Respiration muscles, skin, color, and rate, and depth &

- Function: GAS EXCHANGE rhythm of respiration

- The process of gas exchange between atmospheric - Palpation
air and the blood at the alveoli, and between the - Percussion
blood cells and the cells of the body. o resonant
- Exchange of gases occurs because of differences in - Auscultation
partial pressures.
- Oxygen diffuses from the air into the blood at the DIAGNOSTIC TESTS
alveoli to be transported to the cells of the body. - Chest x-ray
- Carbon dioxide diffuses from the blood into the air - Thoracic cage x-ray (scoliosis) – rib xray
at the alveoli to be removed from the body - Ct scan
- MRI
Brain stem - ABG
- Respiratory center - Pulse oximetry
- Stimuli - Spirometry
- Increase PCO2 = normal
- Decrease PCO2 = COPD LUNG VOLUMES
- Neuromuscular: innervated by nerves (phrenic Tidal volumes
nerve) (SCI, Neuromuscular disorder – MG, GBS, - The volume of air inhaled and exhaled with normal
ALS) quiet breathing
- Lungs & thoracic cage - 500 ml

 Ventilation and perfusion should be normal Inspiratory reserve volume

- The maximum volume that can be inhaled following
Ventilation a normal quiet inhalation.
- The movement of air in and out of the airways - 3000 ml

Perfusion Expiratory reserve volume

- The blood flow to tissues and organ - The maximum volume that can be inhaled following
a normal quiet inhalation
Inspiration - 1300 ml
- Active process.
- contraction of the diaphragm (movement of this Dead space volume / anatomic dead space
chamber floor downward) and contraction of the - That does not participate in gas exchange
external intercostal muscles increases the space in - 150 ml
this chamber. lowered intrathoracic pressure causes
air to enter through the airways and inflate the Physiologic dead space
lungs. - Diseased alveoli

Expiration Residual Volume

- passive process - The volume of air that remains in the lungs after
- with relaxation, the diaphragm moves up and forceful exhalation
intrathoracic pressure increases. this increased - 1200 ml
pressure pushes air out of the lungs. expiration
requires the elastic recoil of the lungs. Functional Volume
- Actuality participates in gas exchange
** Inspiration normally is 1/3 of the respiratory cycle - 350 ml
and expiration is 2/3. Normal: 12 – 20 cpm
Lung Capacity
ASSESSMENT OF RESPIRATORY SYSTEM - Combination of volumes
- Inspection
o Posture, shape, movement, dimensions of 1. Functional Residual Capacity (ERV 1300 mL + RV
chest, flared nostrils, use of accessory 1200 mL = 2500 mL)
 a. The volume of air that remains in the lungs - Spirometry: increase FRC, dec ERV, inc RV
after normal, quiet exhalation - Peak flow meter
2. Inspiratory Capacity (TV 500 mL + IRV 3000 mL = o FEV1 (force expiratory volume in 1 second)
3500 mL)
a. The amount of air that a person can inspire management:
maximally after a normal expiration - Orthopneic position / tripod position/ leaning
3. Vital capacity (IRV 3000 mL + TV 500 mL + ERV 1300 forward
mL = 4800 mL) - Bronchodilator – inhalation
a. The maximum volume of air that can be - O2 administration
exhaled after a maximum inhalation - Provide rest
b. Reduced in COPD - Promote safety
4. Total Lung Capacity (IRV 3000 mL + TV 500 mL + - Prevent infections – anti-infective drugs
ERV 1300 mL + RV 1200 mL = 6000 mL) - Support lung function
a. Total of all four volumes o Bronchodilators
 Xanthines derivatives ex.
Theophylline, aminophylline
RESPIRATORY DISORDERS  Sympathomimetic bronchodilators
ex. Salbutamol, albuterol
OBSTRUCTIVE LUNG DISEASES  Tachycardia, palpitation, tremors
 Anticholinergic bronchodilators –
Bronchial Asthma inhalation only ex. Ipratropium,
- Bronchospasm tiotropium
- Reversible, non-progressive inflammatory lung o Steroids: decreased the swelling
condition caused by hypersensitivity to allergens o Leukotriene receptor antagonist – stop
leading to narrowing of smaller airway bronchospasm ex. Montelukast (before
bedtime)
EXTRINSIC ASTHMA INTRINSIC ASTHMA o Mechanical ventilation: status asthmaticus
Atopic/Allergic Asthma IDIOPATHIC – prolonged asthma attack despite the usual
Allergens – proteins that treatment
stimulate antibody - Prevent and manage complications
formation o Status asthmaticus
Antigen antibody reaction o Acute respiratory failure (ABG = Po2 <50;
will induce inflammation PCO2 >)
Inflammation of the o Infection – Pneumonia
bronchioles o Emphysema
Histamine Leukotriene - Prevent an attack
Swelling of Bronchospasm o Avoid allergens
bronchiole (expiration) o Prophylaxis: mast cell stabilizers ex:
s cromolyn sodium and nedocromil
Goblet cell wheezing
swell COPD
Increase - Irreversible and progressive
mucus - Chronic bronchitis: chronic inflammation of the
production bronchioles, the presence of cough and mucus
cough production for at least 3 months for 2 consecutive
Airway obstruction years
dyspnea - Emphysema: impaired gas exchange resulting from
destruction of the walls of overdistended veins
Diagnostic test:
- chest x-ray (hyperinflated lungs – air trapping) CHRONIC BRONCHITIS
- ABG: Initial (respiratory alkalosis) Later (respiratory - Etiology: environmental pollutants / smoking
acidosis) - Blue bloaters
- Pulse ox: decrease 02 saturation
- Inflammation of the bronchi due to hypertrophy or - Overdistention of thoracic cavity (Barrel chest) 
hyperplasia of goblet mucous producing cells compensatory mechanism  increased AP
leading to narrowing of smaller airways diameter

Pathophysiology of Chronic Bronchitis Etiology:

- Environmental pollutants  injury to the - Environment pollutants: smoking
bronchioles  inflammation of the bronchioles - Chronic asthma
(>6months / permanent, irreversible, and - Hereditary: involves alpha-1 antitrypsin  for
progressive)  swelling of the bronchioles elastase production  for recoil of the alveoli
(hypertrophy of goblet cells, increase mucus
production = COUGH) smoking  followed by short expiratory phase 
collapse of alveolar wall  air trapping  DYSPNEA 
Diagnostic test: overused of accessory muscles  hypertrophy of
- chest x-ray (pneumonia) muscles  hyperinflation of lungs  BARREL CHEST
- ABG: respiratory acidosis
- Pulse ox: decrease 02 hypoxemia  inc. erythropoietin release  inc.RBC 
polycythemia  flushing of face  PINK puffer
Management:
- Position: Orthopneic position / tripod position/ Signs and Symptoms:
leaning forward - Productive cough
- Bronchodilator – inhalation - Dyspnea at rest
- O2 administration – low inflow 02 admin; high flow - Prolonged expiratory grunt
will cause respiratory arrest - Resonance to hyperresonance
- Provide rest - Decreased tactile fremitus
- Promote safety - Decreased breath sounds ( if (-) BS  lung collapse)
- Prevent infections – anti-infective drugs - Barrel chest
- Manage cough - Anorexia and generalized body malaise
o Increase fluid intake - Rales or crackles
o Chest physiotherapy - Alar flaring
o Postural drainage – before eating; oral care - Pursed-lip breathing (to eliminate excess CO2)
o Suction secretions
- Support lung function Diagnostic Test:
o Bronchodilators - CXR – barrel chest, Pnuemonia
o Steroids - Decreased o2 sat
o Mechanical ventilator - ABG: respiratory acidosis
- Prevent and manage complications - Spirometry: dec ERV, inc. RV, inc. FRC, inc. TLC
o Pneumonia
o Acute respiratory failure Management:
o Bronchiectasis – dilatation and destruction - Position: Orthopneic position / tripod position/
of bronchi and bronchioles leaning forward
o Etiology: repeated bacterial infection, foul - Bronchodilator – inhalation
smelling, yellowing, greenish, rusty, halitosis - O2 administration – low inflow 02 admin; high flow
– bad breath will cause respiratory arrest
- Provide rest
PULMONARY EMPHYSEMA - Promote safety
- terminal and irreversible stage of COPD - Prevent infections – anti-infective drugs
characterized by: - Manage dyspnea
- Inelasticity of alveoli o Pursed lip breathing: to prolong expiration
- Air trapping  prevent collapse  promote CO2
- Maldistribution of gasses (d/t increased air elimination  promote gas exchange 
trapping) keep airway open
o Strengthen respiratory muscle
- Prevent and manage complications
- Slow down progression - hematologic disorders (disseminated intravascular
o Avoid smoking, fatigue, infections coagulopathy, massive transfusions,
cardiopulmonary bypass)
Complications: - prolonged inhalation of high concentration of
- Pneumonia: fluid inside the alveoli oxygen, smoke or corrosive substances
- Pneumothorax: rupture of bleb or bullae - localized infection (bacterial, fungal, viral
- Close: simple or spontaneous pneumonia)
- Open - Metabolic disorders (pancreatitis, uremia)
- Traumatic - Shock (any cause)
- Tension - Trauma (pulmonary contusion, multiple fractures,
head injury)
S/Sx: - Major surgery
- dsypnea, tachypnea, chest pain/back pain Same - Fat or air embolism
as pleural effusion sound of percussion: - Systemic sepsis
HYPERRESSONANT OR TYMPANIC
Diagnostic Test
Management: - Chest x-ray
- CTT or 1 way bottle system - BNP *brain natriuretic peptide* level in the blood
- Erythrocytosis/polycthemia - Pulmonary artery catheterization
- Increase RBC production - Transthoracic echocardiography (check function of
- Flushing of face = pink puffer lungs)
- Pulmonary hypertension: increase pulmonary
pressure (normal: 25/9) Management: - Palliative and supportive
- Primary: idiopathic - supportive
- Secondary: COPD, pulmonary embolism, morbid o mechanical ventilator
obesity, kyphoscoliosis o position: prone – 30 to 1hr change position
- Cor Pulmonale: distention of the right ventricle due o bronchodilators
to high blood pressure in the lungs usually cause by o steroids
chronic lung disease (pulmonary heart disease) = - IVF
systemic edema – lower extremities - nutrition
- Right sided heart failure - manage the cause

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) RESTRICTIVE LUNG DISEASES

Etiology: Severe form of acute lung injury
- Destruction of alveolocapillary membrane
- Destruction of alveolar type 2 cell
• Decrease surfactant – decrease surface
tension and prevent collapse of the alveoli
wall, pulmonary edema, atelectasis
- Characterized by a sudden and progressive
pulmonary edema, increasing bilateral infiltrates on
chest x-ray, hypoxemia unresponsive to oxygen
supplementation regardless of the amount of PEEP,
and the absence of an elevated left atrial pressure.
- Reduced Lung compliance
• Elastic
• Stretchable
• distensible
Causes
- aspiration (gastric secretions, drowning,
hydrocarbons)
- drug ingestion and overdose
- Flail chest: trauma to the chest  multiple rib
fracture
- air enters pleural space during inspiration and
cannot escape leading to overdistention of the
thoracic cavity  mediastinal shift to the affected
side (ie. Flail chest)  paradoxical breathing
s/sx:
- paradoxical breathing, dyspnea, chest pain,
tachypnea
Management:
- ventilatory support
- clearing of secretions
- managing pain
- endotracheal intubation and mechanical ventilation
provide pneumatic stabilization
- surgery: open reduction
PLEURAL EFFUSION
- accumulation of fluid in the plural space
- hydrothorax
- primary: Idiopathic
- secondary: infection, pneumonia, tb, malignancy

s/x
- dyspnea, tachypnea, chest/back pain inspiration,
asymmetrical chest expansion, unequal tactile and
vocal fremitus, diminished/absent breath sound
(auscultate), flat to dull (percussion)

diagnostic test:
- chest x-ray (most definitive test)

management:
- thoracentesis
- pleurodesis: procedure that sticks your lung to your
chest wall. This procedure removes the space
between your lung and your chest wall (pleural
space) so that fluid or air no longer builds up
between the layers.

THORACENTESIS
- Position the patient seated on the edge of the bed
- Ultrasound guided