CA – MEDICAL-SURGICAL 1 4.

CT Scan
RESPIRATORY SYSTEM 5. MRI
6. ABG
RESPIRATION – gas exchange 7. Pulse oximeter – O2 test
Respiratory center 8. Spirometry – spirometer – volume & capacities of the lungs
- Pons & medulla VOLUMES
- chemoreceptors 1. Tidal volume (TV) ave:
- Low O2 – COPD (best stimulus) 500 mL – vol of air that goes in and out of the lungs in normal
- High CO2 – normal (best stimulus) breathing
Muscles & nerves 2. Inspiratory reserve volume (IRV) = 3000mL – vol of air that can still
- Inspiratory muscles be inhaled after normal inspiration
- Diaphragm – phrenic nerve (C3 & C4) 3. Expiratory reserve volume (ERV) – 1100mL – vol of air that can still
- External intercostal muscles be exhaled after normal expiration
- Expiratory muscles 4. Residual Volume (RV) – 1200 mL vol of air that remains in the
Expiration = passive = recoil of the lungs lungs after forceful expiration; keep the alveoli open
> Elastic, distensible, stretchable (Compliance) 5. Dead space volume (DSV) – 150 mL – volume of air that does
Expiratory muscles not participate in gas exchange
Sternocleidomastoid 6. Functional volume (FV) – 350 mL – volume of air that actually
Internal intercostals (accessory muscles) participates in gas exchange
Respiratory System – open CAPACITIES – combination of volumes
Upper respiratory tract – nose – larynx – cartilages 1. Inspiratory capacity (IC) – total volume of air maximally inhaled
Lower respiratory tract – trachea – alveoli – trachea – c-shaped TV + IRV
cartilages 2. Functional Residual Volume (FRV) – total volume of air left in the
Bronchi/bronchioles – smooth muscles lungs after normal expiration ERV + RV
Contract – bronchoconstriction 3. Vital Capacity (VC) – total volume of air maximally inhaled and
Relax – bronchodilation maximally exhaled
Protective structures TV + IRV = ERV
1. Hair, cilia, mucus cells, turbunates 4. Total Lung Capacity – total volume of air the lungs can hold VC
2. Respiratory epithelium – pseudostratified + RV
columnar ciliated with goblet cells
3. Alveolar macrophage OBSTRUCTIVE LUNG DISEASES – airway obstruction
4. Alpha 1 antitrypsin – chemical that prevent BRONCHIAL ASTHMA COPD
the destruction of the alveolar wall by the Bronchospasms Permanent impairment
hydrolytic enzymes Reversible Irreversible
5. Surfactant – produced by the alveolar type 2 cells: decreased Acute attack Acute exacerbation
surface tension, prevent collapse of the alveolar wall Non progressive Progressive
(atelectasis) *chronic asthma can lead to emphysema
Adult – ARDS (Acute/Adult Respiratory Distress Syndrome cause
by an acute lung injury BRONCHIAL ASTHMA – bronchospasm (expiration)
DIAGNOSTIC TESTS Etiology:
1. Chest X-ray 1. Intrinsic Asthma – idiopathic
2. Thoracic cage X-ray
3. Bronchoscopy – admit – local anesthesia – awake – monitor
breathing or lung sounds
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 2. Extrinsic Asthma – allergy most à allergens à Ag – Ab reaction b. Prophylactic drugs
àinflammation of the the bronchioles àLeukotriene à Ex: Mast cell stabilizers – inhibit release of histamine à prevent an
bronchospasm à wheezing (partial obstruction) attack
à Histamine à swelling of the bronchioles c. Cromolyn sodium
(goblet cells swell) à inc mucus production à d. Nedocromil
= airway obstruction à dyspnea àuse of MEDICAL MANAGEMENT:
accessory muscles à fatigue, intercostal 1. Bronchodilators
retraction a. Xanthine derivatives (methylxanthines) – caffeine containing
* initially à hyperventilate à respiratory alkalosis Ex: Aminophylline, Theophylline
* later on à respiratory acidosis b. Sympathomimetic bronchodilator
NURSING DIAGNOSIS: Ex: Beta agonists (Beta 1 & beta 2), Salbutamol (Ventolin),
1. Ineffective airway clearance Albuterol, Terbutaline
2. Ineffective breathing pattern c. Anticholinergic bronchodilator – inhalation only, no oral, no
3. Impaired gas exchange parenteral
4. Ineffective tissue perfusion Ex: Ipratropium (Atrovent), Tiotropium
5. Fatigue/Activity Intolerance
6. Risk for infection (Pneumonia) CHRONIC OBSTRUCTIVE PULMOARY DISEASE (COPD)
DIAGNOSTIC TEST: – irreversible and progressive
1. CXR – hyperinflated lung (air trapping) Chronic bronchitis – chronic inflammation of the bronchioles
2. ABG – initial – Resp alkalosis Emphysema – overdistention and destruction of alveoli
Later on – Resp acidosis
3. Pulse Ox – low O2 sat CHRONIC BRONCHITIS – “BLUE-BLOATERS”
4. Spirometry – decrease ERV, increase RV, increase FRC - productive cough for 3 months for 2 consecutive years (clinical
5. Peak flow meter – determine the degree of obstruction definition)
MANAGEMENT: Etiology: environmental pollutants (smoking) à injury to the bronchioles
1. Position – orthopneic, tripod, leaning forward à chronic inflammation of the bronchioles [>6months (permanent
2. Bronchodilators – dilates normal bronchiole first – inhalation changes, progressive & irreversible)] à swelling of the bronchioles &
3. O2 administration hypertrophy of goblet cells à increase mucus production
4. Promote rest period ëà airway obstruction à dyspnea à impaired gas exchange à dec
5. Promote safety pO2 (hypoxemia) inc pCO2 (hypercapnea) à cyanosis (lips, fingertips,
6. Prevent infection nail clubbing)
a. Handwashing NURSING DIAGNOSIS
b. Universal precaution – avoid crowd places 1. Ineffective airway clearance
c. Avoid sick people 2. Ineffective breathing pattern
d. Vaccination – influenza / pneumococcal vaccine 3. Impaired gas exchange
7. Treat infection – anti-infective drugs 4. Fatigue/Activity intolerance
8. Support lung function 5. Ineffective peripheral tissue perfusion
a. Bronchodilators – oral / parenteral DIAGNOSTIC TESTS
b. Steroids – decrease the swelling of the bronchioles 1. CXR – Pneumonia 3. Pulse Ox – low O2 sat
c. Anti-asthma drugs – Leukotriene receptor antagonists 2. ABG – Resp acidosis
Ex: Montelukast – given bedtime MANAGEMENT:
d. Mechanical ventilator 1. Position – orthopneic
9. Prevent another attack 2. Bronchodilator – inhalation
a. Avoid allergens 3. O2 administration – low flow
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 4. Promote rest 2. ABG – respiratory acidosis
5. Promote safety 3. Pulse ox – low O2 sat
6. Prevent infection 4. Spirometry – dec ERV, inc FRC, inc RV, inc TLC
7. Treat infection MANAGEMENT:
8. Most prominent clinical manifestation – cough à inc fluid intake 1. Position: orthopneic
9. Chest physiotherapy chest vibration/ chest tapping 2. Bronchodilator – inhalation
10. Postural drainage – to facilitate removal of the mucus 3. O2 administration – low flow
11. Suction secretion 4. Promote rest
12. Support lung function 5. Promote safety
a. Bronchodilators 6. Prevent infection
b. Steroid 7. Treat infection
c. Mechanical ventilator 8. Prominent dyspnea – teach pursed lip breathing, inhale through
13. Slow down progression the nose and exhale through the mouth
a. Avoid smoking Rationale: to prolong expiration, to prevent collapse of the
b. Avoid infection alveoli, to promote gas exchange, to promote carbon dioxide
c. Avoid fatigue elimination, to maintain, to keep the alveoli open, to strengthen
14. Prevent complications resp muscles
a. Pneumonia 9. Support lung function
b. Acute Respiratory Failure a. Bronchodilators c. Mechanical ventilator
Basis: ABG (pCO2 >50 ; pO2 <50) b. Steroids
c. Bronchiectasis – permanent dilatation and destruction of 10. Slow down progression
bronchi & bronchioles a. Avoid smoking c. Avoid fatigue, stress
Etio: Repeated bacterial infection b. Avoid infection
S/Sx – chronic inflammation, productive cough with sputum 11. Prevent complications
(yellowish, green, rusty) a. Pneumonia
(+) halitosis b. ARF
15. Bronchodilators c. Pneumothorax – air in the pleural space
16. Mechanical ventilator (close/simple/spontaneous P)
d. Polycythemia (secondary)
EMPHYSEMA – “PINK PUFFERS” e. Pulmonary Hypertension
– overdistention & destruction of alveolar wall f. Cor Pulmonale
Etiology: g. Right sided heart failure
1. Environmental pollutants (smoking) PULMONARY HYPERTENSION
2. Alpha 1 antitrypsin deficiency à short expiratory phase à - increase in pulmonary arterial pressure >30 mmHg
collapse of alveolar wall à air trapping à DYSPNEA à use of - Mean pulmonary arterial pressure > 15 mmHg
accessory muscles à hypertrophy of muscles à hyperinflation of - N: 25/9mmHg
the lungs à barrel chest a. Primary – idiopathic
Impaired gas exchange, Chronic hypoxemia/hypercapnea à b. Secondary – known causes: COPD, pulmonary embolism,
erythropoietin release à erythrocytosis à flushing of face kyphoscoliosis, morbid obesity
– substance that protects the alveolar wall from hydrolytic
enzymes COPD à chronic hypoxemia à pulmonary vasoconstriction à
3. Chronic asthma pulmonary hypertension à S/Sx – dyspnea, tachypnea, fatigue,
DIAGNOSTIC TEST: weakness, tachycardia, palpitations, syncope (fainting)
1. Chest X-ray – barrel chest/pneumonia
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*enlargement or distention of the RV à cor pulmonale à increase
venous pressure à bipedal edema à Right sided heart failure à soon
LV will also be affected
PULMONARY HEART DISEASE
a. Pulmonary hypertension
b. Cor pulmonale
c. R sided heart failure

IAPP
Inspection – symmetrical/equal chest expansion
Auscultate
- Abnormal breath sounds
crackles/rales – fluid inside the alveoli
alveoli
wheezing – bronchospasm
stridor
ronchi
Palpate – apex
Percussion
- Lungs – resonant
- Heart – dull

RESTRICTIVE LUNG DISEASE

PLEURAL EFFUSION
PNEUMOTHORAX

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