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Nursing Assessment of Patients with Respiratory Disorders

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1 Nursing Assessment of Patients with Respiratory Disorders
33 Nursing Assessment of Patients with Respiratory Disorders

2 Complete Assessment History Biographic and demographic data
Chief complaint Past medical history Family history Risk factors Social history

3 Complete Assessment Components of Physical Exam Inspection
Auscultation Percussion Pain Genetic and gerontological considerations

4 Social History Patients’ lifestyles and habits and
Risk for developing pulmonary disease Current and previous work settings Home environment Social settings

5 Gerontological Considerations
aging decreases respiratory function lower arterial oxygen values, increase risk of pneumonia Risk of aspiration may increase with aging Aging may affect patient comfort needs during the examination

6 Genetic Considerations
Cystic fibrosis (CF): genetic disorder, typically diagnosed in childhood CF has serious pulmonary complications – thick mucus builds up in lungs

7 Inspection Initial assessment activity General appearance:
Posture, facial expression and movements Changes in mental status Respiratory rates shallow breathing, irregular patterns of breathing Size and shape of the thorax, asymmetry Diminished movement of rib cage, use of accessory muscles

8 Inspection Color and appearance of skin
Pallor may indicate decreased oxygen-carrying capacity of the blood due to anemia Central cyanosis, where the mouth, lips, and mucous membranes are blue-tinged, indicates hypoxia in adults

9 Inspection Inspection of the neck
Appearance of veins, trachea and musculature may indicate chronic cardiac or pulmonary disease, pneumothorax Goiter or lesions may obstruct the upper airway

10 Inspection Palpation of skin and extremities
Edema of lower extremities Skin temperature and moisture Clinical reference points Chest excursion Tactile fremitus Tenderness Crepitus

11 Clinical Reference Points

12 Occupational Impact on Respiratory Disease
Exposure to airborne particles, vapors, and irritants Can result in acute or chronic respiratory disease in susceptible individuals Early recognition, diagnosis, and treatment of occupational asthma can prevent pulmonary complications

13 Auscultating Breath Sounds
Patient should be upright Use the diaphragm of the stethoscope Begin at C7 posteriorly and anteriorly from above the clavicles Move steadily from right to left upper and lower Compare breath sounds bilaterally Do not auscultate over clothing

14 Diaphragm - best for higher pitched sounds, like breath sounds and normal heart sounds.
Bell - is best for detecting lower pitch sounds, like some heart murmurs, and some bowel sounds. It is used for the detection of bruits, and for heart sounds (for a cardiac exam, listen with the diaphragm, and repeat with the bell).

15 Figure In a respiratory assessment, it is important to palpate and count ribs and interspaces to accurately record the location of lesions or adventitious breath sounds.

16 Auscultating Breath Sounds
Figure Lobes of the lung—anterior.

17 Auscultating Breath Sounds
Figure Lobes of the lung—posterior

18 Tracheal Breath Sounds
Auscultated over the trachea Loud and high pitched Cause: airflow through tubular trachea Best heard over the neck and trachea Occurs during upper airway obstruction

19 Bronchial Breath Sounds
Anterior: heard on either side of sternum, over main stems of the bronchus from 2nd to 4th intercostal spaces Posterior: best heard lateral to the spine between 3rd and 6th intercostal spaces Loud, harsh, less turbulent and lower than tracheal sounds

20 Bronchial Breath Sounds
Pause between inspiration and expiration; expiration is heard for a longer time than inspiration Sounds over smaller airways are low pitched and softer

21 Bronchovesicular Breath Sounds
Heard during inspiration and expiration Midway in Pitch and loudness between vesicular and bronchial breath sounds Best heard in 1st and 2nd intercostal spaces of anterior chest, between scapulae of the posterior chest Represent air movement in the moderate airways between the bronchi and the smaller airways

22 Vesicular Breath Sounds
Heard over most of the thorax Soft and low pitched, rustling, from air moving through small airways Heard longer during expiration, which generally lasts twice as long as inspiration

23 Adventitious Breath Sounds
Decreased or no sounds where normal sounds should occur Breath sounds occurring in abnormal locations Diminished breath sounds demonstrate decreased airflow and potentially decreased oxygen exchange

24 Adventitious Breath Sounds
Adventitious/extra sounds: Represent pathologic conditions of heart or lungs Indicate disrupted airflow due to airway spasm, fluid, or secretions Crackles (rales-term not used as much), Wheezes, Stridor, Friction rubs

25 Crackles Caused by fluid in the airways
Intermittent or discontinuous, nonmusical, or popping sounds Caused by fluid, inflammation, infection, or secretions Crackles are described as either fine or coarse Occur when closed airways snap open during inspiration Softer, gentler sound may also be heard on inspiration

26 Wheezes Heard equally during inspiration and expiration
High-pitched musical sounds Caused by air flowing across strands of mucus, swollen pulmonary tissue that narrows the airway, bronchospasm Rhonchi (term for secretions in airways-not used as much) Inspiratory/expiratory, continuous/ discontinuous, mild/moderate/severe Asthma, allergies, reactive airway disease

27 Stridor Heard only during inspiration as air attempts to flow across an obstruction Heard without stethoscope as high-pitched, crowing sound With stethoscope, best heard over large airways, e.g., trachea or bronchus Report to the health care provider immediately Indicates airway obstruction requiring intervention

28 Pleural Friction Rubs Low-pitched, creaking or squeaking sounds
Occur when inflamed pleural surfaces rub together Heard on inspiration Pitch usually increases with chest expansion Have the patient hold breath to distinguish between pleural and pericardial friction

29 Adventitious Lung Sounds

30 Travel and Area of Residence
An important aspect of the history in diagnosing potential respiratory problems Exposure to region-specific infectious diseases Exposure to environmental conditions, e.g. high altitudes

31 High-Altitude Pulmonary Edema (HAPE)
HAPE – can occur with travel to altitudes greater than 5,000 feet Increasing altitude → decreasing atmospheric pressure → decreasing available O2 Rapid onset of hypoxemia may result Compensatory increased respiratory rate may contribute to fatigue

32 High-Altitude Pulmonary Edema (HAPE)
This causes further respiratory insufficiency Initial compensatory mechanisms – pulmonary vascular vasoconstriction Later, inflammatory mediators cause vasodilation

33 Percussion Assess presence of air, fluid, solid mass in underlying tissues Normal lungs produce a resonant, low-pitched clear sound Hyperresonance indicates airways are hyperinflated or air is present outside of lung tissue Dullness indicates that air is absent Pneumonia, pleural effusion, hemothorax, solid tumors

34 Pain Pain during respiration may decrease tidal volumes
Pain management enables participation in rehabilitative activities Also promotes deep breathing to prevent pneumonia and atelectasis

35 Standard of Care For patients with cardiac and respiratory illness, standard is: Continuous or intermittent observation of the patient’s oxygen saturation End-tidal carbon dioxide levels Peak flow is utilized to trend treatment effectiveness in patients with asthma

36 Assessment of Arterial Oxygen Levels
ABG’s Pulse oximetry Physical assessment FiO2 will increase the PaO2 four times (normal patient)

37 Pulse Oximetry Measures O2 saturation of hemoglobin
Reflects light off the hemoglobin molecules Measures the absorption of light by hemoglobin Normal range is from 95% to 100%

38 Factors Interfering with Pulse Oximetry
Nail polish Automated BP cuffs, hemodialysis fistulas, or arterial lines interfere with blood flow Shock and hypovolemia Patient movement, ambient light, and venous pulsations may also cause inaccurate readings

39 Peak Flow Meters Track trends in a patient’s condition, evaluate air movement to determine severity of asthma exacerbation Measure the peak expiratory flow rate Normal values based on age and body size Severity scale: Utilizes red, yellow, and green zones to determine the severity of decrease in peak flow

40 Arterial Blood Gas Studies (ABG)
Provide information on arterial oxygen and carbon dioxide levels Oxygen saturation, bicarbonate, and blood pH are also calculated CO2 is major determinant of respiratory alkalosis/acidosis Bicarbonate level is determinant of metabolic acidosis/alkalosis

41 Capnography Measurement of exhaled CO2
Some utilize paper treated to detect the presence of acid such as CO2 Others use spectrography, generate waveform readings

42 Capnography Useful in determining ventilatory status, readiness for extubation Also used to determine pulmonary vessel perfusion in patients with pulmonary embolus

43 Capnography Monitor

44 Caring for the Patient with Upper Airway Disorders
34 Caring for the Patient with Upper Airway Disorders

45 Facial Bones Mandible Maxilla Zygoma Temporal bones Frontal bone

46 Mandible U-shaped bone
Together with the maxilla, largest and strongest bone of the face Forms lower jaw, holds the lower teeth in place Articulates with temporal bones at the temporomandibular joint Only mobile bone of the facial skeleton; motion is essential for mastication

47 Nursing Management for Mandibular Fractures
Determine patient’s nutritional requirements and knowledge deficits Oral nutrition with high-protein liquid diet and calories is essential Avoid weight loss if possible to ensure nutritional adequacy for healing Nasogastric or oral gastric tube supports nutrition if patient has extensive facial swelling Observe for nausea and vomiting, intervene to prevent aspiration

48 Maxilla Largest component of the middle third of the facial skeleton
Attaches laterally to the zygomatic bones Key bone in the midface, provides structural support Fractures less frequently than mandible or nose due to strong structural support

49 Classification System of Maxillary Fractures
Le Fort I Fracture (horizontal) Le Fort II Fracture (pyramidal) Le Fort III Fracture (transverse)

50 Zygoma A paired bone, commonly called the cheekbone
Articulates with maxilla, temporal, sphenoid, and frontal bones Forms prominence of the cheek The masseter muscle is suspended from the zygomatic arch

51 Temporal Bone Situated at the sides and base of the skull
Houses cochlear and vestibular end organs, facial nerve, carotid artery, jugular vein

52 Nursing Management for Temporal Bone Fractures
Care is conservative Assess for nerve damage and hearing loss Test for otorrhea; may indicate a CSF leak Monitor lumbar drain if inserted If facial nerve injury is present, provide eye care Institute CSF leak precautions – HOB 30o , no straining, bending or lifting

53 Frontal Bone Makes up the forehead, upper edge and roof of the orbit
Forms the anterior portion of the cranium Frontal sinus – air-filled cavity between lamina of the frontal bone Serves as a mechanical barrier to protect the brain

54 Infectious Rhinitis Usually caused by upper respiratory tract infection of viral origin

55 Allergy Inappropriate immune response to usually harmless substance in the environment

56

57 Sinusitis Inflammation of one or more paranasal and frontal sinuses
Occurs with obstruction of the normal drainage mechanism Three classifications of sinusitis Acute (symptoms lasting <3 weeks), Subacute (symptoms lasting 3 weeks to 3 months) Chronic (symptoms lasting >3 months)

58 Sinusitis Can be caused by bacterial, viral, and fungal infections
May occur during a Upper RespiratoryInfection when infection in the nose spreads to the sinuses Contributing factors: Air pollution Diving and underwater swimming Sudden temperature extremes Structural defects

59 Sinusitis Pathophysiology
Paranasal sinuses in direct communication with nasopharynx Proximity can cause bacterial infection When a bacterial or viral infection present, person develops sinus infection Tumors, polyps, trauma or benign growths can cause obstruction

60 Sinusitis Pathophysiology
Ostia (sinus openings) obstruction can impede normal flow of air Reduced flow of air and mucus allows mucus to become stagnant, contributing to growth of bacteria causes inflammation and swelling

61 Figure 34.4 Sites of sinusitis.

62 Sinusitis Clinical manifestations: Fever Weakness Fatigue Cough
Congestion Discharge Pain in face or forehead

63 Sinusitis Nursing management Assessment Thorough history
Education on causes and how to avoid triggers (air pollutants, diving, underwater swimming, allergies, irritants) Education on complications with nasal surgery

64 Sinusitis Postoperative nursing management Patient education
Monitor for bleeding Dressing care

65 Figure 34.5 CT registered with probe for sinus surgery.

66 Loss of Smell 2 million Americans have smell and taste disorders
About 200,000 visit a doctor each year Causes include: nasal congestion, a cold, obstruction, neurological disorder May be idiopathic – without any identifiable cause

67 Causes for Loss of Smell
Temporary anosmia is common with colds and nasal allergies Following a viral illness

68 Causes for Loss of Smell
Disorders preventing air from reaching smell receptors: Nasal polyps Nasal septal deformities Nasal tumors Tumors of the head or brain Head trauma Endocrine and nutritional disorders

69 Categories of Smell Dysfunction
Anosmia: a complete loss of smell Hyposmia: a partial loss of smell Hyperosmia: enhanced smell sensitivity Dysosmia: distortion in odor perception Includes parosmia (distorted sense of smell) and phantosmia

70 Categories of Smell Dysfunction
Parosmia: distortion of perception of external stimulus Phantosmia: smell perception with no external stimulus.

71 Determine the Cause of Anosmia
Complete head and neck examination Focus on the nose to determine whether it is a conductive or sensorineural loss Endoscope is used to provide reliable observations Chemosensory testing (“sniffing sticks) and a neuroradiologic (CT, MRI-to detect problems with olfactory nerve) evaluation also are used

72 Treatment of Anosmia Antihistamines (if the condition is related to allergy) Surgical correction of physical blockages Changes in medication If permanent, dietary counseling may include use of highly seasoned foods and stimulation of taste sensations that remain Caution should be taken to ensure safety around the home

73 MUCORMYSIS Rare often fatal disease caused by fungi
Opportunistic infection – immunocompromised Develops in patients receiving iron chelating drug called Desferal as treatment for actue iron poisioning Can develop in nasal areas, the lungs and brain

74 Disorders Affecting Taste
Hairy tongue is a condition in which the tongue is covered with hairlike papilla due to the overgrowth of the fungus Candida albicans or Aspergillus niger Result of antibiotic therapy that inhibits the growth of normal flora in the mouth Dental caries are the result of the destruction of tooth enamel caused by dental plaque

75 Treatment Good dental hygiene Antibiotics for bacteria Mouth rinse

76 Causes of Airway Obstruction
Foreign object Allergy Lesions Stenosis Swelling Viral and bacterial infections Fire or inhalation burns

77 Causes of Airway Obstruction
Allergic responses to foods, medications, or bee stings Infections after dental extraction that have a large amount of swelling Laryngeal trauma Aspiration of food material Large boluses as well as small pieces of food, such as peanuts

78 Epiglottitis Life-threatening bacterial illness that may lead to airway obstruction Epiglottis is a flap of tissue and cartilage that covers the opening of the trachea during swallowing Seen more frequently in children, but occurs in adults

79 Epiglottitis Cause of the infection usually is Haemophilus influenzae group B Symptoms: cherry red epiglottis, drooling, inspiratory stridor, dyspnea, and high fever

80 Nursing Management of Epiglottittis
Initial treatment focuses on maintaining a patent airway Conservative measures of oxygen, humidification, and inhaled respiratory therapy Administer Corticosteroids to reduce edema

81 Nursing Management of Epiglottittis
Administer antibiotics as prescribed to thwart the infection IV fluids are given for hydration Prepare for tracheotomy or endotracheal tube if the airway is in immediate jeopardy

82 Endotracheal (ET) Tube Intubation
May cause laryngeal trauma Placement of an ET tube may induce laryngeal swelling, which is a cause of upper airway obstruction after extubation Acute complications: perforation or laceration of the trachea or esophagus, bleeding, and arytenoid (cartilage that form larynx) dislocation

83 Nursing Management Ensure the endotracheal tube remains properly positioned and secured in place Unnecessary movement of the tube can irritate and inflame the laryngeal tissue Maintain sedation of the patient as ordered if the patient is restless Prepare to set up for a tracheostomy tube if intubation is anticipated to be necessary for longer than 7 to 14 days

84 Clinical Manifestations of Airway Obstruction
Stridor (partial obstruction) Unable to speak (complete obstruction) Labored respirations and use of accessory muscles Air hunger (mild obstruction) vs. cyanosis (complete obstruction)

85 Clinical Manifestations of Airway Obstruction
Confusion and unconsciousness indicate a progression in the severity of the obstruction If not treated, a partial obstruction can lead to a complete obstruction, rapid suffocation, and death

86 Nursing Management of Airway Obstruction
The initial assessment of objective and subjective data includes: Presence of spontaneous breathing Rate, depth, and effort of respirations Presence of grunting or wheezing Use of accessory muscles of respiration

87 Nursing Management of Airway Obstruction
The initial assessment of objective and subjective data includes: Symmetry of chest expansion (determined through palpation) vital signs Oxygen saturation level Quality of the voice Stridor or any type of noisy breathing

88 Other Nurse Assessment
Monitor the patient’s orientation, mentation, and general demeanor Assess the patient’s ability to handle oral secretions Pain with speaking or swallowing Assess for frequent drooling or productive coughing to clear the airway

89 Planning Care for the Patient with Upper Airway Obstruction
A patient with complete airway obstruction appears very anxious, agitated, and apprehensive, and progresses quickly to cyanosis and respiratory arrest There is no cough and the patient will be cyanotic and unable to speak

90 Planning Care for the Patient with Upper Airway Obstruction
If the patient is unable to speak, a Heimlich maneuver should be performed in case the obstruction is from a foreign object or food Anticipation is the key to saving patients with a complete airway obstruction

91 Planning Care for the Patient with Upper Airway Obstruction
Supplies should be kept at the bedside for creating an immediate artificial airway Resuscitation equipment should be brought to the bedside in case there is a subsequent cardiac arrest

92 Head and Neck Cancer More uncommon cancers; may not present until patient has a large tumor burden If detected early; head and neck cancer is treatable and curable If not treated; very disfiguring, alters normal functions Challenges for patient and family

93 Head and Neck Cancer Ablative surgery may leave patient with facial disfigurement, functional impairment Decisions regarding treatment must be informed decisions that include: Outcome without treatment Implications, risks, and benefits of surgery and radiation therapy

94 Etiology A variety of risk factors are associated with head and neck cancer Some patients do not have any of the known risk factors Not possible to know for sure how much they contributed to causing the cancer

95 Risk Factors for Oral and Oropharyngeal Cancer
Alcohol: six times more likely to develop these cancers Alcohol and smoking combined significantly increase risk over nonsmoking drinkers Ultraviolet light: >30% of lip cancers associated with prolonged exposure to sunlight

96 Risk Factors for Oral and Oropharyngeal Cancer
Tobacco: Approx. 90% of people with oral cavity and oropharyngeal cancer use tobacco Risk increases with amount smoked / chewed and duration Smokers six times more likely than nonsmokers to develop these cancers Tobacco smoke from cigarettes, cigars, pipes all implicated

97 Risk Factors for Oral and Oropharyngeal Cancer
Tobacco: Approx. 90% of people with oral cavity and oropharyngeal cancer use tobacco Can cause cancers anywhere in the oral cavity or oropharynx, and larynx Pipe smoking: significant risk for cancers where lips contact the pipe stem Smokeless tobacco increases risk by about 50 times

98 Risk Factors for Oral and Oropharyngeal Cancer
Tobacco: Approx. 90% of people with oral cavity and oropharyngeal cancer use tobacco Associated with cancers of the cheek, gums, and inner surface of the lips Exposure to secondhand smoke (called passive smoking) also a risk factor

99 Risk Factors for Oral and Oropharyngeal Cancer
Irritation: Long-term irritation to the lining of the mouth from poorly fitting dentures Poor nutrition: A diet low in fruits and vegetables increases risk Human papillomavirus infection: HPV infection may contribute to around 20% of cases

100 Risk Factors for Oral and Oropharyngeal Cancer
Immune system suppression: Immunosuppressive drugs may increase the risk Gender: Twice as common in men as in women Ethnicity: Asian heritage, first generation immigrant, are associated with nasopharyngeal cancer from the Epstein-Barr virus

101 Nursing Management for Patients with Head and Neck Cancer
Priorities are airway maintenance, pain management, and nutrition

102 Nursing Management for Patients with Head and Neck Cancer
If surgery, special needs and consideration: Wound management Drain assessment and care Oral care Wound complications Carotid artery exposure assessment and management

103 Airway Management – Assessment
Airway is the first priority Outcome is to maintain a patent airway and normal gas exchange Ongoing assessment: SOB, stridor, blood-tinged sputum, and infection Monitor increased WOB, use of accessory muscles Assess for increased heart rate and decreased O2 saturation levels Assess the type of airway that is being used

104 Nurse Interventions Secure airway with the appropriate ties
Prevents the possibility of the tube being dislodged or accidentally removed Change ties daily or when soiled to decrease the possibility of infection Clean the tracheostomy site regularly, e.g. every 8 hours

105 Nurse Interventions Clean more frequently p.r.n. to remove secretions that could obstruct the airway For tracheostomy tube with inner cannula, change if disposable or clean at every tie tracheostomy care Frequent assessment of secretions is essential to patient safety

106 Nurse Intervention for Artificial Airway
Humidification to the airway is necessary Bag/suction in early postop period if patient is unable to clear own secretions Patients may require mechanical ventilation in early postop period Monitor pulse oximetry, ABGs, respiratory rate and effort

107 Nurse Intervention for Artificial Airway
Deflate cuff when the patient is off positive pressure ventilation Turn, cough, and deep breathe Perform respiratory treatments with bronchodilators, and chest physiotherapy

108 Nurse Intervention for Artificial Airway
Early mobilization and ambulation greatly improve respiratory status Stimulate coughing Encouraging greater lung expansion Recruiting lung fields Mobilizing secretions Early ambulation also benefits circulation and increasing muscle strength

109 Laryngectomy Stoma Care
Permanent change in their airway Breathe only from their stoma Clean stoma at least every 8 hours, p.r.n. to prevent buildup of secretions, scarring Position patient’s head so as not to occlude the airway Humidification after discharge until the airway becomes used to room air

110 Nurse Management of Pain
Greatest fears for any patient undergoing cancer surgery is the fear of pain High nursing priority to alleviate pain and anxiety related to pain Careful and exact assessment of the type and location of the pain Have the patient set a goal pain level, using a pain rating scale

111 Nurse Management of Pain
Use the pain scale to evaluate effectiveness Note clues for patients who are unable to communicate Teach the patient not to wait until the pain is unbearable to request pain medication Early, immediate, frequent intervention for pain relief in immediate postop period

112 Nurse Management of Pain
Increase the dosage as the patient’s respiratory status tolerates it Consider patient-controlled analgesia (PCA) for alert cooperative patients Transition to oral meds as patient is able to swallow safely and in sufficient quantity to sustain nutrition and medication Treat joint pain with mobility, ambulation, turning, as early as postop day 1

113 Nutrition Management Present with inadequate nutrition caused by the tumor burden, cancer cachexia, or the mechanical difficulty of eating because of tumor impingement into the aerodigestive tract Early recognition of nutritional inadequacy and early intervention is critical Positive nitrogen balance, adequate calories and protein needed for healing

114 Nutrition Management The best test is serum prealbumin, transthyretin, or thyroxin-binding prealbumin (TBPA) Nutritionist in the multidisciplinary team is mandatory Nutritional goal for caloric intake in the postop period – roughly 35 kcal/kg With artificial airway, extra water loss through expiration, suctioning

115 Nutrition Management Carefully calculate replacement requirements to ensure proper hydration Feeding method depends on patient’s level of consciousness and ability to swallow Route may be oral, nasogastric, gastrostomy, jejunostomy Nutrition replacement must begin early and continue throughout the therapy

116 Nutrition Management Most feeding can begin on postop day 1
Advance to goals as quickly as tolerated Dysphagia is a common issue; tumor burden, invasion of the aerodigestive tract, pain Aspiration is a significant concern with patients who are unable to maintain their airway protection

117 Caring for the Patient with Lower Airway Disorders
35 Caring for the Patient with Lower Airway Disorders

118 Restrictive vs. Obstructive Lung Diseases
Restrictive lung diseases (interstitial lung diseases) Result in reduced lung volumes Alteration in lung parenchyma (alveolar tissue w/ terminal bronchioles, respiratory bronchioles, alveolar ducts) Disease of pleura, chest wall or neuromuscular apparatus Characterized by reduced total lung capacity, vital capacity, or resting lung volume

119 Restrictive vs. Obstructive Lung Diseases
Obstructive lung diseases – A group of disorders Common characteristic – chronic and recurring blockage of airways Limit airflow through the airways and out of the lungs

120 Restrictive (Interstitial) Lung Diseases
Divided into two groups based on anatomic structures: Intrinsic lung diseases Extrinsic lung diseases

121 Intrinsic Lung Diseases
Diseases of the lung parenchyma Cause inflammation or scarring of lung tissue or result in filling of the air spaces with exudate and debris Characterized according to etiologic factors Exposure to dust, metals, or organic solvents and agricultural employment increase risk

122 Extrinsic Lung Diseases
Extraparenchymal diseases – diseases of: Chest wall Pleura Respiratory muscles Result in: Lung restriction Impaired ventilatory function Respiratory failure

123 Extrinsic Lung Diseases
Extrinsic disorders of pleura and thoracic cage Total compliance by the respiratory system is reduced Lung volumes are reduced

124 Restrictive (Interstital) Lung Diseases
Clinical Manifestations of Intrinsic Lung Disease Onset can be acute or insidious (subtle gradual) Progressive exertional dyspnea Hemoptysis

125 Restrictive (Interstital) Lung Diseases
Clinical Manifestations of Extrinsic Lung Disease Onset dyspnea, decreased exercise tolerance, and respiratory infections Dyspnea upon exertion, followed by dyspnea at rest, ultimately advancing to respiratory failure Recurrent lower respiratory tract infections

126 Restrictive (Interstital) Lung Diseases
Diagnostic Tests Generally no positive findings revealed in intrinsic lung diseases Chest radiography and CT to diagnose intrinsic disorders Anemia – vasculitis Poycythemia (high RBC count) - hypoxia

127 Restrictive (Interstital) Lung Diseases
Extrinsic disorders – elevated creatinine kinase (CK) may indicate myositis (enflammation of muscle) Fluoroscopy to diagnose extrinsic disorders PFT and tests for extrinsic lung disorders: Bronchoalveolar lavage, lung biopsy, surgical lung biopsy

128 Acute Bronchitis Etiology Most prevalent in children and older adults
Incidence is highest in the winter High Risk People with allergies, other respiratory illnesses Chronic obstructive pulmonary disease (COPD), chronic sinusitis, chronic tonsillitis, infected adenoids Smokers are at a higher risk Sudden inflammation of the tracheobronchial tree Can be acute or chronic One of the most common conditions treated by primary care physicians

129 Acute Bronchitis Pathophysiology
Inflammation of the lower bronchial mucous membranes Commonly follows a respiratory viral illness Causative agents: viruses, bacteria, yeast, fungi, noninfectious triggers Most often the cause is viral; adenovirus, influenza virus, and RSV Common bacterial causes Streptococcus pneumoniae, Haemophilus influenzae, and Bordetella pertussis Other causes: pollutants, such as ammonia and tobacco

130 Acute Bronchitis Clinical Manifestations
Fever, cough, chills, and malaise Mimic pneumonia, but exam and chest x-ray often are normal Cough: Typically gets steadily worse for 10 to 12 days More profound at night Becomes increasing loose over time Most patients have a cough for less than 2 weeks Shortness of breath and wheezing

131 Acute Bronchitis Assessment Assessment findings reveal a cough
Viral bronchitis – nonproductive cough Bacterial bronchitis – productive cough, fever, pain behind the sternum aggravated by coughing

132 Acute Bronchitis Nursing Diagnoses
Priority nursing diagnoses for the patient with bacterial bronchitis include: Ineffective airway clearance Impaired gas exchange Activity Intolerance

133 Acute Bronchitis Outcomes Relief of the clinical manifestations
Return to the previous level of functioning

134 Acute Bronchitis Interventions and Rationales
Assist patients with prescribed therapies Use of antitussives, analgesics, and bronchodilator medications Encourage fluids Teach patients to cough effectively and avoid infections Offer mild analgesics for discomfort

135 Acute Bronchitis Interventions and Rationales
Offer patients deep breathing exercises, incentive spirometer Anticholinergics, antibiotic therapy (when indicated), IV corticosteroids or methylxanthines Antibiotics not shown to be effective except in patients with COPD Beta-2 agonists (brochodilators)

136 Acute Bronchitis Prevention/Evaluation
Relief of the respiratory symptoms including cough, wheezing, and shortness of breath Teach prevention and avoidance of risk factors

137 Influenza A contagious disease caused by the influenza virus
10% to 20% of people in US get influenza yearly An average of 36,000 deaths per year from influenza in US People ages 65+, people with chronic medical conditions more likely to have complications from the flu

138 Influenza Etiology Epidemics occur from December – April in the Northern Hemisphere Yearly epidemics of influenza begin abruptly and last 5 to 6 weeks Influenza A and B are the viruses that cause epidemic human disease

139 Influenza Etiology Pandemics occur when a new virus emerges for which there is no immunity Influenza virus type C has not been classified and usually does not induce illness

140 Influenza Pathophysiology
Transmission by small-particle aerosols – droplets from coughs, sneezes Viruses deposited in the lower respiratory tract Attach to and infect epithelial cells Contact with respiratory droplets, then touches own mouth or nose

141 Influenza Clinical Manifestations
Fever, chills, headache, fatigue, dry, nonproductive cough, sore throat, nasal congestion, and myalgia Cough may be associated with chest pain Fever usually persists for 3-4 days, up to 1 week Common complication is pneumonia, which may be primary influenza

142 Influenza Nursing Management
Primary care goals: relieving symptoms, preventing secondary infection Rest, plenty of fluids, avoid alcohol and tobacco, take mild pain relievers Work with health care provider to ensure medications taken appropriately Antiviral drugs approved for prevention, treatment

143 Influenza Prevention Flu Vaccine
Avoid contact with others who have the flu

144 Pneumonia Inflammatory process resulting in edema of the parenchymal lung tissue Extravasation of fluid into the alveoli causing hypoxemia Primarily affects terminal gas-exchanging portions of the lung

145 Pneumonia Etiology Acute inflammation of lung tissue
Caused by bacteria, viruses, fungi, protozoa, parasites Inhaled into lungs or transported via the bloodstream Classified by causal agent, distribution, setting (hospital -HAP or community - CAP) Causative microorganism influences S&S, treatment, prognosis CAP typically caused by different microorganisms than HAP

146 Pneumonia Pathophysiology
Damage to bronchial membranes causes buildup of infectious debris, exudates Results in dyspnea, ventilation/perfusion (V/Q) mismatching, and hypoxemia

147 Pneumonia Pathophysiology
CAP: begins outside hospital or is diagnosed w/in 48 hours after admission Patient did not reside in a long-term facility prior to admission Incidence of CAP is highest in winter months Smoking an important risk factor

148 Pneumonia Pathophysiology
HAP: occurs > 48 hours after hospital admission HAP has a mortality rate of 20% to 50% 90% of HAP infections are bacterial Compromised immune systems, chronic lung disease, intubation and mechanical ventilation increase risk

149 Pneumonia Clinical Manifestations Fever, chills
Increased respiratory rates Rusty bloody sputum Crackles X-ray abnormalities

150 Pneumonia Clinical Manifestations Nonrespiratory symptoms Headache
Abdominal pain Nausea and vomiting Diarrhea Muscle aches

151 Pneumonia Nursing Management Administer antibiotics (prime treatment)
Primary nursing intervention: Maintain airway and O2 saturation above 93% Common Nursing Diagnosis – Readiness for Enhanced Comfort Promote nutrition and hydration Provide small, frequent, high-carb, high-protein meals

152 Pneumonia Nursing Management Monitor fluid intake closely
Provide oral hygiene before and after meals Promote comfort Monitor for chest pain, note character and location Elevate head of bed 45 to 90 degrees Offer mild analgesics

153 Pneumonia Discharge Priorities/Prevention Teach patient about
Importance of rest, gradual increase in activity to avoid fatigue Maintain resistance with proper nutrition, adequate fluid intake Avoid chilling and exposure to others with URI, viral infections Medications that will be continued at home

154 Pneumonia Discharge Priorities/Prevention Teach patient about
Continue deep breathing and coughing exercises 4x/day, 6-8 weeks Signs and symptoms to report to health care provider

155 Tuberculosis Etiology
Mycobacterium tuberculosis is nonmotile, nonsporulating Transmitted via aerosolization (i.e., an airborne route) Affects people with repeated close contact with an infected but undiagnosed person TB an opportunistic infections common with HIV/AIDS

156 Tuberculosis Etiology
Continuous assessment and intervention to prevent the spread of TB The newest form of TB is multidrug-resistant tuberculosis (MDRTB) Resistant TB is difficult and costly to treat and can be fatal In 1900, TB was leading cause of death in US and Europe TB cases decreased by 7.1% annually from The annual decrease to the current average of 3.8% for Transmission affected by conditions (crowding, prisons), health status (poor nutrition, addiction) Noncompliance is a major cause of drug-resistant TB Multidrug-resistant TB cases declined sharply in US in past 10 years

157 Tuberculosis Pathophysiology
Highly communicable disease transmitted via aerosolization Droplets spread when infected person laughs, sneezes, or sings Droplets may be inhaled by others Tubercle finds a suitable site (bronchi or alveoli), multiplies freely

158 Tuberculosis Pathophysiology
An exudative response occurs, causing a nonspecific pneumonitis Mediated or type IV immunity develops 2-10 weeks after infection Manifested by a significant reaction to a tuberculin test

159 Tuberculosis Clinical Manifestations Dyspnea Weight loss Cough
Sputum production Sleep disturbances Symptoms present when the disease is well advanced

160 Tuberculosis Clinical Manifestations
Lethargy, exhaustive fatigue, activity intolerance, nausea, irregular menses Low-grade fever may have occurred for weeks or months Fever also may be accompanied by night sweats Patient finally notes cough, production of sputum, occasionally streaked with blood

161 Tuberculosis Clinical Manifestations
A dull aching chest pain may accompany the cough Dullness with percussion over involved parenchymal areas Bronchial breath sounds, increased transmission of spoken or whispered sounds Wheezing related to obstruction may also be heard

162 Tuberculosis Laboratory and Diagnostic Procedures Tuberculin skin test
Chest x-ray Acid-fast bacillus smear Sputum culture

163 Tuberculosis Nursing Management
Administer drug therapy as ordered by health care provider Report the diagnosis to the local health department Keep patient in negative pressure room with respiratory airborne isolation Maintain isolation until three consecutive sputum cultures have tested negative Focus on preventing the spread of the infection Discuss pain management, handling fatigue, importance of good nutrition

164 Tuberculosis Health Promotion and Prevention
The main focus of TB management is preventing spread of the infection Patient typically must take drugs for 9 months Test and treat all persons in close contact with the infected individual

165 Lung Abcess Etiology: The incidence of lung abscess is not well known, as it rarely occurs in isolation. Most often such an abscess is secondary to anaerobic and aerobic organisms that colonize the upper respiratory tract.

166 Lung Abcess Etiology: Patients presenting with this problem often have a history of pneumonia, possibly complicated by aspiration of oropharyngeal contents. Formation of multiple abscesses and cavities occurs commonly in patients with TB or fungal infections of the lung.

167 Lung Abcess Clinical Manifestations
Clinical manifestations are often insidious, although often more acute after pneumonia. Typically they include spiking temperature with rigors and night sweats; cough with foul sputum; pleuritic chest pain; tachycardia; dullness on percussion over the abcessed area. Oxygen saturation may decrease with larger abcesses

168 Lung Abcess Laboratory and Diagnostic Procedures CT scan
Pleural fluid and blood cultures may be obtained (thoracentesis) Bronchoscopy Transtracheal aspiration via suction

169 Lung Abcess Nursing Interventions
Assess the patient for adequate cough Administer IV antibiotic therapy if ordered Penicillin G or clindamycin is the pharmacologic therapy of choice Assess for recent history of influenza, pneumonia, febrile illness, cough, and sputum production Auscultate breath sounds

170 Lung Abcess Nursing Interventions
Manage patient’s clinical manifestations Monitor oxygen levels ongoing Assess the work of breathing, respiratory and heart rate Administer antipyretic, antibiotic, and pain medications

171 Lung Abcess Nursing Interventions
Follow-up assessment of effectiveness Space physical care to allow for periods of rest between activities

172 Lung Abcess Outcomes/Prevention Relief of clinical manifestations
Return to the previous level of function

173 Chronic Obstructive Pulmonary Disease
Refers to a group of respiratory disorders Characterized by chronic, recurrent obstruction in pulmonary airways Encompasses chronic bronchitis and emphysema Obstruction is generally permanent and progressive Chronic bronchitis defined in clinical terms

174 Chronic Obstructive Pulmonary Disease
Emphysema defined in terms of anatomic pathology Chronic bronchitis and emphysema typically coexist

175 Chronic Obstructive Pulmonary Disease
Unifying symptoms Dyspnea Wheezing Use of accessory muscles Ventilation/perfusion (V/Q) mismatching Decreased forced expiratory volume

176 Chronic Obstructive Pulmonary Disease
Emphysema: abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis

177 Chronic Obstructive Pulmonary Disease
Chronic bronchitis: characterized by hypersecretion of mucus and chronic productive cough that continues at least 3 months of the year for at least two consecutive years

178 Etiology The primary cause of COPD is exposure to tobacco smoke. Clinically significant COPD develops in 15% of cigarette smokers. Age of initiation, total pack-years, and current smoking status predict COPD mortality

179 Pathophysiology of Chronic Bronchitis
Inflammatory changes in the bronchial walls Causes them to thicken and impinge on the airway lumen Diffuse airway obstruction occurs Initially affects only larger bronchi; eventually involves all airways

180 Pathophysiology of Chronic Bronchitis
Obstructed airways are likely to close on expiration Traps air in the distal portions of the lung, causing: Hypoventilation (increased PaCO2) Ventilation/perfusion mismatching Hypoxemia

181 Pathophysiology of Chronic Bronchitis
Characterized by an increase in mucus production Mucus is thicker and more tenacious than normal Bacteria become embedded in the airway secretions and reproduce Ciliary function is impaired

182 Pathophysiology of Chronic Bronchitis
Edema and accumulation of inflammatory cells lead to bronchial wall inflammation and thickening Airway enlargement, loss of elastic recoil in the alveoli trap air, limit outflow

183 Pathyphysiology of Emphysema
Enzymes called proteases break down elastin, cause alveolar destruction Result is collapse or narrowing of the small airways Eliminates portions of the capillary bed necessary for gas exchange Airway enlargement, loss of elastic recoil combine to trap stagnant air

184 Pathyphysiology of Emphysema
Airway resistance is increased due to compromised alveolar walls Bullae and blebs (thin walled balloon-like extensions or air sacs) develop due to hyperinflation of alveoli inflammatory hyperactivity can lead to additional airway narrowing

185 Nursing Management of COPD Patient
Assess for dyspnea, muscle fatigue,↑ work of breathing, worsening symptoms Monitor ABG results Assist patient to manage the anxiety that often occurs

186 Nursing Management of COPD Patient
A major role of the nurse is patient and family education Breathing retraining Use of postural drainage techniques Energy conservation Physical reconditioning Single most important factor in preventing COPD – smoking cessation

187 Asthma A chronic hyperreactive disorder of the airways (bronchioles)
Episodic reversible airflow obstruction and airway inflammation Inflammatory process causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning

188 Asthma Caused by a complex interaction of genetic and environmental factors Airflow obstruction can be caused by a variety of changes, including: Acute bronchoconstriction Airway edema Chronic mucous plug formation Airway remodeling

189 Clinical Manifestations
Persons with asthma exhibit a wide range of signs and symptoms Episodic wheezing, feelings of chest tightness to acute immobilizing attacks

190 Nursing Management of the Patient with Asthma
A holistic approach to care through the nursing process Educate patient and family about prevention of attacks Thoroughly assess symptoms and history of attacks

191 Nursing Management of the Patient with Asthma
Assesses patient’s respiratory status by monitoring: Severity of symptoms Breath sounds Peak flow meter Pulse oximetry Vital signs

192 Nursing Management of the Patient with Asthma
Administer medication Educate public on symptoms and dangers of asthma

193 Etiology and Pathophysiology - Cystic Fibrosis
A person is born with CF, and it affects boys more than girls Affects Caucasians 5 times more often than African American people Typical features: mucous plugging, chronic inflammation, infection Peripheral bullae or blebs may develop due to obstruction, airway wall weakening Affects mucous glands of the lungs, liver, pancreas, and intestines Causes progressive disability due to multiple-system failure

194 Clinical Manifestations of CF
Acute exacerbation characterized by: Increasing breathlessness Change in sputum volume, color, and viscosity Tiredness Loss of appetite Weight loss

195 Clinical Manifestations of CF
Include barrel chest and digital clubbing GI: malabsorptive symptoms e.g. frequent loose and oily stools, cramping

196 Clinical Manifestations of CF
Signs and symptoms of diabetes including abnormal glucose tolerance, polydipsia, polyuria, and polyphagia Subtle manifestations: chronic sinusitis, nasal polyps, rectal prolapse

197 Nursing Management of CF
Assist patient to maintain adequate airway clearance, reduce risk factors, perform ADLs Prevent complications Involve patient/family in planning and implementing the therapeutic regimen Obtain objective and subjective data from the patient and family

198 Nursing Management of CF
Encourage use of corticosteroids, bronchodilators, and antibiotics Functional health patterns

199 Nursing Management of CF
Assessment of general impressions Mood, anxiety, depression, restlessness, failure to thrive Cyanosis of skin and nail beds Persistent runny nose, diminished breath sounds, sputum characteristics Tachycardia Protuberant abdomen, abdominal distention, foul and fatty stools

200 Nursing Management of CF
Possibly abnormal ABGs and PFTs; abnormal sweat chloride test, chest x-ray, and fecal fat analysis

201 Nursing Diagnoses Ineffective airway clearance related to thick and abundant mucus, weakness, fatigue Ineffective breathing pattern related to bronchoconstriction, anxiety, and airway obstruction Impaired gas exchange related to lung infections Imbalanced nutrition related to dietary intolerances, intestinal gas, and altered pancreatic enzyme production

202 Goals Focus on the patient having adequate airway clearance
Reduced risk factors associated with respiratory infections Assist clients to perform ADLs, stay free of complications, actively participate in planning and implementing a restorative regimeAssist patients in gaining and maintaining independence by assuming responsibility for their own care. Active interventions include relief of bronchoconstriction, airway obstruction, and airflow limitation Encourage frequent hand washing, especially after coughing

203 Goals Frequent mouth care, especially after chest physical therapy regime Avoid exposure to persons who are ill especially with Upper Respiratory Infections

204 Pulmonary Embolism Thrombus breaks loose and blocks a branch of the pulmonary artery Produces widespread pulmonary vasoconstriction Predominantly a disease of older individuals Highest incidence of recognized PE occurs in hospitalized patients

205 Pulmonary Embolism Pulmonary embolism is a complication of a DVT
Most common risk factors for PE are: Prior history of DVT or PE Recent surgery or pregnancy Prolonged immobilization Underlying malignancy Risks also include situations of venous stasis or increased hypercoagulability

206 Pathophysiology and Clinical Manifestations of PE
A pulmonary occlusion occurs when a bloodborne substance occludes a branch of the pulmonary artery and obstructs blood flow Hemoptysis, dyspnea, and chest pain Pleuritic chest pain, chest wall tenderness, a pulmonary friction rub, or hypotension

207 Pathophysiology and Clinical Manifestations of PE
Tachypnea, crackles, an accentuated second heart sound, tachycardia, fever, diaphoresis, S3 or S4 gallop, thrombophlebitis, lower extremity edema, cardiac murmur, and cyanosis Massive PEs typically present with sudden crushing substernal chest pain, shock, and loss of consciousness

208 Nursing Management of PE
The nursing process guides the nursing care for patients with a PE Evaluation of risk factors on admission and throughout the patient’s hospital stay Initially clients may be on bed rest Nurses should encourage maximal mobility, including range of motion and walking where appropriate while also staying alert to symptoms of DVT

209 Nursing Management of PE
Nursing diagnoses: ineffective tissue perfusion and impaired gas exchange Assist the patient to maintain the therapeutic regime during the acute period Anticoagulant medication should be given at the same time each day Monitor liver function when patients receive anticoagulants

210 Nursing Management of PE
Monitor hemoglobin, hematocrit, platelet, and the international normalized ratio (INR) levels, and other clotting studies as needed to assess the effectiveness of anticoagulants Assess for symptoms of bleeding and heparin-induced thrombocytopenia (HIT)

211 Nursing Management of PE
Discharge priorities include educating the patient and family about risk factors and treatment regimes

212 Cor Pulmonale Alteration in the structure and function of the right ventricle Caused by a primary disorder of the respiratory system Chronic lung disease Pulmonary embolism Interstitial lung disease Primary pulmonary hypertension

213 Cor Pulmonale Pathophysiological mechanisms lead to Primary Pulmonary Hypertension and consequently, cor pulmonale Pulmonary vasoconstriction due to alveolar hypoxia Anatomic compromise of the pulmonary vascular bed Increased blood viscosity secondary to blood disorders Idiopathic primary pulmonary hypertension

214 Two Forms of Cor Pulmonale
Acute: usually results from massive PE or injury d/t mechanical ventilation for ARDS Chronic cor pulmonale usually caused by COPD

215 Laboratory and Diagnostic Procedures
Echocardiography gives information about the size of the heart Chest x-rays and CAT scan PFT evaluate ventilation/perfusion mismatch ABG tests identify gas exchange, presence of acidosis and alkalosis

216 Clinical Manifestations
Asymptomatic initially Later, as right ventricular (RV) pressures increase, physical signs commonly include: Left parasternal systolic lift (visible pulsations to left midsternal) Loud pulmonic component of the second heart sound (S2) Murmurs of functional tricuspid and pulmonic insufficiency

217 Clinical Manifestations
Later, as right ventricular (RV) pressures increase, physical signs commonly include: Later, an RV gallop rhythm (third [S3] and fourth [S4] heart sounds) Distended jugular veins, hepatomegaly Lower extremity edema

218 Clinical Manifestations
Later, as right ventricular (RV) pressures increase, physical signs commonly include: Patient may complain of fatigue, dyspnea or chest pain on exertion, cough In advanced stages, hepatic congestion leads to anorexia, RUQ abdominal discomfort

219 Nursing Management Physical assessment findings:
Increased chest diameter Labored respirations with retractions of the chest wall and use of accessory muscles Hyperresonance to percussion Diminished breath sounds Wheezing, rarely Cyanosis

220 Nursing Management Physical assessment findings:
Auscultation of the heart may reveal a split second heart sound, a systolic ejection murmur with a sharp ejection click over the pulmonary artery, along with a diastolic regurgitation

221 The Primary Role of the Nurse
Manage dyspnea by administration of oxygen Administer medications to treat right ventricular hypertrophy and pulmonary hypertension Provide patient education re: managing equipment and medications Refer to home health and pulmonary rehabilitation

222 The Primary Role of the Nurse
Regularly assess oxygen needs and medications Single most preventive measure – encourage smoking cessation Avoid exposure to secondhand smoke and respiratory pollutants

223 LEARNING OBJECTIVE 4 Compare and contrast the etiology and nursing management for patients with a variety of chest trauma and thoracic injuries.

224 Chest Trauma and Thoracic Injuries
16,000 deaths in the United States each year Cause of death in 25% of all trauma patients ↑ hand gun use has contributed to rise in penetrating injuries These injuries impair airway patency, breathing, and circulation

225 Rib Fractures Most common blunt thoracic injury in adults
Associated with other injuries such as flail chest, pulmonary contusion, and pneumothorax

226 Etiology Usually are caused by a direct blow to the ribs
Sternal fractures are most common in motor vehicle accidents Forceful compression of the rib cage

227 Nursing Management Astute assessment for respiratory complications
Diligent patient monitoring for dyspnea, hypoxemia, and pain Administer pain medication and assess for pain relief Auscultate lung fields regularly for adventitious sounds

228 Nursing Management Provide written instructions regarding the plan of care Teach patient and family when to call members of the health team

229 Pneumothorax Partial or complete collapse of the lung on the affected side Under normal circumstances the pleural cavity is free of air When air or gas enters the pleural space pneumothorax results

230 Spontaneous Pneumothorax
Occurs unexpectedly in healthy individuals ages 20-40 More common in tall, thin men Smoking also is a risk factor, due to disease in the small airways Caused by a ruptured, air-filled bleb or blister on the lung surface

231 Spontaneous Pneumothorax
Bleb rupture allows atmospheric air to enter the pleural cavity Results in a loss of negative pressure and collapse of the lung

232 Tension Pneumothorax Rapidly developing complication of blunt chest trauma Occurs as a result of an air leak in the lung or chest wall Caused by blunt chest trauma Parenchymal injury has failed to seal, causes complete collapse of the lung

233 Hemothorax Common problem encountered following blunt chest trauma
Blood loss of <2,000 mL into the thoracic cavity Absence of breath sounds over the lung and dullness to percussion

234 Clinical Manifestations
Pleuritic pain Breathlessness Respiratory distress Breath sounds are unilaterally decreased or absent

235 Nursing Management Assess pulmonary status quickly
The nurse focuses on relieving dyspnea and supporting oxygenation Mobilize health team to provide re-expansion of the lung via a chest tube Prepare for insertion of the chest tube Monitor patency of chest tube

236 Nursing Management Provide the patient with written instructions regarding the plan of care Encourage patients/caregivers to call health team for persistent problems Explain risk of reoccurrence

237 LUNG CANCER - Etiology Prevention efforts target preventing exposure to known risk factors, e.g. smoking Cellular genetic destruction results from repeated exposure to carcinogens

238 Etiology Smoking accounts for 87% of all lung cancer deaths
Other risk factors: occupational hazards, air pollution, genetics, dietary factors, advancing age, and race

239 Pathophysiology Four major histologic types of lung cancer
Small cell carcinoma (SCLC) Squamous cell carcinoma Adenocarcinoma Large cell carcinoma SCLC accounts for 15% of cases in US SCLC disseminates widely by the time of diagnosis, leads to a poor prognosis

240 Pathophysiology 85% of all lung cancers are non-small cell lung cancer (NSCLC) NSCLCs all have unique patterns of growth and clinical appearance Squamous cell tumors malignancies tend to be slow growing

241 Pathophysiology NSCLCs all have unique patterns of growth and clinical appearance Adenocarcinoma – most common form of lung cancer, most common type in nonsmokers Progression is slow Adenocarcinoma invades the lymphatic/blood vessels early Result is a worse prognosis compared to that for SCLCs

242 Pathophysiology NSCLCs all have unique patterns of growth and clinical appearance Large cell lung cancer commonly located in periphery of the lung Often spreads to the subsegmental bronchi or larger airways

243 Clinical Manifestations
Cough Dyspnea Sputum production Wheezing Hemoptysis Chest pain Dysphagia

244 Clinical Manifestations
Hoarseness Fatigue Weakness Nausea Disturbed sleep Memory impairments Anorexia

245 Clinical Manifestations
Night sweats Early diagnosis of lung cancer is difficult Typically no symptoms until disease has metastasized

246 Nursing Management Close postoperatice observation for cardiac and pulmonary complications Dyspnea is the most common postoperative symptom Effective pain management enables participation in progressive mobilization

247 Lung Transplant Viable alternative for patients with advanced pulmonary disease

248 Lung Transplant Indications:
AAT deficiency (Alpha-1 antitrypsin (AAT) deficiency is a condition in which the body does not make enough of a protein that protects the lungs and liver from damage.) Bronchiectasis Cystic fibrosis Emphysema Idiopathic pulmonary fibrosis Interstitial lung disease Pulmonary hypertension

249 Lung Transplant Persons >60 years of age not recommended for single lung transplant

250 Lung Transplant The following do not qualify for lung transplant:
Colonization with antibiotic-resistant organisms Noncompliance with medical regime Inability to walk 600 feet Diagnosis of a malignancy within 2 years Renal or liver insufficiency Positive for HIV

251 Lung Transplant Infection postoperatively is the leading cause of morbidity and mortality

252 Occupational Lung Disorders: Pneumoconiosis
Long-term exposure to toxic dust and particulates can lead to irreversible chronic pulmonary disease Most common causes: silica, asbestos, and coal Dust deposits are permanent

253 Occupational Lung Disorders: Pneumoconiosis
No definitive treatment for the pulmonary fibrotic changes Treatment is palliative Focuses on preventing further exposure and improving workplace safety

254 Occupational Asthma Exposure to particulate matter, workplace chemicals, gases, cereal grains, or irritants Causes inflammation and edema of any portion of the respiratory tract Results in bronchospasm, hypersecretion of mucus, dyspnea, wheezing

255 Occupational Asthma Symptoms are dyspnea, wheezing, and chest tightness Difficult to recognize because symptoms continue when away from the source of exposure

256 Coal Miner Pneumoconiosis
Known as black lung or coal miner’s lung Caused by coal dust deposits in the lung Disease affects about 4.5% of coal miners Patients experience a restrictive disease in which they cannot fully expand their lungs as well as an obstructive disease from secondary emphysema

257 Asbestosis Progressive lung disease
Caused by exposure to microscopic fibers of asbestos Results in diffuse interstitial fibrosis with diaphragmatic calcification Fibrous tissue eventually obliterates the alveoli Latency period years between exposure and symptoms

258 Whose at Risk for Asbestosis?
Asbestos miners, millers Those employed in building trades and shipyards Insulation workers, pipe fitters and steamfitters Sheet metal workers, welders

259 Diagnosis and Clinical Manifestations
PFT findings – restrictive ventilatory defect, restricted lung volume Dyspnea and hypoxemia Removal of the individual from exposure is essential Crackles of a dry quality can be auscultated in 70% to 90% of patients Clubbing also is present frequently

260 Diagnosis and Clinical Manifestations
Chronic cough and sputum production, similar to acute bronchitis Sputum is expectorated in large amounts May contain black fluid, particularly with smokers Respiratory failure and cor pulmonale result

261 Nursing Management Offer supportive care and education for patient and caregiver Address issues: dyspnea, fatigue, and activity tolerance Teach physical conditioning and breathing exercises are helpful Encourage liberal fluids intake

262 Nursing Management Administer bronchodilators, glucocorticoids, and antibiotics Address emotional issues such as depression, anxiety, and anger Educate patient prior to discharge about all aspects of the treatment regime Provide relevant contact numbers to the patient and caregiver

263 Caring for the Patient with Complex Respiratory Disorders
36 Caring for the Patient with Complex Respiratory Disorders

264 Complex Respiratory Disorders
Lead to alteration of oxygen perfusion Caused by problems elsewhere in the body

265 Goals of Treatment Medical Management Nursing Management
Correct and treat hypoxemia Discover and correct primary organ system failure Nursing Management Manage the airway Manage oxygen for perfusion

266 The Alveolar-Capillary (A-C) Membrane
Central component of gas exchange in lungs Oxygen diffuses from alveoli into pulmonary capillaries Attaches to the hemoglobin in the red blood cells Carbon dioxide moves in the opposite direction, into the lungs

267 The Alveolar-Capillary (A-C) Membrane
Figure Alveolar-capillary membrane

268 Ventilation/Perfusion
Ventilation (V) – movement of air Perfusion (Q) – the movement of blood carrying oxygen Near equal relationship of ventilation (4L/min) and perfusion (5L/min) Acute Respiratory Failure commonly caused by mismatch of ventilation and perfusion

269 V/Q is equal to 0.8 – no miss match
Figure Ventilation/perfusion relationships: (A) normal unit; (B) dead space unit; (C) shunt unit; (D) silent unit. V/Q is equal to 0.8 – no miss match V/Q is >0.8 – there is ventilation but no perfusion V/Q is <0.8 – there is perfusion but little or no ventilation V/Q no perfusion and no ventilation (b) Pulmonary Emboli and cardiogentic shock (C) Pulmonary edema pneumonia etc

270 Acute Respiratory Failure
Defined as a failure of gas exchange Respiratory system unable to provide O2 and remove CO2 Results in failure of oxygenation, failure of ventilation, or both

271 Classification of Acute Respiratory Failure (ARF)
Hypoxemia (deprived of oxygen) Caused by failure of oxygenation Hypercapnea (high CO2 in blood) Caused by failure of respiratory system to ventilate Failure of respiratory centers in the brain

272 Classification of ARF Hypoxemia: Hypercapnea:
PaO2 below normal (<60 mmHg) SaO2 <90% on room air Hypercapnea: PaCO2 above normal (>50 mmHg) pH <7.3

273 Pathophysiology Hypoventilation Shunting
Ventilation/perfusion mismatch: most common cause

274 Acute Pulmonary Edema Abnormal accumulation of fluid in the lungs
Occurs rapidly – over minutes or hours Etiologies – all relate to failure of heart and/or lungs

275 Cardiogenic Pulmonary Edema
Initial insult is caused by heart failure ↑ Pulmonary venous pressure leads to ↑ Hydrostatic pressure in pulmonary capillaries Result: pulmonary edema Cardiac dysfunction is most common factor Fluid overload, and chronic hypoxemia may also be present

276 Noncardiogenic Pulmonary Edema
Insult to the A-C membrane Changes the permeability of the A-C membrane Major causes: sepsis, inflammation, inhaled toxins, drugs

277 Neurogenic Pulmonary Edema
Direct insult to central nervous system Examples: seizures, cerebral hemorrhage, head injury Dyspnea (shortness of breath) is primary presenting symptom Other symptoms may be present Crackles, pink frothy sputum

278 Negative Pressure Pulmonary Edema
Caused by ventilation with airway obstruction High pressures required When obstruction is relieved Hydrostatic pressure pushes fluid into lungs

279 PE and Specific Populations
Mountain climbers Heroin users Scuba divers/hyperbaric chamber users Excessive intravenous fluid administration

280 Clinical Manifestations of Cardiogenic PE/Non-Cardiogenic PE
Respiratory clues are identical Agitation, confusion common to both CPE and NCPE Distinguishing factors are subtle Most evident in cardiac assessment, skin appearance

281 Differentiating CPE/Non-CPE
Mostly evident in cardiac assessment, skin appearance Example 1: tachycardia with hypotension and cool diaphoretic skin suggests CPE Example 2: tachycardia with hypertension, bounding pulses and dry skin suggests NCPE

282 Differentiating CPE/Non-CPE
Other Distinguishing Factors Jugular Vein Distension more common in CPE If coronary artery catheter is used, Pulmonary Artery Occlusion Pressures (PAOP) or Pulmonary Capillary Wedge Pressure (PCWP) above 18mmHg confirms CPE

283 Acute Respiratory Distress Syndrome (ARDS)
Most severe type of respiratory failure Caused by injury to A-C membrane Mortality rate = 40% Acute lung injury (ALI) less severe than ARDS

284 Acute Respiratory Distress Syndrome (ARDS)
Lets fluids, proteins etc. flow into the lungs Lung injury → Inflammation → Pulmonary edema → Hypoxemia

285 Acute Injury to the Lungs
Causes of direct injury Aspiration of gastric contents – most common cause of ALI Trauma, Infection Indirect injury – intermediary process causes injury Sepsis, acute pancreatitis, major inflammatory process

286 Treatment of ARDS/ALI Specific therapy to treat underlying cause
Supportive treatment Oxygen Mechanical ventilation Fluid management

287 How the Ventilator Works
Monitors respiratory rate, pressure, volume Delivers specified volume, pressure, or both Controls concentration of oxygen Mixes compressed air with oxygen to reach desired FiO2

288 Nursing Issues Complexity of equipment is increasing
Variety of equipment is increasing No standard terminology among manufacturers

289 Terminology Spontaneous breaths Mandatory breaths Assisted breaths
Types of ventilation Modes

290 Types of Breath Spontaneous breaths Assisted breaths
Patient initiates breath Patient controls switch from inspiration to expiration Assisted breaths Ventilator controls switch to expiration Ventilator controls volume and pressure

291 Terminology Mandatory breaths – controlled entirely by ventilator
Inspiration Expiration Volume/pressure of gas delivery

292 Types of Ventilation Volume – clinician controls tidal volume; pressure can vary – can set rate, set volume Pressure – clinician controls pressure; tidal volume can vary - set rate, set pressure, need to monitor minute volumes No clinical consensus on preferred type

293 Common Ventilator Modes
Mode: describes the pattern of breath delivery Common modes Assist control mode (ACM) Synchronized mandatory intermittent ventilation (SIMV) Pressure support (PS or PSV) Pressure controlled ventilation (PCV)

294 Assist Control Mode ACM delivers a preset volume or a preset pressure for each breath Patient can trigger a breath or the breath can be time triggered (CMV, A/C) Commonly used in care of in the postoperative patient

295 Assist Control Mode Nursing Implications of ACM
As patient awakens, she or he may begin initiating breaths Machine may not have time to deliver set volume Patient can become hypoxic by attempt to breathe faster, stacking breaths Pressure builds; lungs may be injured

296 Assist Control Mode Nursing Implications of ACM
Nurse must monitor to assure that patient and machine are working together

297 Synchronized Intermittent Mandatory Ventilation
Very common mode in US SIMV sets the mandatory respiratory rate (VE ) Ventilator will deliver a set volume or pressure Patient can also initiate a breath Ventilator waits for the patient, to breathe Synchronizes delivery of breath in concert with the patient

298 Synchronized Intermittent Mandatory Ventilation
Nursing Implications of SIMV Desirable for patient to “overbreathe” the machine; i.e. breathe faster than the VE In SIMV, patient may initiate breaths, some are assisted and some are not Team should evaluate VE, level of sedation or analgesia

299 Pressure Support PS is a form of assisted ventilation
Requires stable respiratory effort from patient IF ventilator senses negative pressure on inspiration THEN ventilator supports the patient-initiated breath

300 Pressure Support Does not control the rate or tidal volume
Therefore, usually used with SIMV, CPAP mode PS not triggered unless patient breathes above the VE (mandatory rate)

301 Pressure Support Nursing Implications of PS with SIMV
If patient does not “overbreathe” the machine, no benefit from PS The nurse should assess the patient and talk to the team to determine a course of action

302 Pressure Control Ventilation
Clinician sets rate and pressure Tidal volume is allowed to vary Usually reserved for patients with noncompliant lungs, difficult to ventilate and oxygenate Gas delivery distinguishes PCV from PS Breath triggers rapid delivery of gas to reach set pressure, then the flow is decelerated

303 Pressure Control Ventilation
Nursing Implications of PCV The nurse should trend the VE and the expiratory volume over time Volume decrease may indicate lungs are becoming less compliant Adjust Pressure to Achieve the Same Volume

304 Positive End-Expiratory Pressure
PEEP is a ventilator setting, not a mode Provides resistance at end of exhalation Prevents alveoli from collapsing CPAP – continuous positive airway pressure – related to PEEP

305 Three Types of PEEP Physiological PEEP – 5 cm of H2O
Treatment PEEP – >5 cm of H2O Auto-PEEP For most ventilated patients, PEEP of at least 5 cm of H2O required to prevent alveolar collapse

306 Nursing Implications of PEEP
PEEP of greater than 5 cm of H2O can cause decreased cardiac output Pneumothorax at higher levels of PEEP The nurse should be aware of the level of PEEP

307 Auto-PEEP Potential problems Result: pressure builds in the lungs
Ventilator set rate is too high Overaggressive use of an Ambu bag Result: pressure builds in the lungs Disconnect the ventilator or Ambu briefly Allows the excess pressure to dissipate

308 CPAP Commonly used prior to extubation
Patient is breathing spontaneously Ventilator support at end of expiration only

309 Nursing Assessment in ARF
Priorities are airway and oxygenation status Frequent, ongoing assessment is vital

310 Assessment Data Ask if the patient feels s/he is getting enough air
Evaluate for anxiety Respiratory rate, work of breathing, SO2, vital signs Assess skin and nail beds for cyanosis and pallor

311 Nursing Diagnosis Impaired gas exchange
Ineffective tissue perfusion: cardiopulmonary and peripheral Deficient knowledge related to the disease process Self-care deficit Ineffective airway clearance Ineffective breathing pattern

312 Nursing Interventions in ARF
Encourage deep breathing and coughing Encourage incentive spirometer use, if ordered Frequent turning and repositioning

313 Indications for Endotracheal Intubation
Inability to maintain oxygenation/ ventilation Airway protection Elective surgery

314 Nurse’s Role Know the proper equipment and its use
Anticipate the health provider’s needs Position the patient Preoxygenate the patient Provide suction as necessary Monitor the patient Provide information and reassurance

315 Figure 36.6 Endotracheal tube.
How Intubation Works Figure Endotracheal tube.

316 Documentation Size of ET tube Location of ET tube in airway
Medications administered Patient’s tolerance of procedure

317 Suctioning Performed based on assessment only Never routinely ordered
DO: Hyperoxegenate before/after suctioning DON’T: Routinely instill normal saline before suctioning

318 Complications Hypoxemia Bronchospasm Cardiac arrhythmias Tissue injury
Increased risk of infection

319 Closed Suctioning System
Patient with high PEEP, high FiO2 Closed system keeps pressure up Patient cannot tolerate use of open system Patient with airborne infectious disease Avoids exposing others to aerosolized infectious secretions

320 LEARNING OBJECTIVE 9 State two indications for insertion of a chest tube in a patient in an acute care setting.

321 Chest Tube Another major intervention for respiratory compromise
Tension pneumothorax – common reason for chest tube insertion


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