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Pathophysiology
- 1. Acute inflammation of lower lung parenchyma (alveoli and respiratory bronchioles, aspiration, inhalation, or contaminated respiratory equipment
- 2. Classified as viral versus bacterial, community-acquired versus hospital-acquired, atypical, or pneumocystis
- 3. Causative agent can be infectious (bacteria, viruses, fungi, and other microbes) or noninfectious (aspirated or inhaled substances)
- 4. Most common organism for both community-acquired and hospital-acquired pneumonia is the Gram-positive bacteria Streptococcus pneumoniae
- 5. Other common organisms associated with community-acquired pneumonia in¬clude Klebsiella pneumoniae, Pseudomonas aeruginosa, Escherichia con, haemophilus influenzae, and other influenzae viruses
- 6. Spread of microbes in alveoli activates inflammatory and immune response
- 7. Antigen-antibody response damages mucous membranes of bronchioles and alveoli resulting in edema
- 8. Microbe cellular debris and exudate fill alveoli and can impair gas exchange
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Assessment
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1. Viral
- a. Fever: low-grade
- b. Cough: nonproductive
- c. White blood cell count: normal to low elevation
- d. Chest x-ray: minimal changes evident
- e. Clinical course: less severe than pneumonia of bacterial origin
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2. Bacterial
- a. Fever: high
- b. Cough: productive
- c. White blood cell count: high elevation
- d. Chest x-ray: obvious infiltrates
- e. Clinical course: more severe than pneumonia of viral origin
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Therapeutic management
- Antibiotic therapy, analgesics, antipyretics
- Oxygen therapy to treat hypoxemia, suctioning as necessary
- Maintain patent airway; monitor respiratory and oxygenation status
- Provide supplemental oxygen as indicated
- Be prepared to initiate mechanical ventilatory support
- Provide nutritional support and fluids (2 liters per 24 hours or greater if no traindications) via appropriate route
- Provide adequate opportunities for physical rest
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For all hospitalized clients, take measures to prevent pneumonia
- Identify clients at high risk for pneumonia
- Maintain appropriate infection control measures
- Maintain adequate nutrition
- Initiate aspiration precautions for clients at risk (ex: stroke)
- Encourage activity and mobility as soon as feasible
- Macrolides: erythromycin, azithromycin; Penicillin G; aminoglycosides or cephalosporins
- Alternatives: Augmentin; doxycycline; Bactrim; Levaquin
- Medication therapy: antibiotics or other antimicrobials as indicated, analgesics, antipyretics
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Infection
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Interventions
- Assess VS, temp fluctuations
Assess pulse ox
Assess lung sounds
Assess WBC count
Assess hydration
Assess effectiveness of antibiotics
Chest Xray
Assess WBC count
Administer Abx
Administer antipyretics
Administer O2 and bronchodilators as needed
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Signs and Symptoms
- Fever
Increased WBCs
Positive sputum culture
Tachycardia
Chills
change in character of sputum
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Ineffective Airway Clearance
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Signs and Symptoms
- Adventitious lung sounds
Cough
Dyspnea
Shortness of breath
Infiltrates in C Xray
Purulent sputum
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Nursing Interventions
- Assess respiratory status
Assess cough
Observe sputum for color, amount, consistency
Teach re: positioning, coughing and deep breathing
Suction oropharynx prn
Assist with IS
Teach re: pacing activities
Consult RT for CPT and nebulizer treatments
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Impaired Gas Exchange
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Signs and Symptoms
- Dyspnea
Decreased PaO2
Increased PaCO2
Cyanosis
Tachypnea
Decreased activity tolerance
Restlessness
Disorientation or confusion in older adults, functional decline with or without fever
Loss of appetite
Hypotension
Lung consolidation
Crackles
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Nursing Interventions
- Assess respirations: note quality, rate, rhythm, depth; use of accessory muscles
- Assess VS changes
- Assess skin color for cyanosis
- Assess changes in orientation and increasing restlessness
- Assess ABGs and O2 sat
- Maintain O2, avoid high <> in COPD pts
- Pace activities to reduce oxygen need, fatigue
- Anticipate need for intubation and mechanical ventilation if condition worsens
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Outcome
- Pt will maintain optimal gas exchange as evidenced by respirations between 12-24/min; ABGs WNL (specify ranges here); and no further reduction in mental status, stable ABG
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Blood Gas manifestations
- Respirations: Most PNA pts have hypoxemia and respiratory alkalosis
Hyperventilation = breathing too fast leads to...
Blowing off all your CO2 (acid loss) leads to...
Acute alkalosis (left shift)
Less intake of O2 combined with...
Increased affinity for O2 = less tissue perfusion...
Reduced O2, Increased affinity leads to hypoxemia
Less O2 starts hypotension, vasodilation leads to...
Lack of O2 to brain = confusion, headache, blurred vision leads to
Low O2 to myocardium = bradycardia, arrhythmias = ischemia, coma
- Interventions: Vents
Increase FiO2 (21% on RA) to obtain PO2 (ABG 80-100 about 4-5 times the FiO2)
At 100% O2 and ratio of “21%” to “80 to 100” PO2 should be 400-500!
Increase minute ventilation to remove excess CO2 and increase TV to clear more CO2
(16 BPM x TV 400 cc = 6400cc)
High levels of FiO2 > 60% oxygen is considered toxic and causes fibrotic lung damage
Trade PEEP for O2 reducing the amount of oxygen given on a vent
Use pressure-limited ventilation. Pressure controlled or Pressure support