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7/29/2019 Resp Notes
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Respiratory Sherry Vickers MSN, RN, CNE Influenza
The Flu
The Key Points-Viral infection of upper and lower respiratory tract
-Influenza virus can cause 3 types of infection
1) Uncomplicated URI 2) Respiratory viral followed by bacterial infection 3) Viral pneumonia
Incubation Time- 1-4 days (2 days average) Mode of transmission is aerosol or direct contact Over 250,000 people die every flu season There are three types of influenza
-Type A
-Type B
-Type C
Picture of Flu Virus Type A Influenza S & S: Fever, chills, malaise, muscle aching, headache, profuse water nasal discharge,
nonproductive cough, sore throat, Distinguishing Feature: Rapid Onset
Goals: Provide early recognition and treatment (antiviral meds: Flumadine, Symmetrel), preventcomplications, limit infection to upper respiratory infection
Prevention: wash hands, flu vaccine yearly Acute Respiratory Failure State of disturbed gas exchange resulting in low PaO2 ( 50 mm Hg
with a pH less than 7.30, when the patient is breathing room air
Etiology: precise mechanism unknown
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Causes: central nervous system problems, neuromuscular diseases, chest wall and diaphragmdysfunction, pulmonary parenchymal diseases, airway problems
Acute Respiratory FailureClinical Manifestations
Hypoxemia, hypercapnea, headache, dyspnea, confusion, LOC, agitation, dizziness,restlessness
Dx tests: blood gases, CXR, electrolyte panel, CBC Tx: maintain airway, mechanical ventilation to keep O2 sat >90%, treat underlying problem;
diuretics, if necessary, steroids controversial
Alterations in Pulmonary Vasculature Pulmonary embolus (PE): an undissolved detached material (blood clot, fat emboli, amniotic
fluid, air, tumor, foreign bodies, parasites) that occludes blood vessels
650,000 patients affected annually 50,000 deaths annually 90% in deep veins of lower extremities Alterations in Pulmonary Vasculature (Cont.) Virchows triad: factors causing thromboemboli formation include venous stasis/sluggish blood
flow, hypercoagulability, and damage to the venous wall (intimal injury)
Common risk factors: immobility, trauma, pregnancy, cancer, heart failure, and estrogen use Alterations in Pulmonary Vasculature (Cont.) Pathogenesis: thrombus dislodged from point of origin by direct trauma, exercise, and muscle
action, changes in blood flow
If 50% of the cross-sectional pulmonary circulation is impaired, dangerously high pulmonarypressures are created
PA pressures increase because of mechanical obstruction, release of serotonin, neuralsympathetic stimulation
Alterations in Pulmonary Vasculature (Cont.) Infarction occurs in 10%-15% of cases
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Clinical manifestations: depends on size of thrombus; usually includes restlessness,apprehension, anxiety, dyspnea, tachycardia, tachypnea, chest pain (on inspiration) and
hemoptysis
Dx: ventilation/perfusion scan, helical CT angiography, ABGs, ECG, cardiac enzymes, andpulmonary angiography
Alterations in Pulmonary Vasculature (Cont.)
Tx: treat underlying problems Prevention measures: avoid prolonged bedrest, active ROM, low-dose heparin or low-molecular
weight heparins, compression hose w/pneumatic compression
If PE confirmed, heparin drip, thrombolytics Umbrella filter or embolectomy Alterations in Pulmonary Vasculature: Malignancies Etiology: 180,000 new cases every year in the US; smoking leading cause (85%) Four major types: large cell carcinoma (5%-10% of cases) develop in the periphery; small cell
carcinoma (15%-20%) in central bronchial region; squamous cell carcinoma (20%-30%) in hilar
region; and adenocarcinoma (35%-40% of cases) in the peripheral lung
Alterations in Pulmonary Vasculature: Malignancies (Cont.)
Clinical manifestations: 10% to 25% of cases asymptomatic Extrathoracic manifestations: weight loss, anemia, clubbing, facial and upper extremity edema Intrathoracic manifestations: dyspnea, cough, chest pain, hemoptysis, hoarseness, Horner
syndrome
Alterations in Pulmonary Vasculature: Malignancies (Cont.) Dx: pulmonary function tests show increased volumes, chest x-ray, CT scan Definitive diagnosis requires cytology or histology testing Tx: surgery, if resectable, chemotherapy, radiation, laser therapy or combination of these
therapies: depends on tumor size and location
Obstruction from Conditions in the Wall of the Lumen
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Asthma
Etiology Airway obstruction that is reversible (not completely in some patients) Airway inflammation Increased airway responsiveness to a variety of stimuli
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Statistics Occurs in 5% to 12% of U.S. population Most common chronic disease of children High-risk populations
African Americans Inner-city dwellers Premature/low-birth-weight children
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Predisposing factors Genetic for atopy and structural (smaller airways)
Chromosomes 5, 11, 14 History of hay fever, eczema Family history Positive skin test reactions to allergens
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic (allergic)
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1/3 to of asthma cases An IgE-mediated response is common Clinical manifestations
Elevated IgE levels Allergic rhinitis Eczema Positive family history of allergy Attacks associated with seasonal, environmental or occupational exposure
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic Mechanism of action
Immediate phase Initiated by exposure to specific antigen that has previously sensitized
mast cells in airway mucosa
Antigen reacts with antibody on surface of mast cell Mast cell releases packets of chemical mediator substances
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic Mechanism of action
Chemical mediators released Histamine Slow-reacting substances of anaphylaxis (leukotrienes) Prostaglandins Bradykinins
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Eosinophilic chemotactic factor Serotonin
Obstruction from Conditions in the Wall of the Lumen (Cont.) Obstruction from Conditions in the Wall of the Lumen (Cont.)
Asthma
Extrinsic Mechanism of action
Normal respiratory epithelium is denuded and replaced by goblet cells Alterations in epithelial integrity
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic Mechanism of action
Increased microvascular permeability Mucosal edema Inflammatory exudates Bronchoconstriction Leakage
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic Mechanism of action
Late phase Arrival of recruited leukocytes signals initiation More mediator release causes damage to epithelium
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Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Extrinsic Mechanism of action
Epithelial damage Hypertrophied smooth muscle Edema Mucous gland hypertrophy Mucus in lumen
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Inflammation of airway Causes
Acute bronchospasm (bronchoconstriction) Mucosal edema Mucous plug formation Airway wall remodeling
Obstruction from Conditions in the Wall of the Lumen (Cont.) Obstruction from Conditions in the Wall of the Lumen (Cont.)
Asthma
Pathogenesis Immunohistopathologic features
Denudation of airway epithelium Collagen deposition beneath the basement membrane Edema
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Mast cell activation Inflammatory cell infiltration by neutrophils, eosinophils, and lymphocytes
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Common symptoms Wheezing Feeling of tightness of chest Dyspnea Cough (dry or productive) Increased sputum production (thick, tenacious, scant, and viscid
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Symptoms of severe attack Use of accessory muscles of respiration Intercostal retractions Distant breath sounds with inspiratory wheezing Orthopnea Agitation Tachypnea Tachycardia
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Diagnosis Physical findings
Cough
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Wheezing Hyperinflated chest Decreased breath sounds
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Diagnosis Radiographic finding
Hyperinflation with flattening of the diaphragm Sputum examination
Charcot-Leyden crystals (formed from crystallized enzymes from eosinophilicmembranes)
Eosinophils Curschmann spirals (mucous casts of bronchioles)
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Diagnosis Pulmonary function tests (What goes on during this test? Should the patient be NPO
after the test?
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Diagnosis ABG
Normal during mild attack Respiratory alkalosis (short fast breaths) and hypoxemia as bronchospasm
increases in intensity
PaCO2 elevation (this is bad because patient is not able to breath fast and blowoff CO2 now)
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Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Diagnosis Skin testing
Young patients with extrinsic asthma Bronchial provocation testing
Test with histamine or methacholine CBC
Elevated WBCs Elevated eosinophils
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Treatment Avoid triggers Environmental control
Removal of allergens Air purifiers Air conditioners
Preventive therapy Desensitization (allergen specific immunotherapy)
Obstruction from Conditions in the Wall of the Lumen (Cont.)Asthma
Treatment Medications
O2 therapy
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Small-volume nebulizers B2 agonists Corticosteroids Leukotriene modifiers Mast cell inhibitors
Obstruction from Conditions in the Wall of the Lumen (Cont.) Obstruction from Conditions in the Wall of the Lumen (Cont.)
Acute Bronchitis
Etiology Acute inflammation of the trachea and bronchi Causes
Viral Influenza virus A or B Parainfluenza virus Respiratory syncytial virus Coronavirus Rhinovirus Coxsackievirus Adenovirus
Nonviral Streptococcus pneumoniae Haemophilus influenzae Mycoplasma Moraxella Chlamydia pneumoniae
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Obstruction from Conditions in the Wall of the Lumen (Cont.)Acute Bronchitis
Etiology Causes
Heat Smoke inhalation Inhalation of irritant chemicals Allergic reactions
Obstruction from Conditions in the Wall of the Lumen (Cont.)Acute Bronchitis
Pathogenesis Airways become inflamed and narrowed from capillary dilation Swelling from exudation of fluid Infiltration with inflammatory cells increased mucus production Loss of ciliary function Loss of portions of the ciliated epithelium
Obstruction from Conditions in the Wall of the Lumen (Cont.)Acute Bronchitis
Clinical manifestations Cough (productive or nonproductive) Low-grade fever Substernal chest discomfort Sore throat Postnasal drip Fatigue
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Obstruction from Conditions in the Wall of the Lumen (Cont.)Acute Bronchitis
Diagnosis Clinical presentation Chest x-ray to distinguish acute bronchitis from pneumonia
Treatment Antibiotic therapy (bacterial) Codeine-containing medications (for cough) Increase fluid intake Avoid smoke Use a vaporizer in bedroom (some pulmonologists suggest cool mist humidifier)
Obstruction from Conditions in the Wall of the Lumen (Cont.)Chronic Bronchitis
Etiology Type B COPD, blue bloater Chronic or recurrent productive cough >3 months >2+ successive years Persistent, irreversible Typical patient is overweight (1:2 male to female ratio) >30-40 years Commonly associated with emphysema
Obstruction from Conditions in the Wall of the Lumen (Cont.)Chronic Bronchitis
Cause Cigarette smoking (90%) Repeated airway infections
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Genetic predisposition Inhalation of physical or chemical irritants
Obstruction from Conditions in the Wall of the Lumen (Cont.)Chronic Bronchitis
Pathogenesis Hyperplasia of bronchial mucous gland/goblet cells
Increased mucus production Mucus combines with purulent exudate (bronchial plugs) to form mucous plug Obstruction from Conditions in the Wall of the Lumen (Cont.)
Obstruction from Conditions in the Wall of the Lumen (Cont.)Chronic Bronchitis
Pathogenesis Increased bronchial wall thickness
Resistance increases work of breathing Increased O2 demands Produce ventilation-perfusion mismatch with hypoxemia and hypercarbia
Increases pulmonary artery resistance Obstruction from Conditions in the Wall of the Lumen (Cont.)
Chronic Bronchitis
Pathogenesis Pulmonary hypertension
Inflammation in bronchial walls with vasoconstriction of pulmonary bloodvessels and pulmonary arteries
Right-sided heart failure may occur r/t high pulmonary resistance Obstruction Conditions in the Wall from of the Lumen (Cont.) Obstruction Conditions in the Wall from of the Lumen (Cont.)
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Chronic Bronchitis
Diagnosis Chest x-ray
Increased bronchial vascular markings Congested lung fields Enlarged horizontal cardiac silhouette Evidence of previous pulmonary infection
Obstruction Conditions in the Wall from of the Lumen (Cont.)Chronic Bronchitis
Diagnosis Pulmonary function tests
Normal total lung capacity (TLC) Increased residual volume (RV)
Obstruction Conditions in the Wall from of the Lumen (Cont.)Chronic Bronchitis
Diagnosis Arterial blood gas (ABG)
Elevated PaCO2 Decreased PO2
Develop early in disease process Diagnosis
ECG Atrial arrhythmias Evidence of right ventricular hypertrophy
Secondary polycythemia
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R/t continuous or nocturnal hypoxemia Obstruction Conditions in the Wall from of the Lumen (Cont.)
Chronic Bronchitis
Treatment Medications
Inhaled short-acting B2 agonists Inhaled anticholinergic bronchodilators Cough suppressants Antimicrobial agents (bacterial infections) Inhaled/oral corticosteroids Theophylline products
Low-dose O2 therapy Patients with PaO2 levels
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Emphysema
Etiology Type A COPD Pink puffer Young to middle-age adults 50 years (develops over time) Causes
Smoking >70 pack/year Air pollution Certain occupations (mining, welding, working with or near asbestos) 1-Antitrypsin deficiency Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Etiology Smoking causes alveolar damage
Inflammation in lung tissue leading to release of proteolytic enzymes Inactivates 1-antitrypsin (protects lung parenchyma)
Obstruction Related to Loss of Lung Parenchyma (Cont.) Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Pathogenesis Release of proteolytic enzymes from inflammatory cells (neutrophils, macrophages)
leading to alveolar damage
Reduction in pulmonary capillary bed Exchange of O2 and CO2 between alveolar and capillary blood impaired
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Loss of elastic tissue in lung Results in decrease in size of smaller bronchioles Results in loss of radial traction (holds airway open) Obstruction Related to Loss of Lung Parenchyma (Cont.)
Obstruction Related to Loss of Lung Parenchyma (Cont.) Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Clinical manifestations Progressive, exertional dyspnea Increased SOB for past 3-4 years Thin
R/t increased caloric expenditure and decreased ability to consume adequatecalories
Use of accessory muscles Pursed-lip breathing Cough (minimal or absent)
Obstruction Related to Loss of Lung Parenchyma (Cont.) Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Diagnosis Patient history and physical finding
Thin, wasted individual hunched forward Barrel chest Digital clubbing Decreased breath sounds, lack of crackles and rhonchi with prolonged
expiration
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Decreased heart sounds Decreased diaphragmatic excursion
Digital Clubbing Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Diagnosis Pulmonary function tests (PFTs)
Increased functional residual capacity Increased RV Increased TLC Decreased FEV Decreased FVC
Chest x-ray Hyperventilation Low, flat diaphragm Presence of blebs or bullae Narrow mediastinum Normal or small vertical heart
Obstruction Related to Loss of Lung Parenchyma (Cont.)Emphysema
Diagnosis ABG
Mild increase in PaO2 Normal PaCO2 (elevated in late stages)
ECG Obstruction Related to Loss of Lung Parenchyma (Cont.)
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Normal, show tall P waves Sinus tachycardia Supraventricular arrhythmias Ventricular irregularities Obstruction Related to Loss of Lung Parenchyma (Cont.)
Emphysema
Treatment O2 therapy Medications
Inhaled short-acting B2 agonists Inhaled anticholinergic bronchodilators Cough suppressants Antimicrobial agents (infections) Inhaled/oral corticosteroids Theophylline products
Obstruction of Airway LumenAcute Tracheobronchial Obstruction
Etiology Causes
Aspiration of foreign body (most often in right lung) Malpositioned endotracheal tube Laryngospasm Epiglottitis Trauma Swelling (smoke inhalation)
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Postsurgical blood clot Compression of bronchus/trache (tumor, enlarged lymph nodes
Obstruction of Airway Lumen (Cont.)Acute Tracheobronchial Obstruction
Clinical manifestations Partial obstruction
Stridor Sternal and intercostal retractions Wheezing Nasal flaring Tachypnea, dyspnea Tachycardia Use of accessory muscles
Obstruction of Airway Lumen (Cont.)Acute Tracheobronchial Obstruction
Clinical manifestations Complete obstruction
No air movement heard with auscultation (complete obstruction) Inability to talk Tachycardia Cyanosis Rapid progression to unconsciousness
Obstruction of Airway Lumen (Cont.)Acute Tracheobronchial Obstruction
Diagnosis
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Based on clinical features ABG
Hypoxemia, hypercarbia Chest x-ray
Location of obstruction Treatment
Open obstructed airway as soon as possible Heimlich to expel foreign body Suction Emergency tracheostomy (obstruction in subglottic region or above)
Diagnostic TestsPulmonary Function Testing (PFT)
Demonstrates obstruction of airflow in lungs Spirometry
Determines severity and diagnosis of COPD Patient inhales deeply and exhales as quickly as possible until maximal air is exhaled Forced vital capacity
Total volume of air exhaled Time required for exhaling the air is also measured
Forced expiratory volume in 1 second Volume exhaled in 1st second is reliable and index of obstructive airway disease
Diagnostic Tests (Cont.)Pulmonary Function Testing (PFT)
Spirometry Airflow obstruction
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FEV1/FVC ratio >75% No significant obstruction
FEV1/FVC ratio between 60% and 70% Mild obstruction
FEV1/FVC ratio 50% to 60% Moderate obstruction
FEV1/FVC ratio 15% = positive bronchodilator response Partially reversible bronchospasm of smooth muscle (asthma, asthmatic
bronchitis)
Atelectatic DisordersAcute (Adult) Respiratory Distress
Syndrome (ARDS)
Etiology Occurs in association with other pathophysiologic processes 125,000-150,000 cases/year in United States Mortality rate 30%-60%
Causes Severe trauma Sepsis (>40%) Aspiration of gastric acid (>30%) Fat emboli syndrome Shock
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Atelectatic Disorders (Cont.) Atelectatic Disorders (Cont.)
ARDS
Pathogenesis Widespread pulmonary inflammation leads to:
Noncardiogenic pulmonary edema associated with leaky pulmonary capillaries Atelectasis associated with lack of surfactant
Decreases surface tension in small alveoli and prevents them fromcollapsing
Fibrosis (hyaline membranes) Associated with inflammatory deposition of proteins
Characteristic abnormalities Injury to alveoli from a wide variety of disorders Changes in alveolar diameter Injury to pulmonary circulation Disruptions in O2 transport and utilization Severe hypoxemia caused by intrapulmonary shunting of blood
Perfusion of large numbers of alveoli that are poorly (areas of lowventilation-perfusion) or not ventilated (areas of shunt)
Atelectatic Disorders (Cont.)ARDS
Pathogenesis Common findings
Decrease in lung compliance Due to loss or inactivation of surfactant with subsequent increased
recoil pressure
Proteinaceous fluid fills alveoli and impairs ventilation
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Decrease in FRC Very stiff, noncompliant lungs associated with alveolar edema and
exudate exaggerate surface tension forces
Alveolar closure leads to atelectasis and loss of lung volume Diffuse, fluffy alveolar infiltrates Noncardiogenic pulmonary edema
Atelectatic Disorders (Cont.)ARDS
Clinical manifestations Early
Sudden marked respiratory distress Slight increase in pulse rate Dyspnea Low PaO2 Shallow, rapid breathing
Late Tachycardia Tachypnea Hypotension Marked restlessness Crackles, rhonchi on auscultation Use of accessory muscles Intercostal and sternal retractions Cyanosis
Atelectatic Disorders (Cont.)ARDS
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Diagnosis Hallmark is hypoxemia refractory to increased levels of supplemental O2 ABG
Hypoxia Acidosis Hypercapnia
PFTs Decrease in FVR Decreased lung volumes Decreased lung compliance VA/Q mismatch with large right-to-left shift
Atelectatic Disorders (Cont.)ARDS
Diagnosis Chest x-ray
Normal with progression to diffuse whiteout Open-lung biopsy shows
Atelectasis Hyaline membranes Cellular debris Interstitial and alveolar edema
Atelectatic Disorders (Cont.)ARDS
Treatment Mostly supportive
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Enhance tissue oxygenation until inflammation resolves Identify underlying cause Address cause (ex: sepsis) Maintain fluid and electrolyte balance
Increased fluid administration can produce or intensify pulmonary edema Block system inflammatory cells Adequate oxygenation
Volume ventilator using pressure support Mechanical ventilation with positive end-expiratory pressure (PEEP)
Increases FRV and prevents alveolar collapse at end-expiration Forces edema out of alveoli
Atelectatic Disorders (Cont.)ARDS
Treatment Adequate oxygenation
Supplemental O2 >60% contributes to ARDS related to absorption atelectasis FIO2 reduced as soon as possible
High-frequency jet ventilation (HFJV) Inverse ratio ventilation (IRV) Inhaled nitric oxide
Atelectatic Disorders (Cont.) Pleural Space Disorders
Pneumothorax
Etiology
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Accumulation of air in the pleural space Primary pneumothorax
Spontaneous Occurs in tall, thin men 20-40 years No underlying disease factors Cigarette smoking increases risk
Secondary pneumothorax 20,000 new cases annually Result of complications from preexisting pulmonary disease
Asthma, emphysema, cystic fibrosis, infectious disease (pneumonia, TB) Tension pneumothorax
Traumatic origin Results from penetrating or nonpenetrating injury
Pleural Space Disorders (Cont.)Pneumothorax
Pathogenesis Primary
Rupture of small subpleural blebs in apices Air enter pleural space, lung collapses, and rib cage springs out
Secondary Result of complications from complications from an underlying lung problem May be due to rupture of cyst of bleb
Tension Results form buildup of air under pressure in pleural space Air enters pleural space but cannot escape during expiration
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Lung on ipsilateral (same) side collapses and forces mediastinum towardcontralateral side
Decreases venous return and cardiac output Pleural Space Disorders (Cont.)
Pneumothorax
Pathogenesis Open sucking chest wall wound
Air enters during inspiration but cannot escape during expiration Leads to shift of mediastinum
Pleural Space Disorders (Cont.) Pleural Space Disorders (Cont.)
Pneumothorax
Clinical manifestations Small pneumothoraces (
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Neck vein distention Hyperresonance Subcutaneous emphysema
Diagnosis ABG
Decreased PaO2, acute respiratory alkalosis Chest x-ray
Expiratory films show better demarcation of pleural line than inspiratory Decompression of hemidiaphragm on side of pneumothorax Pleural line with absence of vessel markings peripheral to this line
Pleural Space Disorders (Cont.) Pleural Space Disorders (Cont.)
Pneumothorax
Treatment Management depends on severity of problem and cause of air leak Lung collapse 15%-25% Chest tube placement with H2O seal and suction
Pleural Space Disorders (Cont.)Pleural Effusion
Etiology Pathologic collection of fluid or pus in pleural cavity as result of another disease process Normally, 5-15 ml of serous fluid is contained in pleural space
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Constant movement of pleural fluid from parietal pleural capillaries to pleuralspace
Reabsorbed into parietal lymphatics Causes
Changes associated with various types r/t changes in pleural capillary hydrostaticpressure, colloid oncotic pressure, or intrapleural pressure
Imbalance in pressure associated with fluid formation exceeding fluid removal Pleural Space Disorders (Cont.)
Pleural Effusion
Clinical manifestations Vary depending on cause and size of effusion May be asymptomatic with
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Signs of CHF Hilar adenopathy Loculation of fluid
Thoracentesis Analyze fluid and reduce amount of fluid
pH, LDH, glucose Presence of pathologic bacteria
CT or ultrasonographic tests Assist in complicated effusions Distinguish mass from large effusion
Pleural Space Disorders (Cont.)Pleural Effusion
Treatment Directed at underlying cause and relief of symptoms Tension and spontaneous pneumothorax are medical emergencies requiring treatment
to remove pleural air and re-expand lung
Closed chest tube drainage (adults) Controversial in pediatrics
Thoracentesis Ultrasound useful for thoracentesis guidance
Thoracotomy Control bleeding (>200 ml/hr)
Chest Wall Deformities (Cont.)Flail Chest
Etiology Results from multiple rib fractures r/t trauma to chest wall
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Ribs fractured at two distant sites Results in unstable, free-floating chest wall segment Moves paradoxically inward on inspiration Sternal fractures can cause flail segment
Infection or Inflammationof the Lung
Pneumonia
Inflammatory reaction in the alveoli and interstitium caused by an infectious agent Causes
Aspiration of oropharyngeal secretions composed of normal bacterial flora or gastriccontents (25%-35%)
Present as lung abscess, necrotizing pneumonia, empyema Bacteroides, fusobacterium
Inhalation of contaminants Virus Mycoplasma
Contamination from the systemic circulation
Infection or Inflammation of the Lung (Cont.)
Pneumonia
Classifications Community acquired Hospital acquired Bacterial
Bacterial Gram negative Haemophilus influenzae Klebsiella
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Pseudomonas aeruginosa Serratia marcescens, Escherichia coli,Proteus spp
Viral Legionella Lives in H2O Transmitted by portable H2O, condensers, cooling towers Fever, diarrhea, abdominal pain, liver and kidney failure, pulmonary
infiltrates
Treatment: macrolide antibiotic(Mycoplasma pneumoniae)
Infection or Inflammation of the Lung (Cont.)
Fungal Aspergillus
Released from walls of old buildings under reconstruction
Infection or Inflammation of the Lung (Cont.)
Pneumonia
Pathogenesis Acquired when normal pulmonary defense mechanisms are compromised Organism enters lung, multiply, and trigger pulmonary inflammation Inflammatory cells invade alveolar septa Alveolar air spaces fill with exudative fluid
Consolidates and difficult to expectorate Viral pneumonia doesnt produce exudative fluids
Infection or Inflammation of the Lung (Cont.)
Pneumonia
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Clinical manifestations Severity of disease and patient age cause variation in symptoms Crackles (rales) and bronchial breath sounds over affected lung tissue Chills Fever Cough, purulent sputum Viral
Upper respiratory prodrome Fever, cough, hoarseness, coryza accompanied by wheezing/rales
Mycoplasma Fever Cough Headache Malaise
Infection or Inflammation of the Lung (Cont.)
Pneumonia
Diagnosis Chest x-ray
Parenchymal infiltrates (white shadows) in involved area Sputum C&S
Sputum from deep in lungs Laboratory
WBC >15,000 (acute bacterial Treatment
Antibiotic therapy
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Based on sensitivity of culture
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Etiology Estimated 10 million infected in United States Multidrug-resistant TB
15% of cases Mortality 70%-90% Median survival of 4-16 weeks High-risk individuals
Prior infection (90%) Malnourishment, immunosuppression Living in overcrowded condition Incarcerated persons Immigrants Elderly
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Etiology Causes
Infection Inhalation of small droplets containing bacteria Droplets expelled with cough, sneeze, or talking
Mycobacterium tuberculosis
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Acid-fast aerobic bacillus Infects lungs and lymph nodes
Involvement of distant organ systems Hematogenous spread during primary or reactivation phase
Disseminated disease Miliary tuberculosis causes hematogenous dissemination of organisms
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Etiology Classifications
Primary (usually clinically/radiographically silent) May lie dormant for years or decades
Reactivating May occur many years after primary infection Impaired immune system causes reactivation
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Pathogenesis Entry of mycobacteria into lung tissue Alveolar macrophages ingest and process microorganisms
Microorganisms destroyed or persist and multiply Lymphatic and hematogenous dissemination
T-cells and macrophages surround organisms in granulomas Impairs immune system
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Reactivation occurs if immunosuppressed Pathologic manifestation is Ghon tubercle or complex
Parenchymal complex Well-circumscribed necrotic nodule that becomes fibrotic and calcified
Lymph components
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Clinical manifestations History of contact with infected person Low-grade fever Cough Night sweats Fatigue Weight loss Malaise Anorexia
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Clinical manifestations Physical examination
Apical crackles (rales) Bronchial breath sounds over region of consolidation Malnourished
Infection or Inflammation of the Lung (Cont.)
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Pulmonary Tuberculosis
Diagnosis Sputum culture (definitive diagnosis)
Three consecutive, morning specimens Identify slow-growing acid-fast bacillus Take 1-3 weeks for determination
DNA or RNA amplification techniques (diagnosis) Chest x-ray
Nodules with infiltrates in apex and posterior segments TB skin test
Doesnt distinguish between current disease or past infection
Infection or Inflammation of the Lung (Cont.)
Infection or Inflammation of the Lung (Cont.)
Pulmonary Tuberculosis
Treatment Administer multiple drugs (antibiotics) to which organism is susceptible
Therapy is for 9-12 months for active disease Therapy shorter in persons exposed with no active disease
Add at least 2 agents to drug regimen when treatment failure is suspected Providing safest, most effective therapy for shortest period of time Ensuring adherence to therapy by using directly observed therapy
Nonadherence to therapy is major cause of treatment failure