Respiratory Failure

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Transcript Respiratory Failure

Acute Respiratory Failure
Respiratory System
• Consists of two parts:
• Gas exchange organ (lung): responsible for
OXYGENATION
• Pump (respiratory muscles and respiratory control
mechanism): responsible for VENTILATION
NB: Alteration in function of gas exchange unit
(oxygenation) OR of the pump mechanism (ventilation)
can result in respiratory failure
Normal Lung
Lung Anatomy
Normal Alveoli
Gas Exchange Unit
Fig. 66-1
Normal ABGs
• pH = 7.35-7.45
• CO2 = 35-45
• HCO3= 23-27
Respiratory and Metabolic
Acidosis and Alkalosis
• CO2 is an acid and is controlled by the
Respiratory (Lung) system
• HCO3 is an alkali and is controlled by the
Metabolic (Renal) system
• Respiratory response is immediate; Metabolic
response can take up to 72 hours to respond
(except in patients with COPD who are in a
constant state of Compensation!)
ABG Interpretation
Step 1:
Check the pH: Is it acidotic or alkalotic or
normal? pH below 7.35 is acidotic; pH
above 7.45 is alkalotic
If pH is normal, then the ABG is
compensated; if pH not normal, then the
ABG is uncompensated
ABG Interpretation (cont’d)
Step 2.
Check the CO2 and HCO3:

If the CO2 (acid) is above 45, the pt is
acidotic; if the CO2 is below 35, the pt is
alkalotic

If the HCO3 is above 27, the patient is
alkalotic; if the HCO3 is below 23, the patient
is acidotic
ABG Interpretation (cont’d)
Step 3
If the CO2 is high (above 45), then the patient is in
Respiratory Acidosis; if the CO2 is low (below
35), then the patients is in Respiratory Alkalosis.
If the HCO3 is high (above 27), then the patient is in
Metabolic Alkalosis; if the HCO3 is low (below
23), then the patient is in Metabolic Acidosis.
ABG Example #1
• pH = 7.36
• CO2 = 41
• HCO3 = 27
Diagnosis: ?
ABG Example #2
• pH = 7.49
• CO2 = 37
• HCO3 = 32
Diagnosis: ?
ABG Example #3
• pH = 7.29
• CO2 = 50
• HCO3 = 26
Diagnosis: ?
ABG Example #4
• pH = 7.40
• CO2 = 32
• HCO3 = 30
Diagnosis: ?
Acute Respiratory Failure
• Results from inadequate gas exchange
 Insufficient O2 transferred to the blood
• Hypoxemia
 Inadequate CO2 removal
• Hypercapnia
Acute Respiratory Failure
with Diffuse Bilateral
Infiltrates
Acute Respiratory Failure
• Not a disease but a condition
• Result of one or more diseases involving
the lungs or other body systems
• NB: Acute Respiratory Failure: when
oxygenation and/or ventilation is
inadequate to meet the body’s needs
Acute Respiratory Failure
• Classification:
– Hypoxemic respiratory failure (Failure
of oxygenation)
– Hypercapnic respiratory failure
(Failure of ventilation)
Classification of Respiratory Failure
Fig. 66-2
Acute Respiratory Failure
• Hypoxemic Respiratory Failure
– PaO2 of 60 mm Hg or less
(Normal = 80 - 100 mm Hg)
– Inspired O2 concentration of 60% or
greater
Acute Respiratory Failure
• Hypercapnic Respiratory Failure
– PaCO2 above normal (>45 mm Hg)
– Acidemia (pH <7.35)
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
• Causes:
– Ventilation-perfusion (V/Q) mismatch
– Shunt
– Diffusion limitation
– Alveolar hypoventilation
V-Q Mismatching
I) V/Q mismatch
• Normal ventilation of alveoli is comparable to
amount of perfusion
• Normal V/Q ratio is 0.8 (more perfusion than
ventilation)
• Mismatch d/t:
 Inadequate ventilation
 Poor perfusion
Range of V/Q Relationships
Fig. 66-4
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes V/Q mismatch
– COPD
– Pneumonia
– Asthma
– Atelectasis
– Pulmonary embolus
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
II) Shunt
– An extreme V/Q mismatch
– Blood passes through parts of respiratory
system that receives no ventilation
• d/t obstruction OR fluid accumulation
• Not Correctable with 100% O2
Diffusion Limitations
III) Diffusion Limitations
• Distance between alveoli and pulmonary
capillary is one- two cells thick
• With diffusion abnormalities: there is an
increased distance between alveoli (may
be d/t fluid)
• Correctable with 100% O2
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes Diffusion limitations
– Severe emphysema
– Recurrent pulmonary emboli
– Pulmonary fibrosis
– Hypoxemia present during exercise
Diffusion Limitation
Fig. 66-5
Alveolar Hypoventilation
IV) Alveolar Hypoventilation
• Is a generalized decrease in
ventilation of lungs and resultant
buildup of CO2
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
Causes Alveolar hypoventilation
– Restrictive lung disease
– CNS disease
– Chest wall dysfunction
– Neuromuscular disease
Hypoxemic Respiratory Failure
Etiology and Pathophysiology
• Interrelationship of mechanisms
– Hypoxemic respiratory failure is frequently caused
by a combination of two or more of these four
mechanisms
• Effects of hypoxemia
–
–
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Build up of lactic acid → metabolic acidosis → cell death
CNS depression
Heart tries to compensate → ↑ HR and CO
If no compensation: ↓ O2, ↑ acid, heart fails, shock, multisystem organ failure
Hypercapnic Respiratory Failure
Etiology and Pathophysiology
• Imbalance between ventilatory supply
and demand
• Occurs when CO2 is increased
Causes Hypercapnic
Respiratory Failure
I) Alveolar Hypoventilation and VQ
Mismatch:
– Ventilation not adequate to eliminate CO2
– Leads to respiratory acidosis
– Eg. Narcotic OD; Guillian-Barre, ALS, COPD,
asthma
Causes Hypercapnic
Respiratory Failure
II) VQ Mismatch:
- Leads to increased work of breathing
- Insufficient energy to overcome
resistance; ventilation falls; ↑PCO2;
respiratory acidosis
Hypercapnic Respiratory Failure
Categories of Causative
Conditions
• I) Airways and alveoli
– Asthma
– Emphysema
– Chronic bronchitis
– Cystic fibrosis
Hypercapnic Respiratory Failure
Categories of Causative
Conditions
• II) Central nervous system
– Drug overdose
– Brainstem infarction
– Spinal cord injuries
Hypercapnic Respiratory Failure
Categories of Causative
Conditions
• III) Chest wall
– Flail chest
– Fractures
– Mechanical restriction
– Muscle spasm
Hypercapnic Respiratory Failure
Categories of Causative
Conditions
• IV) Neuromuscular conditions
– Muscular dystrophy
– Multiple sclerosis
Respiratory Failure
Tissue Oxygen Needs
• Major threat is the inability of the lungs
to meet the oxygen demands of the tissues
Respiratory Failure
Clinical Manifestations
• Sudden or gradual onset
• A sudden  in PaO2 or rapid  in PaCO2
is a serious condition
Respiratory Failure
Clinical Manifestations
• When compensatory mechanisms fail,
respiratory failure occurs
• Signs may be specific or nonspecific
Respiratory Failure
Clinical Manifestations
• Severe morning headache
• Cyanosis
– Late sign
• Tachycardia and mild hypertension
– Early signs
Respiratory Failure
Clinical Manifestations
• Consequences of hypoxemia and hypoxia
– Metabolic acidosis and cell death
–  Cardiac output
– Impaired renal function
Respiratory Failure
Clinical Manifestations
• Specific clinical manifestations
– Rapid, shallow breathing pattern
– Sitting upright
– Dyspnea
Respiratory Failure
Clinical Manifestations
• Specific clinical manifestations
– Pursed-lip breathing
– Retractions
– Change in Inspiratory:Expiratory
ratio
Respiratory Failure
Diagnostic Studies
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Physical assessment
ABG analysis
Chest x-ray
CBC
ECG
Respiratory Failure
Diagnostic Studies
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Serum electrolytes
Urinalysis
V/Q lung scan
Pulmonary artery catheter (severe cases)
Acute Respiratory Failure
Nursing and Collaborative
Management
• Nursing Assessment
– Past health history
– Medications
– Surgery
– Tachycardia
Acute Respiratory Failure
Nursing and Collaborative
Management
• Nursing Assessment
– Fatigue
– Sleep pattern changes
– Headache
– Restlessness
Acute Respiratory Failure
Nursing and Collaborative
Management
• Nursing Diagnoses
– Ineffective airway clearance
– Ineffective breathing pattern
– Risk for imbalanced fluid volume
– Anxiety
Acute Respiratory Failure
Nursing and Collaborative
Management
• Nursing Diagnoses
– Impaired gas exchange
– Imbalanced nutrition: less than body
requirements
Acute Respiratory Failure
Nursing and Collaborative
Management
• Planning
– Overall goals:
• ABGs and breath sounds within
baseline
• No dyspnea
• Effective cough
Acute Respiratory Failure
Nursing and Collaborative
Management
• Prevention
– Thorough physical assessment
– History
Acute Respiratory Failure
Nursing and Collaborative
Management
• Respiratory Therapy
– Oxygen therapy
– Mobilization of secretions
• Effective coughing and positioning
Acute Respiratory Failure
Nursing and Collaborative
Management
• Respiratory Therapy
– Mobilization of secretions
• Hydration and humidification
• Chest physical therapy
• Airway suctioning
Acute Respiratory Failure
Nursing and Collaborative
Management
• Respiratory Therapy
– Positive pressure ventilation (PPV)
Acute Respiratory Failure
Nursing and Collaborative
Management
• Drug Therapy
– Relief of bronchospasm
• Bronchodilators
Acute Respiratory Failure
Nursing and Collaborative
Management
• Drug Therapy
– Reduction of airway inflammation
• Corticosteroids
Acute Respiratory Failure
Nursing and Collaborative
Management
• Drug Therapy
– Reduction of pulmonary congestion
• IV diuretics
Acute Respiratory Failure
Nursing and Collaborative
Management
• Drug Therapy
– Treatment of pulmonary infections
• IV antibiotics
Acute Respiratory Failure
Nursing and Collaborative
Management
• Drug Therapy
– Reduction of severe anxiety, pain, and
agitation
• Benzodiazepines
• Narcotics
Acute Respiratory Failure
Nursing and Collaborative
Management
• Medical Supportive Therapy
– Treat the underlying cause
– Maintain adequate cardiac output and
hemoglobin concentration
– Monitor BP, O2 saturation, urine
output
Acute Respiratory Failure
Nursing and Collaborative
Management
• Nutritional Therapy
– Maintain protein and energy stores
– Enteral or parenteral nutrition
– Supplements