Administer medications as ordered. Check the
apical heart rate before administering digoxin.
 Expect to administer electrolyte replacement
therapy (especially potassium) after the
administration of diuretics to prevent such
imbalances such as hypokalemia and the
arrhythmias that they may cause.
 Monitor serum potassium levels regularly and
report any abnormalities.
 Assess respiratory status frequently, at least every
hour.Auscultate lungs for abnormal breath sounds,
such as crackles, wheezes, and rhonchi.

 Obtain a baseline weight and observe for
peripheral edema.
 Monitor hourly urine output.Also, monitor
fluid intake, including IV fluids.
 Assist the patient schedule all activities to
provide maximum rest periods.
 Assess for signs of decreased activity
tolerance, such as increased shortness of
breath, chest pain, increased arrhythmias,
heart rate greater than 120 beats per
minute, and ST segment changes, and have
the patient stop activity.

 Monitor vital signs, including blood pressure, before
and after administering ACE inhibitors e.g. captopril;
ARBs e.g. Lorsartan;Vasodialtors e.g. hydralazine
 Educate the patient about the importance of
adhering to a low-sodium diet and restricting fluid
intake.
 Educate the patient about the importance of
compliance with medication regimen and regular
follow-up appointments.
 Observe the color of skin, mucous membranes, and
nail beds, noting the presence of peripheral
cyanosis.

 Instruct patient in effective coughing and
deep breathing
 Provide comfort, psychological support,
and teach anxiety management
techniques.
 Encourage patient expression of
concerns and involve them in decision-
making.
 Educate patients about heart failure, its
impact, prognosis, lifestyle modifications,
medication adherence, and seeking timely
care to prevent worsening of symptoms.

 Monitor vital signs, especially pulse and blood
pressure every 15 minutes or more frequently
if unstable.Watch out for any reduction greater
than 20 mm Hg over the patient’s baseline or
related changes such as dizziness and changes in
mental status.
 Monitor for and manage complications such as
pulmonary edema, arrhythmias, and
thromboembolism through close
monitoring, medication administration and
patient education.
 Prepare the patient for surgical intervention or
transfer to the CCU if indicated.

Nursing Evaluation
The following are evaluated:
 Demonstration of tolerance for
increased activity.
 Maintenance of fluid balance
 Less anxiety.
 Controlled blood pressure
 Makes sound decisions about care and
treatment.
 Adherence to self-care regimen.

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