Includes :

1. Airways

2. Lungs – responsible
for gas exchange
3. Respiratory
muscles
Functions:
1.Oxygen
transport
2.Respiration
3.Ventilation
4.Gas exchange
 Gas Exchange
- a major function of the respiratory
Gas system
- occurs at the alveoli
Exchange - facilitates oxygenation of the blood
and removal of CO2 and other
gaseous metabolic wastes from
the circulation
Gas
exchange
METABOLIC AND ENDOCRINE FUNCTION OF THE
LUNGS

1. manufacture surfactant
- a fluid that lines the
alveoli and bronchioles

2. contains fibrinolytic system

3. release substances that enters the

systemic arterial blood
ACUTE RESPIRATORY
FAILURE

- a sudden and life-threatening deterioration of the gas

exchange function of the lung and indicates failure of
the lungs to provide adequate oxygenation or
ventilation for the blood

PaO2 - less than 60mm Hg (hypoxemia)

PaCO2 - greater than 50 mm Hg (hypercapnia)
pH - less than 7.35
 ACUTE RESPIRATORY
FAILURE

Causes

1. Impaired ventilation

2. Impaired gas exchange

3. Airway obstruction

4. Ventilation-perfusion abnormalities
 A. IMPAIRED VENTILATION
- conditions that disrupts the muscle of
respirations or their neurologic control
Musculoskeletal
Neuromuscular
Pulmonary Impaired CNS
Impaired ↓ movement of gas
dysfunction:dysfunction: function:
respiratory muscle into the lungs
- Chest trauma,
- MG,
COPD,GBS, - Drug
ALS,
movement
kyphoscoliosis,
spinal
asthma, cystic overdose, head
cord
malnutritiontrauma
fibrosis trauma,
- hemorrhage,
CO2 retention and sleep apnea
hypoxemia hypoventilation
 B. IMPAIRED GAS EXCHANGE
- conditions that damage the alveolar-
capillary membrane
Causes: ( Pneumonia)
1. increase alveolar permeability
↓
increases the potential for interstitial
fluid to leak into the alveoli
↓
noncardiac pulmonary edema
Causes:
2. decrease in surfactant production
↓
- increase alveolar surface tension
↓
alveolar collapse
↓
hypoxia
 Causes:
3. fluid leaks from intravascular
space to the pulmonary interstitial
space (excess fluid)
↓
- increases the distance between the
alveolus and the capillary
↓
- decrease efficiency of gas exchange
process
↓
hypoxia
C. AIRWAY OBSTRUCTION
Causes:
- conditions that obstruct
1. block on inner airway
airways increase resistance to
lumen
airflow into the lungs
2. increase airway wall
↓ thickness
hypoventilation and 3. peribronchial
↓ gas exchange compression of the airway
↓
hypoxia
D. VENTILATION-PERFUSION
ABNORMALITIES
- conditions disrupting alveolar
ventilation or capillary perfusion
↓
decreases the efficiency of
respiratory gas exchange process
↓
inadequate CO2 removal, O2
absorption, or both
 SIGNS AND SYMPTOMS
Early signs:
1. Restlessness As hypoxemia progresses….
2. Fatigue 1. Confusion
3. Headache 2. Lethargy
3. Tachycardia
4. Dyspnea
4. Tachypnea
5. Air hunger 5. Central cyanosis
6. Tachycardia 6. Diaphoresis
7. Increased BP 7. Resp arrest
Diagnostic Tests
1. ABG
Ph ≤ 7.30
PaO2 ≤ 60mmhg
PaCO2 ≥ 50mmhg
MANAGEMENT

Goal
1. improving oxygenation and
ventilation
2. treating the underlying disease
state
3. reducing anxiety
4. preventing and managing
complications
 IMPROVING OXYGENATION
AND VENTILATION
1. Provide supplemental O2

2. Improve ventilation:
a. Bronchodilators,
b. mucolytics
c. other airway
modalities
3. Intubate and initiate mechanical
ventilation

4. Suctioning

5. Verify adequacy of ventilatory support

equipment during transport
Treating the underlying
disease state
- correction of the underlying
cause must be done ASAP
 REDUCING ANXIETY
1. Maintain a calm, supportive
environment

2. Teach diaphragmatic breathing

3. Administer mild doses of anxiolytics

PREVENTING AND MANAGING
COMPLICATIONS
1. Pulmonary aspiration

2. GI bleeding
3. Barotrauma
- rupture of the lung after
forceful exhalation against a
close glottis
4. Volutrauma
- a lung damage caused
by overdistention by a mechanical
ventilator set for an excessively high
tidal volume (Vt)
1.
2.
3. Assess respiratory status
a. level of responsiveness
b. ABG
c. Pulse oximetry – O2 saturation
d. vital signs
Phases
One: injury reduces normal blood flow to the lungs; platelets aggregate
and release histamines, serotonins and bradykinins
Two: released substances inflame and damage the alveolar capillary
membrane increasing capillary permeability; fluids then shift into the
interstitial space
Three: capillary permeability increases and proteins and fluids leak
out, increasing interstitial osmotic pressure thus causing pulmonary
edema
Fourth: decreased blood flow and fluids in the alveoli damage
surfactant and impair the cell's ability to produce more; the alveoli then
collapse, hence impairing gas exchange
Fifth: oxygenation is impaired but CO2 easily crosses the alveolar
capillary membrane and is expired; blood O2 and CO2 are low;
pulmonary edema worsens and inflammation leads to fibrosis; gas
exchange is further impeded
-
Medical
Management
1. Identification and treatment of the underlying
cause
2. Supportive therapy
a. endotracheal intubation and mechanical
ventilation
3. Pharmacological therapy
4. Adequate fluid volume
5. Nutritional support
Nursing
Management
1. Frequent assessment of the patient’s status
2. oxygen administration
3. nebulizer therapy
4. chest physiotherapy
5. endotracheal intubation or tracheostomy
6. mechanical ventilation
7. suctioning
8. Positioning
9. Reduce patient’s anxiety
Risk Factors
1.congenital heart disease, Vascular injury
2. anorexigens (specific
appetite depressants)
3.chronic use of stimulants,
- vascular smooth muscle
4.portal hypertension
hypertrophy
5. HIV infection - adventitial and intimal
proliferation
- advanced vascular lesion
formation
Pathophysiology
Damaged pulmonary vascular
bed
right ventricular
Unable to handle whatever hypertrophy and
blood flow or volume it receives failure

increases the pulmonary artery

pressure
affect right
increase pulmonary vascular
ventricular function.
resistance
1. Manage the underlying conditions
2. Diuretics
3. Oxygen
4. Anticoagulant
5. Digoxin
6. Exercise
7. Lung transplantation
8. Atrial septostomy
ASSESSMENT AND DIAGNOSTIC
FINDINGS
End of topic!
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