OBSTRUCTIVE PULMONARY
DISEASES
Obstructive pulmonary disease
-describes conditions in which airflow
in the lungs is obstructed.
- Resistance to inspiration is
decreased, whereas resistance to
expiration is increased, so that the
expiratory phase of respiration is
prolonged (Bullock & Henze, 2000).
Chronic obstructive pulmonary
disease:
-(COPD) is an umbrella term for
chronic lung diseases that
have limited airflow in and out of the
lungs.
-Symptoms include chronic cough and
expectoration, dyspnea,
shortness of breath, wheezing, and
impaired expiratory airflow.
-COPD- diseases that cause airflow
obstruction or a combination.
- emphysema, chronic bronchitis and
other diseases such as cystic
fibrosis, bronchiectasis and asthma.
Pathophysiology:
- airflow limitation is both progressive
and associated with an abnormal
inflammatory response of the lungs to
noxious particles or gases.
- the inflammatory process occurs
throughout the airways, parenchyma
and pulmonary vasculature.
- the chronic inflammation and the
body’s attempts to repair it, narrowing
occurs in the small peripheral airways.
- this injury-and-repair process causes
scar tissue formation and narrowing
of the lumen.
- airflow obstruction may also be due
to parenchymal destruction,
(emphysema), a disease of the alveoli
or gas exchange units.
• In addition to inflammation;
processes relating to imbalances of
proteinases and anti-proteinases
in the lung;- responsible for
airflow limitation.
• When activated by chronic
inflammation, proteinases and
other substances may be released,
damaging the parenchyma of the
lung.
• The parenchymal changes may
also be consequences of
inflammation, environmental, or
genetic factors.
• Early course of COPD; the
inflammatory response causes
pulmonary vasculature changes
that are characterized by
thickening of the vessel wall.
• Occur as a result of exposure to
cigarette smoke or use of tobacco
products or as a result of the
release of inflammatory mediators.
• Categories of COPD:
• A. Emphysema- disease of the
airways characterized by
destruction of the walls of over
distended alveoli.
- a pathological term that describes an
abnormal distention of the walls of
alveoli.
- the End Stage- walls of the alveoli are
destroyed (process accelerated by
recurrent infections),
a. the alveolar surface area in direct
contact with the pulmonary capillaries
continually decreases, causing an
increase in dead space (no gas
exchange);
b. impaired oxygen diffusion which
leads to hypoxemia.
Later Stage- carbon dioxide tension in
arterial blood (hypercarpnia) and
causing respiratory acidosis.
-As the alveolar walls continue to
break down, the pulmonary bed is
reduced.
­ Pulmonary blood flow increased,
forcing the right ventricle to
maintain a higher blood pressure
in the pulmonary artery.
­ Hypoxemia increase pulmonary
pressure, thus right- sided heart
failure (cor pulmonale) as a
complication.
==congestion, dependent edema,
distended neck veins, or pain in the
region of the liver.
• Two main types of Emphysema:
1. Panlobar (panacinar)- there is
destruction of the respiratory
bronchiole, alveolar duct and
alveoli.
- all air spaces within the lobule are
essentially enlarged, but there is little
inflammatory disease.
- manifestations-hyperinflated
(hyperexpanded), chest (barrel chest),
marked dyspnea on exertion and
weight loss.
= negative pressure during
inspiration- to move air and out of the
lungs.
= adequate level of positive pressure
must be attained and maintained
during expiration.
2. Centrilobular (Centroacinar)- take
place mainly in the center of the
secondary lobule, preserving the
peripheral portions of the acinus.
- derangement of ventilation
-perfusion ratios, producing chronic
hypoxemia, hypercarpnia (increased
CO2 in the arterial blood),
polycythemia and episodes of right
sided heart failure; leads to central
cyanosis, peripheral edema and
respiratory failure.
Risk Factors:
a. cigarette smoking/ passive smoking
1. depresses the activity of scavenger
cells and affects the respiratory tract’s
ciliary cleansing mechanism,
2. irritates the goblet cells and mucus
glands, causing an increased
accumulation of mucus.
3. carbon monoxide (byproduct of
smoking)- combines
with hemoglobin to form
carboxyhemoglobin- cannot carry
oxygen efficiently.
b. prolonged and intense exposure to
occupational dusts and
chemicals, indoor air pollution and
outdoor air pollution.
c. deficiency of alpha, antitrypsin, an
enzyme inhibitor that
process the lung parenchyma from
injury.
• Clinical manifestations:
- cough, sputum production
and dyspnea in exertion, weight loss,
- barrel chest (chronic
hyperinflation)- loss of lung elasticity
• Assessment and Diagnostic
findings:
- pulmonary function studies-
determine disease severity
- spirometry- evaluate airflow
obstruction
- arterial blood gas- obtained to assess
baseline oxygenation and gas
exchange.
- chest x-ray-
- alpha1 antitrypsin deficiency
screening
• Complications:
- Respiratory insufficiency and
failure, pneumonia, atelectasis,
pneumothorax and cor
pulmonale (pulmonary heart disease).
• Medical management:
1. Smoking cessation
2. Pharmacologic therapy:
a. bronchodilators- relieve
bronchospasm and reduce airway
obstruction by allowing increased
oxygen distribution throughout the
lungs and improving alveolar
ventilation.
= metered-dose inhaler (MDI)-
pressurized device containing an
aerosol powder of medication.
b. Corticosteroids-
• Management of Exacerbation:
• Causes: tracheobronchial infection
and air pollution; pneumonia,
pulmonary embolism,
pneumothorax, rib fractures or
chest trauma.
• Treatment: indications for
hospitalization:
1. optimization of bronchodilator
medication-first line therapy.;
2. antibiotic agents.
3. oxygen therapy
4. intensive respiratory intervention
• Oxygen therapy- long-term
continuous therapy
• Surgical management:
1. bullectomy- reduce dyspnea and
improve lung function. Done
thoracoscopically ( video
assisted thoracoscope).
2. lung volume reduction surgery-
removal of a portion of the diseased
lung parenchyma. Allows the
functional tissue to expand, resulting
in improved elastic recoil of the lung
and improved chest wall and
diaphragmatic mechanism.
3. lung transplant- viable alternative
for definitive surgical treatment of
end stage emphysema.
• Nursing management:
1. Patient education
2. Breathing exercises- pursed-lip
breathing helps to slow expiration,
prevent collapse of small airways,
helps the patient to control the
rate and depth of respiration.
3. Inspiratory muscle training-
diaphragmatic breathing; to
strengthen the muscles
4. Self care activities- take short walks,
resting as needed to avoid fatigue
and excessive dyspnea. Fluid should
always available and patient should
begin to drink fluids without having to
be reminded.
5. Physical conditioning- breathing
exercise and general exercises to
conserve energy and increase
pulmonary ventilation.
6. oxygen therapy at home- portable
oxygen system; proper flow rate and
requires number of hours for oxygen
use.
- precaution – smoking is not allowed
(explode)
7. nutritional therapy- caloric needs
and counseling about meal planning
• Coping measures- patient and
family
B. Chronic Bronchitis- chronic
inflammation of the lower respiratory
tract characterized by excessive mucus
secretion, cough and dyspnea
associated with recurring infections of
the lower respiratory tract.
• Pathophysiology:
- smoke or other environmental
pollutants irritate the airways,
resulting in hyper secretion of mucus
and inflammation.
- Constant irritation causes the mucus-
secreting glands and goblet cells to
increase in number, ciliary function is
reduced.
- the bronchial walls thickened, the
bronchial lumen is narrowed,
and mucus plug the airway.
- alveoli adjacent to the bronchioles
may be damaged and fibrosed
resulting in altered function of the
alveolar macrophages.
• Signs/symptoms:
a. presence of cough and sputum
production for at least three months in
each of 2 consecutive years.
b. production of thick, gelatinous
sputum, greater amounts producing
superimposed infections
c. wheezing and dyspnea as disease
progresses
Diagnostic evaluation:
1. pulmonary function test-
demonstrate airflow obstruction-
- reduced FEV to FVC ratio
- increased residual volume to total
lung capacity (TLC )ratio
2. ABG’s decreased PaO2,pH and
increased O2
3. CXR- (late stage)- hyperinflation,
flattened diaphragm, increased
retrosternal space, decreased vascular
markings, possible bullae.
• Management:
1. smoking cessation
2. bronchodilators
- symphathomimetics;
metaproterenol-to protect against
bronchospasm ( aerosol
formulations); MDIs.
- methylxanthines- theophylline
3. Antimicrobial agents- infection
4. corticosteroids- acute exacerbations
for anti-inflammatory effect.
5. Chest physical therapy
6. Low-flow oxygen
7. Pulmonary rehabilitation- limit
activity
• Complications:
- respiratory failure
- pneumonia- overwhelming
respiratory infection
- right heart failure; dysrythmias
- depression;
Nursing Management:
1. Improving airway clearance
2. Improving breathing pattern
3. Controlling infection
4. Improving gas exchange
5. Nutrition
6. Increased activity tolerance
7. Improving sleep patter
8. Enhancing coping
Other Classified Diseases as
COPD:
A. ASTHMA:
Asthma is usually a reversible
obstructive disease of the lower
airway. Inflammation of the airway
and hyper responsiveness of the
airway to internal or external stimuli
characterize asthma.
Pathophysiology and Etiology:
There are two types of asthma:
1. allergic asthma (extrinsic),- which
occurs in response to allergens, such
as pollen, dust, spores, and animal
dander; and
2. non-allergic asthma (intrinsic),-
associated with factors such as upper
respiratory infections, emotional
upsets, and exercise. ***Many clients
experience mixed asthma, which has
characteristics of allergic and non-
allergic asthma.
• Acute asthma results from
increasing airway obstruction
caused by bronchospasm and
bronchoconstriction, inflammation
and edema of the lining of the
bronchi and bronchioles, and
production of thick mucus that can
plug the airway.
• The airways in people with
asthma are hyper-reactive in
response to stimuli.
• Allergic asthma causes the
immunoglobulin E (IgE)
inflammatory response.
• These antibodies attach to
mast cells (granulocyte contain
histamine and heparin) within the
lungs.
• Reexposure to the antigen
causes the antigen to attach to the
antibody, releasing mast cell
products such as histamine.
• Because alveoli cannot expel
air, they hyperinflate and trap air
in the lungs.
• The client breathes faster,
blowing off excess CO2.
• Although the client tries to
force the air out, the narrowed
airway makes it difficult.
• Wheezing usually is audible
with expiration, resulting from air
being forced out of the narrowed
airway.
• Other pathophysiologic
changes include interference with
gas exchange, poor perfusion,
possible atelectasis, and
respiratory failure if inadequately
treated.
• Asthma may develop at any
age.
• Significant relationship
between bronchiolitis
(inflammation
of the bronchioles) in the first
year of life and development of
asthma in early childhood.
• Assessment Findings:
• Signs and Symptoms:
=paroxysms of shortness of
breath, wheezing, and coughing and
the production of thick,
tenacious sputum.
= Duration of acute episodes
varies; it may be brief (less
than 1 day) or extended
(lasting for several weeks).
=During an acute episode, the
work of breathing greatly
increases, and the client
may suffer from a sensation of
suffocation.
-The client frequently
assumes a classic sitting position,
with the body leaning
slightly forward and the arms at
shoulder height.
- This position facilitates
chest expansion and more
effective excursions of
the diaphragm.
• Diagnostic Findings:
1. Chest auscultation reveals
expiratory and sometimes inspiratory
wheezes and diminished breath
sounds.
2. Pulmonary function studies;
- Forced expiratory volume
- abnormal
- Total Lung Capacity (TLC) and
Functional Residual Volume (FRV)
increased secondary to trapped air.
Forced Expiratory Volume (FEV) and
Forced Vital Capacity (FVC) are
decreased.
3. During acute attacks, blood gases
(ABG) show hypoxemia.
- The partial pressure of carbon
dioxide (PaCO2) level may be elevated
if the asthma becomes worse, but
usually the PaCO2 level is decreased
because of the rapid respiratory rate.
- A normal PaCO2 level in the latter
part of an asthma attack may indicate
impending respiratory failure.
• Medical Management:
1. If the history and diagnostic tests
indicate allergy as a causative factor,
treatment includes avoidance of the
allergen, desensitization, or
antihistamine therapy.
2. Oxygen usually is not necessary
during an acute attack because most
clients are actively hyperventilating.
Oxygen may be necessary if cyanosis
occurs.
3. Pharmacologic management:
- metered-dose inhalers (MDIs).
- Bronchodilators are used to manage
acute breathing disorders
• Nursing Management:
1. administers oxygen if indicated and
puts the client in a sitting position.
2. Rest and adequate fluid intake-
secretions less tenacious and replaces
the fluids lost through perspiration.
3. checks the intravenous (IV) site
frequently for signs of extravasation.
4. when the client is receiving
epinephrine or other adrenergic
agents, which may cause palpitations,
nervousness, trembling, pallor, and
insomnia.
5. instructs the client in using the peak
flow meter to monitor the degree of
asthma control.
• Nutrition:
1. Encourage clients with asthma to
consume adequate calories and
protein to optimize health and resist
infection.
2. Large meals may aggravate asthma
by distending the stomach; small
frequent meals may be better
tolerated.
3. Certain vitamins and minerals are
important for immune function,
especially vitamins A, C, B6, and the
mineral zinc.
4. Food allergens that may trigger
asthma include milk, eggs, seafoods
and fish.
• B. Bronchiectasis- a chronic,
irreversible dilatation of the
bronchi and bronchioles.
• Causes:
- bronchial obstruction by tumor or
foreign body,
- congenital abnormalities,
- exposure to toxic gases,
- chronic pulmonary infections.
Pathophysiology:
- damage to the bronchial wall, which
leads to buildup of thick sputum,
causing obstruction.
- severe coughing result in permanent
dilatation of bronchial walls.
• The structure of the wall tissue
subsequently changes, resulting
in formation of saccular
dilatations, which collect purulent
material.
• Airway clearance is further
impaired, and the purulent
material remains, causing more
dilatation, structural damage,
and more infection.
• Nursing Management for the
Elderly;
• The goals of therapy in the
elderly with COPD:
• to treat and prevent chronic
symptoms,
• decrease emergency room
visits and hospitalizations,
optimize and preserve activity
level,
• optimize pulmonary function
with minimal adverse effect from
medications.
• Management should also focus
on improving health status
(quality of life), which is greatly
impaired by respiratory symptoms
such as breathlessness and by
symptoms of anxiety and
depression.
• Clinical manifestations:
1. persistent cough with production of
copious amounts of purulent sputum.
2. intermittent hemoptysis;
breathlessness
3. recurrent fever and bouts of
pulmonary infection
4. crackles and rhonchi
( whistling/snoring) heard over
involved lobes
5. finger clubbing
Diagnostic evaluation;
-CXR- may reveal areas of atelectasis
with widespread dilatation of bronchi.
- sputum examination- pathogens
• Medical Management
1. drainage of purulent material from
the bronchi; antibiotics,
bronchodilators, and mucolytics to
improve breathing and help raise
secretions;
2. humidification to loosen secretions;
3. surgical removal if bronchiectasis is
confined to a small area.
Nursing management:
1. instructing the client in postural
drainage techniques, which help the
client mobilize and expectorate
secretions.
2. Chest percussion and vibration may
be performed during this time.
3. Encourage increased intake of fluid
to reduce viscosity of sputum and
make expectoration easier.
C. Cystic Fibrosis - an inherited
multisystem disorder that affects
infants, children, and young adults.
- It obstructs the lungs, leading to
major lung infections, as well as
obstructing the pancreas.
• Pathophysiology and Etiology
- CF results from a defective autosomal
recessive gene.
- A person with CF inherits a defective
copy of the CF gene from both parents.
- A person who is a carrier has one
normal copy of the gene and one
defective copy.
- When two carriers give birth to a
child, the child has a 25% chance of
having CF, a 50% chance of being a
carrier, and a 25% chance of not
being a carrier.
• The genetic defect causes
inadequate synthesis of a protein
(CF gene product) referred to
as the CF transmembrane
conductance regulator (CFTR).
• CFTR molecules are located in
the cells lining the ducts of the
exocrine glands, particularly the
lungs, pancreas, intestine, and
sweat ducts.
• Clients with CF cannot
synthesize adequate CFTR to
regulate the
combination of water and
electrolytes with exocrine secretions
and mucus.
Subsequently, thick, viscous secretions
and protein plugs eventually block the
ducts of the exocrine glands.
Eventually, ducts may become
fibrotic and convert into cysts
(Bullock & Henze, 2000).
• Airflow obstruction is a key
feature in the presentation CF.
• This obstruction is due to
bronchial plugging by purulent
secretions, bronchial thickening
due to inflammation resulting
airway obstruction.
• Chronic retained secretions in
the airways set up an excellent
reservoir for continuous bronchial
infection.
• Clinical manifestations:
• respiratory infections, ranging
from URIs with increased cough
and purulent sputum to the
production of thick, tenacious
mucus.
• Finger clubbing is common.
• Hemoptysis also may occur as successfully and have the benefit of
blood vessels are damaged in the decreasing systemic absorption.
lungs, secondary to frequent • Nursing management:
coughing and constant efforts to 1. chest physical therapy (including
clear mucus. postural drainage, percussion, and
• Sinusitis and nasal polyps vibration) two to four times daily,
• Assessment and diagnostic 2. deep-breathing and coughing
findings: exercises, nebulized treatments, and
• Pilocarpine iontophoresis medications.
sweat test. Up to 20 years of age, 3. prophylactic antibiotic therapy to
levels decrease recurrence of infection
higher than 60 mEq/L are
diagnostic, and those between 50
and 60 mEq/L are highly
suggestive for CF.
• Chest radiography
demonstrates widespread
consolidation, fibrotic changes,
and overaerated lungs.
Pulmonary function tests assist in
determining current function as well
as progression of the disease.
• Radiographic studies of the GI
system show fibrous
abnormalities.
• In 80% of those with CF, tests
for pancreatic enzymes in
duodenal contents fail to show
evidence of trypsin.
• Medical management;
• promoting the removal of the
thick sputum through postural
drainage,
• chest physical therapy with
vigorous percussion and vibration,
breathing exercises,
• hydration to help thin
secretions,
• bronchodilator medications,
nebulized mist treatments with
saline or mucolytic
• lung infections with antibiotics.
• Inhaled antibiotics, such as
tobramycin, are being used

Chronic Illness/ Conditions
Heart disease,
Hypertension,
Chronic obstructive Pulmonary
Disease COPD
Diabetes,
Cancer and
Dementia,
Stroke
A. Heart Disease
Principle cause of death
Accounts for significant morbidity,
disablement and inactivity
Dominant factors; atherosclerosis
(build-up of fatty deposits within
arterial walls
Pathophysiology/Mechanism
Atherosclerosis buildup
Narrowing of arteries supplying blood
to the heart
Ischemia ( inadequate blood supply)
Ischemic heart disease known as;
a. Coronary heart disease (CHD)
b. Coronary artery disease (CAD)
c. Myocardial infarction (heart
attack)-
persistence of deficient blood
supply,
tissue dies.
- Dead area (Necrosis): an infarct
Heart attack may result from;
- cardiac arrest- some interruption
of normal pattern of cardiac
contraction
- Coronary thrombosis- sudden
blockage of coronary artery with a
blood clot,
- Strenuous exercises resulting in
suddenly increased need for oxygen.
Mortality associated with MI
Over 70 and 2x under the age 70
Symptoms of MI may differ in older
people than in younger ones.
- complete absence of chest pain is
very rare in acute MI up to middle age,
it is a “mundane occurrence” in old
people.
- “only about 1/3 of elderly patients
present with classical prolonged
episode of chest pain”. (Kart & Kinny)
Gerontology:
- elderly patients: more likely to
experience silent MIs have atypical
symptoms- hypotension, low body
temperature, vague complaints of
discomfort, mild perspiration, stroke-
like symptoms ( dizziness, change in
sensorium).
Etiology
1. Acute Coronary thrombosis (partial
or total)– associated with 90% of Mis.
a. severe coronary artery disease
 (greater then 70% narrowing of
the
artery) precipitates thrombus
formation.
b. Intramural hemorrhage into
atheromatous plaques causes
lesion to
enlarge and occlude the vessel;
dissecting
hemorrhage can also occur.
c. plaque ruptures into the vessel
lumen and a thrombus forms on
top of the ulcerated lesion, with
resultant vessel occlusion.
2. Other etiologic factors;
- coronary artery spasm, coronary
artery embolism, infectious disease
causing arterial inflammation,
hypoxia, anemia severe exertion or
stress on the heart in the presence of
significant coronary artery disease.
3. Degrees of Damage occur to the
heart muscle:
a. Zone of necrosis- death to the
heart muscle caused by extensive
and complete oxygen deprivation;
(Irreversible damage).
b. Zone of Injury – region of the
heart
muscle surrounding the area of
necrosis;
- inflamed and injured, but still
viable if adequate oxygenation can
be
restored.
c. Zone of ischemia- region of the
heart muscle surrounding the
area of injury, which is ischemic and
viable;
- not endangered unless extension
of the infarction occurs.
4. Layers of the layers of the heart
muscle
involved; Classified as:
a. Transmural (Q wave) infarction-
area of necrosis occurs throughout the
entire thickness of the heart muscle.
b. Subendocardial
(nontransmural/non-Q) infarction-
area of necrosis is
confined to the innermost layer of the
heart lining the chambers.
5. Location of damaged heart muscle
within the left ventricle; inferior,
anterior, lateral and posterior;
a. left ventricle- most common and
dangerous location- main pumping
chamber of the heart.
b. right ventricular infarctions – occur
in conjunction with damage to the
inferior and/or posterior wall of the
left ventricle.
6. Region of the heart muscle that
becomes damaged- determined by the
coronary artery that becomes
obstructed.
7. Amount of heart muscle damage
and the location of the MI- determines
prognosis.
Heart Disease: Modifiable Factors:
Cigarette smoker: 2x MI rate of non-
smokers
High B/p
High serum cholesterol levels
Diabetes
Obesity
Sedentary lifestyle
Healthy people 2000
1. Increase proportion of people
whose high B/P is under control
2. reduce mean-serum cholesterol
levels
3. reduce dietary fat intake and
average unsaturated fat intake
4. reduce prevalence rates of
obese/overweight adults
5. increase proportion of children and
adults engaging in regular, daily
physical activity at least 30min/day.
6. reduce cigarette smoking among
people age 20 and older
(.http://www.health.gov/healthypeop
le).
Management:
A. oxygen therapy- improves
oxygenation
B. Pain Control;
i. Opiate analgesic therapy=
- morphine- improve cardiac
hemodynamics by reducing
preload and afterload; provide
anxiety relief.
- Meperidine (demerol)- allergic to
morphine or sensitive to
respiratory depression.
ii. Vasodilator therapy-
- nitroglycerine (sublingual, paste)
- myocardial oxygen demand
- persistent chest pain – IV
nitroglycerin
iii. Anxiolytic therapy-
- benzodiazepines- with
analgesic.
C. Pharmacologic therapy-
i. Thrombolytic agents- tissue
plasminogen activator; steptokinase,
urokinase; reestablish blood flow in
coronary vessels by dissolving
obstructing thrombus.
ii. Anticoagulant therapy- adjunct
to thrombolytic therapy.
iii. Beta-adrenergic blocking agents-
improve O2 supply and demand,
decrease sympathetic stimulation to
the heart, promote blood flow in the
small vessels of the heart; have anti
-dysrhythmic
effects
iv. Anti-dysrhythmic therapy;
lidocaine- decreases ventricular
irritability.
v. Calcium channel blockers
(Dilzem)- improve the balance b/w O2
and demand by decreasing HR, B/P
and dilating coronary vessels.
D. Percutaneous Transluminal
Coronary Angioplasty (PTCA)-
mechanical opening of the coronary
vessel can be performed during an
evolving infarction.
E. Surgical Revascularization-
coronary artery bypass surgery (w/in
6hrs of evolving infarction)
- definite treatment of the stenosis
and less scar formation of the heart.
Gerontology Consideration:
Elderly patients are extremely
susceptible to respiratory depression
in response to narcotics.
Analgesic agents with less profound
effects on the respiratory center
should be used.
Anxiolytic agents
Nursing care:
Reducing pain- administer O2,
medication;
Alleviating anxiety- explain
equipment, procedures and need for
frequent assessment
Maintaining hemodynamic stability-
monitor v/s.
Increasing activity tolerance- promote
rest with early gradual increase in
mobilization
Preventing bleeding- monitor V/s;
thrombolytic agent.
Assignment:
Read about Hypertension, COPD and
Diabetes mellitus.
Hypertension: High Blood Pressure
Disease of the vascular regulation in
which the mechanism that control
arterial pressure within normal range
are altered.
Mechanism control:
- CNS
- renal pressure system (renin-
angiotensin-aldosterone system
- extracellular fluid volume.
B/p elevation- increased cardiac
output and peripheral vascular
resistance.
Hypertension
Pathophysiology/Etiology:
A. Primary or Essential Hypertension
- approx. 90% of patients with hpn
- diastolic pressure is 90mmHg or
higher and other causes of
hypertension are absent.
- considered hpn when the average of
3 or more B/p readings taken at rest
several days apart exceeds the upper
limits.
Causes:
Unknown
Hyperactivity of sympathetic
vasoconstricting nerves
Presence of blood component
containing a vasoconstrictor that acts
on smooth muscle, sensitizing it to
constrictor substances
Increases cardiac output, followed by
arteriole constriction.
Prostaglandins affect regulatory
mechanism, which include the renin-
angiotensin system, renal Na and
water excretion and vascular smooth
muscle tone.
Familial (genetic) tendency.
Decsription:
Labile- intermittently elevated B/P
Accelerated- sudden and severe
escalation in arterial pressure,
producing many symptoms and
vascular damage
Resistant- hpn that is not responsive
to usual treatment
Atrial natriuretic peptide (ANP) or
atrial natriuretic factor (ANF) is a
natriuretic peptide hormone secreted
from the cardiac atria.
cardiac hormone which gene and
receptors are widely present in the
body.
Main functions:
To lower blood pressure and to
control electrolyte homeostasis.
Causing a reduction in expanded
extracellular fluid (ECF) volume by
increasing renal sodium excretion.
B. Secondary hypertension
- approx. 5%-10% of patients with
hypertension
Causes:
1. follows other pathology
2. Renal Pathology-
a. congenital anomalies,
pyelonephritis, renal artery
obstruction, acute and chronic
glomerulonephritis.
b. reduced blood flow to kidney
(atherosclerotic plaque) release
of renin.
- renin reacts with serum protein in
liver (a2- globulin) angiotensin I;
and angiotensin-converting enzyme
(ACE)
Angiotensin II leads to increase
B/P.
Renal artery disease can cause of
narrowing of the vessel lumen
(stenosis).
Reduced lumen diameter decreases
the pressure at the afferent arteriole
in the kidney and reduces renal
perfusion.
Stimulates renin release by the kidney,
which increases
circulating angiotensin II (AII)
and aldosterone.
These hormones increase blood
volume by enhancing renal
reabsorption of sodium and water.
Increased AII also causes systemic
vasoconstriction and enhances
sympathetic activity.
Chronic elevation of all promotes
cardiac and vascular hypertrophy.
The net effect of these renal
mechanisms is an increase in blood
volume that augments cardiac output
by the Frank-Starling mechanism.
Therefore, hypertension caused by
renal artery stenosis results from both
an increase in systemic vascular
resistance and an increase in cardiac
output.
Frank–Starling law of the heart
represents the relationship between
stroke volume and end diastolic
volume.
- states that the stroke volume of
the heart increases in response to an
increase in the volume of blood in the
ventricles, before contraction, when
all other factors remain constant..
Hypertension- the leading causes of
CKD due to the deleterious effects that
increased BP has
on kidney vasculature.
- damage impairs the kidney's ability
to filter fluid and waste from the
blood, leading to an increase of fluid
volume in the blood causing an
increase in BP
3.Coarctation of aorta (stenosis of
aorta)- blood flow to upper
extremities is greater than flow to
lower extremities hpn of upper
body part.
Coarctation (narrowing) of the aorta is
a congenital defect that most
commonly is found just distal to the
left subclavian artery in the arch of the
aorta.
Obstruction of the aorta at this point
reduces distal arterial pressures and
elevates arterial pressures in the head
and arms.
The reduced systemic arterial
pressure activates the renin-
angiotensin-aldosterone system,
which leads to an increase in blood
volume.
This further increases arterial
pressures in the upper body and may
largely offset the reduction in lower
body arterial pressures.
This condition is readily diagnosed by
comparing arterial pressures
measured in the arms and legs.
4. Endocrine disturbances –
a. Pheochromocytoma- tumor of the
adrenal gland – causes release of
epinephrine and norepinephrine and a
rise in b/p
b. Adrenal cortex tumors- leads to
increase in aldosterone secretion and
an elevated blood pressure.
Increased secretion of aldosterone
generally results from adrenal
adenoma or adrenal hyperplasia.
Increased
circulating aldosterone causes renal
retention of sodium and water, which
causes blood volume and arterial
pressure to increase.
Plasma renin levels are generally
decreased as the body attempts to
suppress the renin-angiotensin
system; there is also hypokalemia
associated with the high levels of
aldosterone.
c. Cushing syndrome leads to an
increase in adrenocortical steroids
and hypertension.
d. Hyperthyroidism.
C. Accelerated Hypertension-
Hypertensive Crisis Blood pressure
elevates very rapidly, threatening one
or more of the target organs; brain,
kidney heart
Classification
Prevalence and Risk factors
No Symptoms- is termed as “silent
killer”
Factors;
- age-30-70
- race- african american
- birth control pills
- overweight
- family history
- smoking
- sedentary lifestyle
- stress
- diabetes mellitus
Clinical manifestation
Usually asymptomatic
Headache,
dizziness,
blurred vision when greatly elevated
Diagnostic evaluation
ECG– left ventricular hypertrophy,
ischemia
Chest x-ray- cardiomegaly
Proteinuria- elevated BUN, creatinine
Serum K- decreased in primary
aldosteronism- elevated in cushing
syndrome
Urine catecholamines- increased
pheochromocytoma
Nursing Management
Goal: to help achieve a normal blood
pressure through independent and
dependent interventions.
Assessment:
On antihypertensive medication,-
blood pressure is
assessed to determine the
effectiveness and detect changes in
the blood pressure.
Complete history should be obtained
to assess for signs and symptoms that
indicate target organ damage.
Pay attention to the rate, rhythm, and
character of the apical and peripheral
pulses.
Major goals for a patient with
hypertension are as follows:
Understanding of the disease process
and its treatment.
Participation in a self-care program.
Absence of complications.
BP within acceptable limits for
individual.
Cardiovascular and systemic
complications prevented/minimized.
Disease process/prognosis and
therapeutic regimen understood.
Necessary lifestyle/behavioral
changes initiated.
Plan in place to meet needs after
discharge.
Nursing Priorities
Maintain/enhance cardiovascular
functioning.
Prevent complications.
Provide information about disease
process/prognosis and treatment
regimen.
Support active patient control of
condition.
Nursing Interventions
Objective: focuses on lowering and
controlling the blood pressure without
adverse effects and without undue
cost.
1. Encourage the patient to consult a
dietitian to help develop a plan for
improving nutrient intake or for
weight loss.
2. Encourage restriction of sodium and
fat
3. Emphasize increase intake of fruits
and vegetables.
4. Implement regular physical activity.
5. Advise patient to limit
alcohol consumption and avoidance
of tobacco.
6. Assist the patient to develop and
adhere to
an appropriate exercise regimen.
Evaluation:
Maintain blood pressure at less than
140/90 mmHg with lifestyle
modifications, medications, or both.
Demonstrate no symptoms of angina,
palpitations, or visual changes.
Has stable BUN and serum creatinine
levels.
Has palpable peripheral pulses.
Evaluation;
Adheres to the dietary regimen as
prescribed.
Exercises regularly.
Takes medications as prescribed and
reports side effects.
Measures blood pressure routinely.
Abstains from tobacco and alcohol
intake.
Exhibits no complications.
Discharge and Home care Guidelines
The nurse can help the patient achieve
blood pressure control
through education about managing
blood pressure.
Assist the patient in setting goal blood
pressures.
Provide assistance with social
support.
Encourage the involvement of family
members in the education program to
support the patient’s efforts to control
hypertension.
Provide written information about
expected effects and side effects.
Encourage and teach patients to
measure their blood pressures at
home.
Emphasize strict compliance of follow-
up check up.
DASH Guidelines
• 6 to 8 servings of grains per day
• 4 to 5 servings of fresh fruits per day
• 4 to 5 servings of fresh vegetables
per day
• 2 to 3 servings of low-fat dairy per
day
• 6 or less servings of lean protein per
day
• 4 to 5 servings of legumes or
nuts/seeds per week
• Limited fats and sweets
Physiological Changes and COPD in
the Elderly
Aging affects the structure, function,
and control of the respiratory system.
The elastic recoil of the lungs is the
major determinant of maximal
expiratory flow and is diminished with
aging, causing increased lung
compliance at high lung volumes.
Bronchiolar diameters diminish and
alveolar ducts enlarge as a result of
the change in lung matrix and elastic
properties of lungs.
These changes result in decreased
expiratory flow and decreased surface
area for gas exchange, respectively.
Airways in dependent portions of the
lung close at higher volumes with
advancing age, so that more airways
are closed during all or part of the
respiratory cycle.
Lower portions of the lung are better
perfused at all ages, but higher closing
volume with age increases ventilation
perfusion mismatch and accounts for
the declining Pao2 (oxygen pressure)
with age.
In contrast to the lungs, the chest wall
stiffens with age and compliance
decreases.
Costochondral cartilages become
calcified, and intercostal muscle
contraction accounts for less chest
expansion.
Respiratory muscle strength and
endurance diminish with age,
especially above the age of 55 years.
The anterior-posterior diameter of the
thorax and the kyphosis of the
thoracic spine also increase with age.
Changes in skeletal muscle and the
thoracic wall may affect clearing of the
airway in states where airway mucus
hypersecretion occurs.