Acute Respiratory failure

1. NCM 106: ACUTE BIOLOGIC CRISIS
Acute Respiratory Failure

3. Respiratory Failure
It is a sudden and life-threatening
deterioration of the gas
exchange function of the lungs.
Indicates failure of the lungs to
provide adequate oxygenation
or ventilation for the blood.

4. Acute Respiratory Failure
Conditions:
1. Hypoxemia
- decrease in arterial oxygen tension
(PaO2) to less than 50 mmHg
2. Hypercapnia
- increase in arterial carbon dioxide
tension (PaCO2) to greater than 50
mmHg
3. Arterial pH of less than 7.35.

5. Causes of Respiratory Failure
Site Examples
Respiratory centre (CNS) Depressant drugs, opiates; traumatic and
ischemic lesions
Loss of respiratory sensitivity to CO2
Spinal cord and peripheral
nerves
Spinal injury, Guillain Barre, poliomyelitis
Neuromuscular junction Myasthenia, neuromuscular blocking drugs
Muscle Myopathies, respiratory muscle fatigue in
COPD
Pleura and thoracic cage Flail chest, pneumothorax, hemothorax
Deformities, trauma (e.g. rib fractures), loss of
optimal shape due to chronic lung
hyperinflation
Airways Extrathoracic: foreign bodies, croup
Intrathoracic: asthma, bronchiolitis, bronchitis
Gaseous exchange Emphysema, pulmonary edema, ARDS,
pneumonia
Lung vasculature Pulmonary embolus, ARDS

8. Classification:
A. Hypoxemic respiratory failure (type I) a PaO2 of
less than 60 mm Hg with a normal or low
PaCO2.
-Generally involves fluid filling or collapse of
alveolar units.
Examples:
1. cardiogenic or noncardiogenic pulmonary
edema
2. Pneumonia
3. Pulmonary hemorrhage

9. Pathophysiology: Hypoxemic Respiratory Failure
V/Q mismatch intrapulmonary/ intracardiac
shunt
↓ ↓
low ventilation mixing of venous
(deoxygenated) blood
↓
bypassing of ventilated alveoli
↓ ↓
venous admixture
↓
Widening of the alveolar-arterial oxygen difference
↓
Hypoxemia

10. Pathophysiology
A. Ventilation-Perfusion Mismatch
‰1. Vascular obstruction
„ Pulmonary embolism
‰2. Air-space consolidation
„ Pneumonia, Pulmonary edema
† 3. Airway obstruction
„ Asthma, COPD
† 4. Diffuse parenchymal lung diseases
„
Interstitial lung disease

11. Pathophysiology
‰
B. Shunt:
Blood pathway which does not allow contact between
alveolar gas and red blood cells
‰
Abnormal shunting:
„ a. Congenital defects in the heart or vessels ASD,
VSD, Pulmonary AVM
„ b. Lung atelectasis or consolidation ,Pneumonia,
Cardiogenic or Non-cardiogenic
pulmonary edema
‰
Shunt (right-to-left shunt)
Resistant to O2 supplementation when shunt
fraction of CO > 30%

12. ‰
Etiologies of Shunt physiology
• „Diffuse alveolar filling
• „Collapse / Consolidation
• „Abnormal arteriovenous channels
• „Intracardiac shunts
Hallmark of shunt is poor or no response to O2 therapy
‰
Shunt can lead to hypercapnia when there is
more than 60% of the cardiac output and
‰
ventilatory compensation fails
• ‰
↑RR → Increased dead space
• ‰
↓ total alveolar ventilation
• ‰
Respiratory muscle fatigue

13. Classification:
B. Hypercapnic respiratory failure (type II)
- characterized by a PaCO2 of more than 50 mm Hg.
- Common in patients with hypercapnic respiratory failure
who are breathing room air.
- The pH depends on the level of bicarbonate, which, in
turn, is dependent on the duration of hypercapnia.
Common causes:
1. Drug overdose
2. Neuromuscular disease
3. Chest wall abnormalities
4. Severe airway disorders- COPD

15. Pathophysiology
Decreased functional components of the respiratory system
and CNS
↓
Reduction in overall (minute) ventilation / increase in the
proportion of dead space ventilation
↓
Decrease in alveolar ventilation
↓
Increased work of breathing

16. 1. Decreased minute ventilation
† CNS disorders
„ Stroke, brain tumor, spinal cord lesions,
drug overdose
† Peripheral nerve disease
„ Guillain-Barre syndrome, botulism,
myasthenia gravis
† Muscle disorders
„ Muscular dystrophy, respiratory muscles
fatigue

17. Chest wall abnormalities
„ Scoliosis, kyphosis, obesity
† Metabolic abnormalities
„ Myxedema, hypokalemia
Airway obstruction
Upper airway obstruction, Asthma,
COPD

18. 2. Increase dead space- Increased RR
† a. Airway obstruction
„ Upper airway obstruction
„ Asthma, COPD
„ Foreign body aspiration
† b. Chest wall disorder
„ Kyphoscliosis, thoracoplasty

19. 3. Increase CO2 production
† a. Fever, sepsis, seizure, obesity, anxiety
† b. Increase work of breathing (asthma,
COPD)
† c. High carbohydrate diet with underlying
lung disease

20. Diagnostic Tests:
• Arterial blood gases
• Complete blood count
• Chemistry panel – renal and hepatic function
• Creatine kinase with fractionation and
troponin I
• Chest radiograph
• Echocardiography
• ECG

21. Clinical Manifestations:
• Early signs: Impaired oxygenation
- restlessness
- fatigue
- headache
- dypnea
- air hunger
- tachycardia
- increased blood pressure

22. Clinical Manifestations:
• Disease progression: Hypoxemia
- confusion
- lethargy
- tachycardia
- tachypnea
- central cyanosis
- diaphoresis
- respiratory arrest
• Use of accessory muscles
• Decreased breath sounds

23. Medical Management:
Objectives of treatment:
To correct the underlying cause.
To restore adequate gas exchanges in the lungs.
1. Intubation
2. Mechanical ventilation

24. Nursing Management:
1. Assist in airway management
a. The mode of ventilation should be suited to
the needs of the patient. Ventilator settings
should be adjusted based on the patient's lung
mechanics, underlying disease process, gas
exchange, and response to mechanical
ventilation.
b. Supplemental oxygen is administered via
nasal prongs or face mask. In patients with
severe hypoxemia, intubation and mechanical
ventilation are often required.

25. Nursing Management:

26. Nursing Management:
*The lowest FiO2 that produces an SaO2 greater
than 90% and a PaO2 greater than 60 mm Hg
generally is recommended.
Maintain a PaO2 sufficient to give an arterial Hb
saturation of at least 85%.
Hyperoxia should be avoided, particularly in the
bronchitic who is a CO2 retainer and dependent
on hypoxic ventilatory drive.

27. Nursing Management:
2. Repeated assessments should be done, which
may range from bedside observations to
monitorings (ABGs, Pulse oximetry, VS and
responsiveness)
3. Constant monitoring in a critical care setting is a
must.
4. After the patient's hypoxemia is corrected and
the ventilatory and hemodynamic status have
stabilized, every attempt should be made to
identify and correct the underlying
pathophysiologic process that led to respiratory
failure.

28. Nursing Management:
5. Implement strategies such as turning schedule,
mouth care, skin care and range of motion
activities.
6. Assess patient’s understanding of the
management strategies that are done.
7. Assess if patient is able to initiate some form of
communication to enable the patient to express
concerns and needs to the health care team.
8. Assess patient’s knowledge of the underlying
disorder and provide teaching appropriately.

29. NCM 106 Lecture Series:
Acute Respiratory Failure