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COPD physiology

Alveolar sacs lose elasticity and narrow/collapse,↓gas exchange

↑ Air trapped in lungs, loss of elastic recoil
Lung over stretch resulting in hyperinflation (Barrel Chest)

Hard to blow out CO2, inhalation begins before exhalation, uncoordinated breathing

COPD Pt. at risk for

1. Respiratory acidosis due to CO2 retention
Low PAO2 because body cannot move O2 into the bloodstream through the diseased lung
2. Hypoxemia
3. Respiratory infection
4. Cardiac Failure
5. Cor Pulmonale (right sided heart failure) (pumps blood to the lungs)
6. Cardiac dysrhythmias (from hypoxia, acidosis)

People who have COPD

Emphysema- smokers, chronic exposure to inhalation irritants

Chronic Bronchitis (same as above)

Alpha1-antitrypsin deficiency

Cor Pulmonale

Enlarged, tender liver
cyanotic hands/feet
bounding pulses
cyanotic lips
Distended neck viens
visible pulsations at neck
Pulmonary hypertension

Respiratory Acidosis

pH < 7.35, PaCO2 > 45, HCO3 >26,

PaCO2 >45 mm Hg; compensation metabolic alkalosis,

acidity caused by abnormal retention of carbon dioxide resulting from impaired ventilation.

Chronic Airflow Limitation

Chronic diseases including asthma,
chronic bronchitis. Pulmonary
emphysema ----- COPD
COPD : S/S brpnchospasms, and Dyspnea, irreversible lung damage

Asthma intermittent disease with reversible airflow obstructuin and wheezing


Destruction of walls of alveoli/portions of pulmonary capillary bed lost
Loss of elastic recoil—lungs permanently over distended
Increased airway resistance, destruction of small airways (collapse, narrowed) air is trapped increased CO2 levels

Assessment of client with Emphysema

Usually Pt presents to HCP/ ER with S/S of RTI
prolonged expiratory phase,
pursed lip breathing,
tripod position,
crackles—if infection, decreased breath sounds ???,
hyperresonant with percussion,
increased AP diameter,
anorexia, decreased muscle mass,

Pt History questions

Cultural background

Trouble breathing lying down? Talking?
Activities that trigger problems?
Color of sputum
When is cough most productive, morning?
Compare wieghts
Diet, fluid intake

Chronic Bronchitis

Defined as productive cough 3 or more months in 2 consecutive years
thick sputum bronchial edema, narrowed airways

Assessment: stocky build, overweight, chronic cough with sputum production

Diagnosis of COPD

History long time smoking 20 years +
exposure to 2 nd hand smoke, long time air pollution

Physical exam

CXR not really diagnostic—enlarged heart, hyper inflated lungs, flatted diaphragm,

COPD What would ABG values be

↑ PaO2 <80, pH >7.45, PaCO2 >45mm/mg
↓O2 >94%

Hematocrits compensate for lack of O2

Diagnosis of COPD

History long time smoking 20 years +
exposure to 2 nd hand smoke, long time air pollution

Physical exam

CXR NOT DIAGNOSTIC—enlarged heart, hyper inflated lungs, flatted diaphragm,

Pulmonary Function tests

Used to evaluate degree of airway
Evaluates lung volumes and airflow

Used to evaluate response to bronchodilator drug therapy
Used to evaluate progression of disease/diagnose COPD

Example pt. breaths into a spirometer—lung volumes recorded onto a graph

FEV Forced expiratory Volume--- amount of air that can be exhaled in one second
COPD decreased elastic recoil, narrowed airways "obstructive lung disease" FEV is decreased

Nursing Diagnoses

Nursing Diagnoses :
Ineffective airway clearance
Ineffective Breathing Patterns
Imbalanced Nutrition
Decisional Conflict Smoking
Alteration in Gas exchange

Oxygen Therapy

O2 therapy low flow N/C oxygen
1-3 L at home

Long term management 12-15 hours/day to continous therapy
may help relieve S/S, delay development pulmonary HTN, increase exercise tolerance, improve mental function

Why low flow O2 ?? Normally, stimulus to breathe triggered by high CO2 levels
COPD have high CO2 levels and stimulus to breathe triggered by low O2 levels. If increase O2 knocks out stimulus== respiratory failure

Nursing Care

Respiratory assessment, LOC, R/R dyspnea, ability to speak, chest movement, breath sounds, cough sputum production, skin color

Interventions ; Fowlers position, V/S, IV breathing treatment with aerosol bronchodilators ABG, CXR, Oxygen, steriods,

Pt admitted to M/S unit

2-3 liters fluid/day
Chest pt. 02,
Small frequent meals—fats/protein vs CHO (CO2 natural end product of CHO metabolism
Labs: CBC, Electrolytes,
Bronchodilators, steriods, ?? Antibiotics,


Heart pumps venous blood through pulmonary arteries to lungs CO2 expelled, O2 restored

COPD Hypercapnia—potent vasoconstrictor, narrowed airways causes increased pressure in pulmonary arteries
Decreased size of pulmonary vascular bed, obstruction, constriction==blood stagnates

ASSESSMENT : lower extremity edema, liver enlargement, enlarged R ventricle, coarse crackles, wheezes, Nausea/vomiting -congestion of GI tract blood vessels
Polycythemia- body tries to compensate for hypoxia


abnormally high level of RBCs in blood sample

COPD teaching cough

1. Inhale by sniffing to prevent mucus from moving back into deep airways.
2. Cough twice, the first time to loosen mucus, the second to expel secretions.
3. Rest
4. Follow prescribed bronchodilator treatment
5 .Hold breath briefly
6. Inhale deeply

Pulmonary Hypertension

pressure on the right side of the heart must increase to push blood into the lungs (eventually right sided heart failure develops)

Pulmonary Hypertension Treatment

Oxygen therapy
Phlebotomy for polycythemia
Salt and water restriction
Diuretic therapy
Bilateral lung or heart-lung transplant

Pulmonary Hypertension Nursing Diagnoses

Anticipatory grieving
Decreased cardiac output
Excess fluid volume
Ineffective individual coping

Teach health management

Diaphramatic breathing
relaxation therapy
energy conservation
deep breathing
purse lipped breathing

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