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NCM 106: ACUTE BIOLOGIC CRISIS
Acute Respiratory Failure
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.
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.
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
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
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
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
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%
‰
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
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
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
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
Chest wall abnormalities
„ Scoliosis, kyphosis, obesity
† Metabolic abnormalities
„ Myxedema, hypokalemia
Airway obstruction
Upper airway obstruction, Asthma,
COPD
2. Increase dead space- Increased RR
† a. Airway obstruction
„ Upper airway obstruction
„ Asthma, COPD
„ Foreign body aspiration
† b. Chest wall disorder
„ Kyphoscliosis, thoracoplasty
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
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
Clinical Manifestations:
• Early signs: Impaired oxygenation
- restlessness
- fatigue
- headache
- dypnea
- air hunger
- tachycardia
- increased blood pressure
Clinical Manifestations:
• Disease progression: Hypoxemia
- confusion
- lethargy
- tachycardia
- tachypnea
- central cyanosis
- diaphoresis
- respiratory arrest
• Use of accessory muscles
• Decreased breath sounds
Medical Management:
Objectives of treatment:
To correct the underlying cause.
To restore adequate gas exchanges in the lungs.
1. Intubation
2. Mechanical ventilation
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.
Nursing Management:
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.
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.
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.
NCM 106 Lecture Series:
Acute Respiratory Failure

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Acute Respiratory failure.ppt

  • 1. NCM 106: ACUTE BIOLOGIC CRISIS Acute Respiratory Failure
  • 2.
  • 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
  • 6.
  • 7.
  • 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
  • 14.
  • 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.
  • 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