gagal napas .ppt
TRANSCRIPT
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Focus onRespiratory Failure
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Acute Respiratory Failure
Results from inadequate gas
exchange
Insufficient O2transferred to the blood Hypoxemia
Inadequate CO2removal
Hypercapnia
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Gas Exchange Unit
Fig. 68-1
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Acute Respiratory Failure
Not a disease but a condition
Result of one or more diseases
involving the lungs or other bodysystems
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Acute Respiratory Failure
Classification
Hypoxemic respiratory failure
Hypercapnic respiratory failure
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Classification of Respiratory
Failure
Fig. 68-2
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Acute Respiratory Failure
Hypoxemic respiratory failure
PaO260%
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Acute Respiratory Failure
Hypercapnic respiratory failure
PaCO2above normal ( >45 mm Hg)
Acidemia (pH
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Range of V/Q Relationships
Fig. 68-4
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Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes
Ventilation-perfusion (V/Q) mismatch
COPD
Pneumonia
Asthma
Atelectasis
Pulmonary embolus
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Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes
Shunt
Anatomic shunt Intrapulmonary shunt
An extreme V/Q mismatch
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Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes
Diffusion limitation
Severe emphysemaRecurrent pulmonary emboli
Pulmonary fibrosis
Hypoxemia present during exercise
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Diffusion Limitation
Fig. 68-5
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Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes
Alveolar hypoventilation
Restrictive lung diseaseCNS disease
Chest wall dysfunction
Neuromuscular disease
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Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Interrelationship of mechanisms
Combination of two or more
physiologic mechanisms
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Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Imbalance between ventilatory
supply and demand
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Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Airways and alveoli
Asthma
EmphysemaChronic bronchitis
Cystic fibrosis
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Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Central nervous system
Drug overdose
Brainstem infarctionSpinal chord injuries
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Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Chest wall
Flail chest
FracturesMechanical restriction
Muscle spasm
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Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Neuromuscular conditions
Muscular dystrophy
Multiple sclerosis
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Respiratory FailureTissue Organ Needs
Major threat is the inability of the
lungs to meet the oxygen demands of
the tissues
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Respiratory FailureClinical Mani festations
Sudden or gradual onset
A sudden decrease in PaO2or rapid
increase in PaCO2indicates a seriouscondition
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Respiratory FailureClinical Mani festations
When compensatory mechanisms
fail, respiratory failure occurs
Signs may be specific or nonspecific
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Respiratory FailureClinical Mani festations
Severe morning headache
Cyanosis
Late sign
Tachycardia and mild hypertension
Early signs
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Respiratory FailureClinical Mani festations
Consequences of hypoxemia and
hypoxia
Metabolic acidosis and cell deathDecreased cardiac output
Impaired renal function
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Respiratory FailureClinical Mani festations
Specific clinical manifestations
Rapid, shallow breathing pattern
Tripod positionDyspnea
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Respiratory FailureClinical Mani festations
Specific clinical manifestations
Pursed-lip breathing
RetractionsChange in I:E ratio
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Respiratory FailureDiagnostic Studies
History and physical assessment
ABG analysis
Chest x-rayCBC, sputum/blood cultures, electrolytes
ECG
UrinalysisV/Q lung scan
Pulmonary artery catheter (severe cases)
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Acute Respiratory Failure
Nursing Assessment
Health information
Health history
Medications
Surgery
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Acute Respiratory Failure
Nursing Assessment
Functional health patterns
Health perceptionhealth management
Nutritional-metabolic
Activity-exercise
Sleep-rest
Cognitive-perceptual
Copingstress tolerance
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Acute Respiratory Failure
Nursing Assessment
Physical assessment
General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal
Neurologic
Laboratory findings
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Acute Respiratory Failure
Nursing Diagnoses
Impaired gas exchange
Ineffective airway clearance Ineffective breathing pattern
Risk for fluid volume imbalance
Anxiety
Imbalanced nutrition: Less than body
requirements
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Acute Respiratory Failure
Planning: Overall goals
ABG values within patient
s
baseline
Breath sounds within patient
s
baseline
No dyspnea or breathing patternswithin patient
s baseline
Effective cough and ability to clear
secretions
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Acute Respiratory Failure
Prevention
Thorough history and physical
assessment to identify at-risk
patients
Early recognition of respiratory
distress
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Acute Respiratory Failure
Respiratory therapy
Oxygen therapy: Delivery system
should
Be tolerated by the patient
Maintain PaO2at 55 to 60 mm Hg or
more and SaO2at 90% or more atthe lowest O2concentration possible
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Acute Respiratory Failure
Respiratory therapy
Mobilization of secretions
Hydration and humidificationChest physical therapy
Airway suctioning
Effective coughing and positioning
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Augmented Cough
Fig. 68-6
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Acute Respiratory Failure
Respiratory therapy
Positive pressure ventilation (PPV)
Noninvasive PPVBiPAP
CPAP
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Noninvasive PPV
Fig. 68-7
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Acute Respiratory Failure
Drug Therapy
Relief of bronchospasm
Bronchodilators
Reduction of airway inflammation
Corticosteroids
Reduction of pulmonary congestion Diuretics, nitrates if heart failure present
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Acute Respiratory Failure
Drug Therapy
Treatment of pulmonary infections
IV antibiotics
Reduction of severe anxiety, pain, andagitation
Benzodiazepines
Narcotics
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Acute Respiratory Failure
Nutritional Therapy
Maintain protein and energy stores
Enteral or parenteral nutritionNutritional supplements
A i i
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Acute Respiratory Failure
Medical Supportive Therapy
Treat the underlying cause
Maintain adequate cardiac output andhemoglobin concentration
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Acute Respiratory FailureGerontologic Considerations
Physiologic aging results in
Ventilatory capacity
Alveolar dilationLarger air spaces
Loss of surface area
Diminished elastic recoilDecreased respiratory muscle strength
Chest wall compliance
A i i
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Acute Respiratory FailureGerontologic Considerations
Lifelong smoking
Poor nutritional status
Less available physiologic reserveCardiovascular
Respiratory
Autonomic nervous system