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Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

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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Not a disease but a condition

Result of one or more diseases

involving the lungs or other bodysystems


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Classification

Hypoxemic respiratory failure

Hypercapnic respiratory failure


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Classification of Respiratory

Failure

Fig. 68-2


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Hypoxemic respiratory failure

PaO260%




Hypercapnic respiratory failure

PaCO2above normal ( >45 mm Hg)

Acidemia (pH



Range of V/Q Relationships

Fig. 68-4



Hypoxemic Respiratory Failure

Etiology and Pathophysiology

Causes

Ventilation-perfusion (V/Q) mismatch

COPD

Pneumonia

Asthma

Atelectasis

Pulmonary embolus





Causes

Shunt

Anatomic shunt Intrapulmonary shunt

An extreme V/Q mismatch





Causes

Diffusion limitation

Severe emphysemaRecurrent pulmonary emboli

Pulmonary fibrosis

Hypoxemia present during exercise



Diffusion Limitation

Fig. 68-5





Causes

Alveolar hypoventilation

Restrictive lung diseaseCNS disease

Chest wall dysfunction

Neuromuscular disease





Interrelationship of mechanisms

Combination of two or more

physiologic mechanisms



Hypercapnic Respiratory Failure


Imbalance between ventilatory

supply and demand





Airways and alveoli

Asthma

EmphysemaChronic bronchitis

Cystic fibrosis


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Central nervous system

Drug overdose

Brainstem infarctionSpinal chord injuries


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Chest wall

Flail chest

FracturesMechanical restriction

Muscle spasm


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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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When compensatory mechanisms

fail, respiratory failure occurs

Signs may be specific or nonspecific


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Severe morning headache

Cyanosis

Late sign

Tachycardia and mild hypertension

Early signs


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Consequences of hypoxemia and

hypoxia

Metabolic acidosis and cell deathDecreased cardiac output

Impaired renal function


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Specific clinical manifestations

Rapid, shallow breathing pattern

Tripod positionDyspnea


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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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Nursing Assessment

Health information

Health history

Medications

Surgery


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Nursing Assessment

Functional health patterns

Health perceptionhealth management

Nutritional-metabolic

Activity-exercise

Sleep-rest

Cognitive-perceptual

Copingstress tolerance


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Nursing Assessment

Physical assessment

General

Integumentary

Respiratory

Cardiovascular

Gastrointestinal

Neurologic

Laboratory findings


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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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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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Prevention

Thorough history and physical

assessment to identify at-risk

patients

Early recognition of respiratory

distress


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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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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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Respiratory therapy

Positive pressure ventilation (PPV)

Noninvasive PPVBiPAP

CPAP


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Noninvasive PPV

Fig. 68-7


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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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Drug Therapy

Treatment of pulmonary infections

IV antibiotics

Reduction of severe anxiety, pain, andagitation

Benzodiazepines

Narcotics


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Nutritional Therapy

Maintain protein and energy stores

Enteral or parenteral nutritionNutritional supplements

A i i


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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

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