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Pathophysiology Treatment

Impaired Gas exchange R/T damaged


Chronic Bronchitis
alveoli and or terminal bronchioles,
And bronchospasm air trapping
Emphysema Sx. Relieve
Chronic Emphysema Bronchodialators
Bronchitis Inhailed cortico
steroids
Oxygen therapy
: is degenerative, nonreversible Pulmonary rehab
*Inflammation characterized by characterized by enlargement of the (walking or pedaling)
increased production of mucus airway. Nutrition * because
and chronic cough mofor more 1. Centrilobular Nursing Dx. malnutrition causes
than 3 months, caused by *Cigarret smoking and respiratory energy resistance to
irritants. bronchioles enlargeband breakdown, infection* supplement
alveoli remain intact. diet.
*smoke causes blood vessesl *Elastic coil diminish and airway
to dialate and mucosa to become collapse.
endentamous. *Rupted blebs can cause the lungs to
*Cor Pulmonale: R side-heart collapse Goal
failure secondary to pulmonary 2. Panlobular Improve air exchange , v/s and arterial
disease. *Affect the respiratory bronchioles
blood gases consistent with patient norm
and the alveoli, caused by hereditary
deficiency of the enzymes inhibitor
alpha-antitrypsin.
S/S

Productive Cough
Exertional dyspnea
Wheezing S/S
*With chronic
hypoxemia, the RBC Dyspnea on exertion
typically elevated. Pt. may also be thin
* Pt. with pulmonate and have barrel chest.
S/S are heart failure, *Despite dyspnea pt.
dyspnea, cyanosis may have a normal
peripheral edema. arterial gases until
disease has progressed.
Skin may appear
normal pink puffer is
the term used to
describes the pt.
ASTHMA
Characterized Assessment
Inflammation
Hyperresponsiveness
Sensitive to stimuli
Obstruction COPD Meds, allergies, cardiac
disease sleep disruption

DX. Test
Pulmonary Function Health Hx
Pathophysiology: Airway dynamic
Innate inborn immunity, Genetics, Ability to inhale exhale by force
Environmental factors Vital capacity
1. Phase one: Allergens, irritants, Inspiratory capacity Frequency, severity, factors
infection, exercise, gastroesophageal Expiratory reserve volume that trigger, strategies to
reflux, and stress. These activate the Residual Volume manage, source of stress
inflammatory process. Total lung capacity and knowledge of illness.
Mucus Lung volume
Tenacious sputum Diffusion capacity
Obstruction causes air to be Ability of gases to diffuse across the alveolar PE
trapped in the alveoli are capillary membrane
perfused with blood but not
ventilated with fresh air.
The effect is hypoxemia with VS
Auscultation of lungs
compensatory hyperventilation
Occur 30 to 60 minutes and resolve Skin color
30 -90 minutes after Respiratory effort
2. 5-6 hours after exposureRBC and WBC
infiltratethe swollen tissue of the
Medications:
airway. Interventions
Bronchodilator and anti-inflammatory drugs:
( Controllers) : Glucocorticoid agents, leukotine
modifiers, mast cell
stabilizersimmunomodulator omalizumbad, Monitor: Impaired Gas
long-acting beta-abrenergic agonist and
Exchange
methylxanthine agents. Impending respiratory
failure: Tachypnea ,
Complications: Severe bronchospasm is called Tx.: shallow breathing, ,
status asthmaticus. If not corrected can lead to
S/S Assesing and monitoring diaphoresis, reddening,
R side heart failure, pneumothorax, worsening Dyspnea Education HTN, hypotension,
Productive cough Control environment restlessnessg skin,
hypoxemia, acidosis, and respiratory or cardiac
arrest. Hypertrophy of bronchial smooth wheezing Comorbid condition that drowsiness, loss of
Tachycardia affect asthma conciousness
muscle.
Tachypnea Drink 10-14 8oz glasses of Pt. R rate
fluids Fowlers position
Use inhaler 30 min pre- Give O2
exercise Meds