resp notes

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


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


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


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



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


Normal respiratory epithelium is denuded and replaced by goblet cells Alterations in epithelial integrity



Increased microvascular permeability Mucosal edema Inflammatory exudates Bronchoconstriction Leakage



Late phase Arrival of recruited leukocytes signals initiation More mediator release causes damage to epithelium


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Epithelial damage Hypertrophied smooth muscle Edema Mucous gland hypertrophy Mucus in lumen


Inflammation of airway Causes

Acute bronchospasm (bronchoconstriction) Mucosal edema Mucous plug formation Airway wall remodeling


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


Common symptoms Wheezing Feeling of tightness of chest Dyspnea Cough (dry or productive) Increased sputum production (thick, tenacious, scant, and viscid


Symptoms of severe attack Use of accessory muscles of respiration Intercostal retractions Distant breath sounds with inspiratory wheezing Orthopnea Agitation Tachypnea Tachycardia


Diagnosis Physical findings

Cough


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Wheezing Hyperinflated chest Decreased breath sounds


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)


Diagnosis Pulmonary function tests (What goes on during this test? Should the patient be NPO

after the test?


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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Diagnosis Skin testing

Young patients with extrinsic asthma Bronchial provocation testing

Test with histamine or methacholine CBC

Elevated WBCs Elevated eosinophils


Treatment Avoid triggers Environmental control

Removal of allergens Air purifiers Air conditioners

Preventive therapy Desensitization (allergen specific immunotherapy)


Treatment Medications

O2 therapy


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Small-volume nebulizers B2 agonists Corticosteroids Leukotriene modifiers Mast cell inhibitors


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


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


Clinical manifestations Cough (productive or nonproductive) Low-grade fever Substernal chest discomfort Sore throat Postnasal drip Fatigue


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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


Cause Cigarette smoking (90%) Repeated airway infections


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Genetic predisposition Inhalation of physical or chemical irritants


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.)


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.)


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)


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


Clinical manifestations Complete obstruction

No air movement heard with auscultation (complete obstruction) Inability to talk Tachycardia Cyanosis Rapid progression to unconsciousness


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


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



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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



Normal with progression to diffuse whiteout Open-lung biopsy shows

Atelectasis Hyaline membranes Cellular debris Interstitial and alveolar edema


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


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)


Fungal Aspergillus

Released from walls of old buildings under reconstruction


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


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


Pneumonia


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


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



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



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



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



Clinical manifestations History of contact with infected person Low-grade fever Cough Night sweats Fatigue Weight loss Malaise Anorexia



Clinical manifestations Physical examination

Apical crackles (rales) Bronchial breath sounds over region of consolidation Malnourished



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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




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

resp notes

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