1. Invasive Mechanical Ventilation
Weaning Intolerance Indicators (Box 16-1)
Decreased LOC
SBP increased or decreased by 20 mmHg
DBP > 100 mmHg
HR increased by 20 beats/min
Resp. rate increase by 10/min (> 30 or < 10)
Use of accessory muscles
PaCO2 increase of 5-8 &/or pH < 7.3
SpO2 < 90%
Assess NIF, and spontaneous TV
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2. Noninvasive Mechanical Ventilation
Advantages
Decreased incidence of nosocomial pneumonia
Increased comfort
More efficient delivery of preset tidal volume
Nursing Management
Assessment and patient compliance
Properly fitted mask
Skin integrity
Head of bed elevated 45 degrees to prevent aspiration
Avoid sedation
VAP and VAP precautions
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3. Acute Respiratory Failure
Description
Acute Respiratory Failure abbreviated as ARF
A clinical condition where the pulmonary system fails to maintain adequate gas exchange
Mortality rate of 22% - 75%
May be classified as: Type I or Type II
Type I: Low PaO2 and Normal PaCO2
Type II: Low PaO2 and High PaCO2
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4. Acute Respiratory Failure(P. 285)
Pathophysiology of Type I ARF
Hypoxemia is a hallmark sign caused by:
Alveolar hypoventilation – ventilation to alveoli is insufficient d/t ↑ metabolic O2 needs or ↓ ventilation (extrapulmonary disorders)
Ventilation / Perfusion (V/Q) mismatching – blood, passing through under ventilated alveoli, leaves without adequate O2
Intrapulmonary shunting – extreme form of V/Q mismatching; blood reaches the arterial system w/out participating in gas exchange
Intrapulmonary shunting is the most extreme form of V/Q mismatch. Caused by alveolar collapse or alveolar flooding with pus, blood, or fluid
Type I is hypoxemic/normocapneic
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5. Acute Respiratory Failure
Complications
If the hypoxemia (blood) is not corrected, it will lead to hypoxia within the body cells
Tissue hypoxia develops because of the oxygen demand / supply imbalance
Low tissue oxygen can lead to lactic acidosis and place organs at major risk
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6. Acute Respiratory Failure
Nursing Management- maximize oxygenation
Positioning
Position patient to best match ventilation/ perfusion
Place least affected area of lung in a dependent position (healthy lung down) gravity and perfusion
If both lungs are equally affected, position with right (larger lung) down
Reposition every 2 hours
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7. Acute Respiratory Distress Syndrome (ARDS)
Description
Acute in onset (severe form of ALI-Acute Lung Injury)
Alveolar collapse due to damage to surfactant producing Type II cells
Ratio of PaO2 / FIO2 equal or below <200 mm Hg
Example:
PaO2 of 80 mm Hg receiving 70% (0.7) O2
80 divided by 0.7 = 114 mm Hg
Bilateral infiltrates on chest x-ray-differs for pulmonary edema
PAOP less or equal to 18 mm Hg
PAOP = pulmonary artery occlusion pressure
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10. Acute Respiratory Distress Syndrome (ARDS)
Etiology (Box 15-3) Pathophysiology Fig. 15-1) p.275
Direct Injury
Aspiration or inhalation injury
Near-drowning
Pneumonia
Indirect Injury
Sepsis
Severe pancreatitis
Embolism – air, fat
Shock
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11. Acute Respiratory Distress Syndrome (ARDS)
Medical Management
Ventilation
Assist Control or SIMV (traditional methods)
Permissive Hypercapnia
Smaller tidal volumes (5 - 8 ml/kg)
Pressure Control Ventilation (PCV)
Maintain plateau pressure < cm H2O
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13. Pneumonia Description Acute inflammation of the lung
Caused by an infectious agent
Can lead to alveolar consolidation
May be classified by where or how contracted:
Community acquired pneumonia (CAP)
Hospital acquired pneumonia (HAP)
Ventilator associated pneumonia (VAP)
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14. Pulmonary Embolism (PE)
Etiology (Box 15-3, p. 301)
Hypercoagulability
Venous stasis
Injury to vascular endothelium
Atrial fibrillation
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15. Status Asthmaticus Description
Asthma a chronic obstructive airways disease with:
Partially reversible airflow obstruction
Airway inflammation
Hyper-responsiveness to a variety of stimuli
Status asthmaticus is a SEVERE asthma attack that fails to respond to conventional therapy and can result in acute respiratory failure
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