Chronic Bronchitis

And
Emphysema
Pathophysiology
*Inflammation characterized
by increased production of
mucus and chronic cough
mofor more than 3 months,
caused by irritants.
*smoke causes blood
vessesl to dialate and mucosa
to become endentamous.
*Cor Pulmonale: R side-
heart failure secondary to
pulmonary disease.
: is degenerative, nonreversible
characterized by enlargement of
the airway.
1. Centrilobular
*Cigarret smoking and respiratory
bronchioles enlargeband
breakdown, alveoli remain intact.
*Elastic coil diminish and airway
collapse.
*Rupted blebs can cause the
lungs to collapse
2. Panlobular
*Affect the respiratory
bronchioles and the alveoli,
caused by hereditary deficiency of
the enzymes inhibitor alpha-
antitrypsin.
Chronic
Bronchitis
Emphysem
a
Treatmen
t
S/S
S/S
Productive
Cough
Exertional
dyspnea
Wheezing
*With chronic
hypoxemia, the RBC
typically elevated.
* Pt. with pulmonate
S/S are heart failure,
dyspnea, cyanosis
peripheral edema.
Dyspnea on exertion
Pt. may also be thin
and have barrel chest.
*Despite dyspnea pt.
may have a normal
arterial gases until
disease has
progressed. Skin may
appear normal pink
puffer is the term
used to describes the
pt.
Nursing Dx.
Sx. Relieve
Bronchodialators
Inhailed cortico
steroids
Oxygen therapy
Pulmonary rehab
(walking or
pedaling)
Nutrition * because
malnutrition causes
energy resistance
to infection*
supplement diet.
Impaired Gas exchange R/T
damaged alveoli and or terminal
bronchioles, bronchospasm air
trapping
Improve air exchange , v/s and arterial
blood gases consistent with patient
norm
Goal

Characterized
Inflammation
Hyperresponsiveness
Sensitive to stimuli
Obstruction
Pathophysiology:
Innate inborn immunity, Genetics,
Environmental factors
1. Phase one: Allergens, irritants,
infection, exercise,
gastroesophageal reflux, and stress.
These activate the inflammatory
process.
Mucus
Tenacious sputum
Obstruction causes air to be
trapped in the alveoli are
perfused with blood but not
ventilated with fresh air.
The effect is hypoxemia
with compensatory
hyperventilation
Occur 30 to 60 minutes and
resolve 30 -90 minutes after
2. 5-6 hours after exposureRBC and
WBC infiltratethe swollen tissue of
the airway.

Complications: Severe bronchospasm is
called status asthmaticus. If not corrected can
lead to R side heart failure, pneumothorax,
worsening hypoxemia, acidosis, and
respiratory or cardiac arrest. Hypertrophy of
bronchial smooth muscle.
S/S
Dyspnea
Productive cough
wheezing
Tachycardia
Tachypnea

Tx.:
Assesing and monitoring
Education
Control environment
Comorbid condition that
affect asthma
Drink 10-14 8oz glasses of
fluids
Use inhaler 30 min pre-
exercise

Medications:
Bronchodilator and anti-inflammatory drugs:
( Controllers) : Glucocorticoid agents, leukotine
modifiers, mast cell stabilizersimmunomodulator
omalizumbad, long-acting beta-abrenergic
agonist and methylxanthine agents.


Meds, allergies, cardiac
disease sleep disruption
ASTHMA
Assessment

Health Hx
Frequency, severity, factors
that trigger, strategies to
manage, source of stress
and knowledge of illness.
PE
VS
Auscultation of lungs
Skin color
Respiratory effort
Intervention
s
Monitor: Impaired Gas
Exchange
Impending respiratory
failure: Tachypnea ,
shallow breathing, ,
diaphoresis, reddening,
HTN, hypotension,
restlessnessg skin,
drowsiness, loss of
conciousness
Pt. R rate
Fowlers position
Give O2
Meds

DX. Test
Pulmonary Function
Airway dynamic
Ability to inhale exhale by force
Vital capacity
Inspiratory capacity
Expiratory reserve volume
Residual Volume
Total lung capacity
Lung volume
Diffusion capacity
Ability of gases to diffuse across the alveolar
capillary membrane

COPD