Common Respiratory Disorders Flashcards
Exam 1
1
Q
Pneumonia: What is it?
A
An infection involving the lower respiratory tract,
2
Q
Pneumonia: What is it caused by?
A
caused by any class of organism (ie, bacteria, viruses, fungi, amoebae, or parasites) associated with human infections.
3
Q
What is the leading cause of death worldwide?
A
Pneumonia is the leading cause of death worldwide in the United States.
4
Q
What is the ninth leading cause of death?
A
Pneumonia combined with influenza is the ninth leading cause of death
5
Q
Types of Pneumonia that exist?
A
Community Acquired Pneumonia (CAP)
Hospital-acquired pneumonia (HAP)
Health care–associated pneumonia (HCAP)
Ventilator-associated pneumonia (VAP)
6
Q
Types of Pneumonia that exist:
Community Acquired Pneumonia (CAP): What is it? What are people with this at low risk of developing?
A
Pneumonia diagnosed in people who have limited contact with the health care system and are at low risk for developing MDR infections
7
Q
Types of Pneumonia that exist:
Hospital-acquired pneumonia (HAP): What is it?
A
Pneumonia occurring more than 48 hours after admission to a hospital
8
Q
Types of Pneumonia that exist:
Health care–associated pneumonia (HCAP):
What is it?
A
An expansion of HAP to include patients who reside in residential treatment centers or nursing homes, or who have risk factors (such as recent chemotherapy) for developing MDR infections
9
Q
Types of Pneumonia that exist:
Ventilator-associated pneumonia (VAP):
What is it?
A
Pneumonia occurring in patients who have been intubated for more than 48 hours
10
Q
Pneumonia—Etiology
What causes it?
A
Bacteria, viruses, mycoplasmas, fungi, and foreign material
11
Q
Pneumonia—Etiology
What is the most predominant pathogen?
A
Streptococcus pneumoniae (pneumococcus) is the predominant pathogen and most common cause in patients hospitalized for pneumonia.
12
Q
Pneumonia—Etiology
Other pathogens that cause Pneumonia?
A
Others include Haemophilus influenzae, Staphylococcus aureus, and other Gram-negative bacilli.
13
Q
Pneumonia—Etiology
What is frequently seen in individuals older than 65?
A
Drug-resistant S. pneumoniae is frequently seen in individuals older than 65 years of age.
14
Q
Pneumonia—Etiology
What is typical pneumonia?
A
S. pneumoniae, S. pyrogenes, and S. aureus
15
Q
Pneumonia—Etiology
What are atypical pneumonia?
A
Mycoplasma pneumoniae, C. pneumoniae, influenza virus, adenovirus, and Legionella species
16
Q
Pneumonia—Assessment
What to look for in the history?
A
Risk Factors
Signs and symptoms
17
Q
Pneumonia—Assessment
Physical findings
A
Hypoxemia, dyspnea, new onset respiratory symptoms (cough, sputum production, dyspnea, pleuritic chest pain, hemoptysis), fever, and chills
18
Q
Pneumonia—Assessment
Physical findings: Having to do with breathing?
A
Dullness with percussion, decreased breath sounds, tactile fremitus, crackles or bronchial breath sounds
19
Q
Pneumonia—Assessment
Physical findings: Other findings?
A
Myalgia, new-onset seizures, periodontal disease, GI symptoms, nonexudative pharyngitis, splenomegaly, and confusion in elderly patients
20
Q
Pneumonia—Diagnostic Studies
A
Chest radiograph (AP and lateral)
Blood cultures
CBC
Electrolytes
Renal and liver function
ABG
Thoracentesis
WBC with differential
Pretreatment gram stain of sputum
UAT (urine antigen test) to rule out Legionella and Streptococcus
Respiratory viral testing
21
Q
Pneumonia—Management
A
Antibiotic therapy
Supportive therapy
Prevention
22
Q
Pneumonia—Management
Antibiotic therapy:
What is it considered?
When is the first dose given?
A
Cornerstone of treatment
First dose within 3 hours of arrival to hospital
23
Q
Pneumonia—Management
Supportive therapy: What does it include?
A
Oxygen, mechanical ventilation, pulmonary toilet, nutritional support
24
Q
Pneumonia—Management
Prevention: What does it include?
A
Influenza and pneumococcal vaccine
25
Pleural Effusion—Pathophysiology
Caused by at least one of the five following mechanisms:
26
Pleural Effusion—Pathophysiology
Caused by at least one of the five following mechanisms:
An increase in...
Increased pressure in pulmonary capillaries (eg, heart failure, massive PE)
Increased capillary permeability (eg, pneumonia, malignancy, infection, pancreatitis)
Increased intrapleural negative pressure (eg, atelectasis, trapped lung)
27
Pleural Effusion—Pathophysiology
Caused by at least one of the five following mechanisms:
An decrease in...
Decreased plasma osmotic pressure (eg, hypoalbuminemia, hypoproteinemia, cirrhosis)
28
Pleural Effusion—Pathophysiology
Caused by at least one of the five following mechanisms:
An impaired...
Impaired lymphatic drainage of the pleural space (eg, pleural malignancy or infection)
29
Pleural Effusion—Pathophysiology
What can pleural effusion be a complication of?
Pleural effusion is a complication of pneumonia.
30
Pleural Effusion—Pathophysiology
What is pleural effusion?
Accumulation of fluid in the pleural space.
31
Pleural Effusion—Assessment
What does it include?
History and physical findings
Subjective findings:
Objective findings:
32
Pleural Effusion—Assessment
What are subjective findings?
Subjective findings: shortness of breath and pleuritic chest pain, depending on the amount of fluid accumulation
33
Pleural Effusion—Assessment
What are Objective findings?
Objective findings:
tachypnea and hypoxemia if ventilation is impaired,
dullness to percussion,
and decreased breath sounds over the involved area
34
Pleural Effusion—Diagnostic Studies
What does it include?
Chest radiograph, ultrasound, or a CT scan
When physical exam and CXR confirm diagnosis pleural fluid exam via thoracentesis is performed.
35
Pleural Effusion—Diagnostic Studies
What does thoracentesis do?
Thoracentesis distinguishes transudate from exudate.
36
Pleural Effusion—Management: What is included?
Treat the underlying cause.
Drainage of the pleural effusion by thoracentesis
Chest tube placement or surgery may be indicated depending on the etiology and size
37
Pleural Effusion—Management:
Chest tube placement or surgery may be indicated depending on what?
the etiology and size.
38
Pleural Effusion—Management:
Drainage of the pleural effusion by
thoracentesis
39
Pneumothorax:
What occurs in this? What does it produce?
Air enters the pleural space between the visceral and parietal pleurae, producing partial or complete lung collapse.
40
Pneumothorax:
Pathophysiology
Sudden communication of the pleural space with alveolar or external air
Pleural pressure rises and the elasticity of the lung causes collapse.
41
Pneumothorax:
What are the two types?
Spontaneous or traumatic
42
Pneumothorax:
Spontaneous
Any pneumothorax that develops without trauma.
43
Pneumothorax:
Traumatic:
From trauma.
44
Pneumothorax—Assessment
History and physical findings
Sudden onset of pleuritic chest pain
Shortness of breath, dyspnea, increased work of breathing
Uneven chest wall movement
Distant or absent breath sounds
Hyperresonant to percussion
Tachycardia
45
Pneumothorax—Diagnostic Studies
Chest radiograph,
CT
46
Pneumothorax—Diagnostic Studies
Management:
Supplemental oxygen
Chest tube
47
Pneumothorax—Diagnostic Studies
Tension pneumothorax
—life threatening
When pressure of the air in the pleural space exceeds atmospheric pressure.
As pressure in the thorax increase, the mediastinum shifts to the collateral side, placing torsion on the inferior vena cava and decreasing venous return to the right side of the heart.
48
Pneumothorax—Diagnostic Studies
Tension pneumothorax: Intervention
Large-bore (16- or 18-gauge) needle should be placed into the anterior second intercostal space.
49
Tension pneumothorax: What is heard? What else?
Tension pneumothorax: breath sounds absent. You may also found distended neck vessels.
50
Pulmonary Embolism: What is it?
Thrombus migrates to pulmonary arteries.
51
Pulmonary Embolism: What does it include?
Venous thromboembolism includes pulmonary embolism and deep vein thrombosis
52
Pulmonary Embolism: What is it called (the three things)
Virchow’s triad (venous stasis, hypercoagulability, vein wall damage)
53
Pulmonary Embolism
Virchow’s triad (venous stasis, hypercoagulability, vein wall damage)
What contributes to this?
Immobility, heart failure, dehydration, and varicose veins contribute to decreased venous return, increased retrograde pressure in the venous system, and stasis of blood with resultant thrombus formation.
54
Pulmonary Embolism—Assessment
What are PE's called? Why?
PE called “the great masquerader” because of nonspecific signs and symptoms
55
Pulmonary Embolism—Assessment
What are symptoms that are assessed?
New onset of dyspnea, tachycardia or sustained hypotension without other explanation
Chest pain, cough (with or without hemoptysis), clinical signs of DVT, and syncope
56
Pulmonary Embolism—Assessment
Diagnosis: Using what?
Computed pulmonary angiography
Ventilation–perfusion (VQ) scans
Transthoracic echocardiogram (TEE)
57
Pulmonary Embolism—Management
Using what to treat?
Heparin and thrombolytics
Continue oral anticoagulants for 3 to 6 months.
58
Pulmonary Embolism—Management
Heparin and thrombolytics: What types of heparin are used?
Subcutaneous LMWH,
unfractionated heparin IV,
subcutaneous fondaparinux and
adjusted-dose heparin
59
Pulmonary Embolism—Management
How long should LMWH be continued?
LMWH should be continued for at least 5 days.
60
Pulmonary Embolism—Management
How long should oral anticoagulants be continued?
Continue oral anticoagulants for 3 to 6 months.
61
Pulmonary Embolism—Management
Prevention:
Prophylactic measures are based on the patient's specific risk factors
62
Chronic Obstructive Pulmonary Disease (COPD):
What is this disease characterized by?
Disease state characterized by airflow limitation that is not fully reversible
63
Chronic Obstructive Pulmonary Disease (COPD)
Pathophysiology—changes occur in the following order:
Mucous hypersecretion
Ciliary dysfunction
Airflow limitation
Pulmonary hyperinflation
Gas exchange abnormalities
Pulmonary hypertension
Cor pulmonale
64
COPD—Assessment
What is assessed?
Detailed medical history
65
COPD—Assessment
Detailed medical history
Exposure to risk factor
Past medical history
Family history
Pattern of symptom development
History of exacerbations or previous hospitalizations for respiratory disorder
Comorbidities
Appropriateness of current medical treatments
Impact of disease on patient’s life
Social and family support
Possibility for reducing risk factors, especially smoking
66
COPD—Physical Findings
Inspection: What are you inspecting for middle of body?
Central cyanosis, horizontal ribs, barrel-shaped chest, protruding abdomen
resting muscle activation
67
COPD—Physical Findings
Inspection: What are you inspecting for lower part of body?
Ankle or lower leg edema
68
COPD—Physical Findings
Inspection: What are you inspecting for breathing?
Flattening of hemidiaphragms, increased
resting respiratory rate, pursed-lip breathing
Supraclavicular wasting and nasal flaring;
69
COPD—Physical Findings
What is not helpful for diagnosis?
Palpation and percussion—not helpful in diagnosis
70
COPD—Physical Findings
Auscultation
Reduced breath sounds,
wheezing during quiet respiration,
inspiratory crackle,
displaced heart sounds,
evidence of right heart failure (increased second heart sound,
jugular venous distention,
and right ventricular heave)
71
COPD—Diagnostic Studies
Spirometry
Diffusing capacity
Bronchodilator reversibility
Chest radiography
CT ABGs
a1-antitrypsin deficiency screening if <45 years old and strong family predisposition
Exercise testing
72
COPD—Management
What types of therapy?
Nonpharmacologic therapy
Pharmacologic therapy
Oxygen therapy
73
COPD—Management
Pharmacologic therapy like what?
Bronchodilators
Corticosteroids
Other (theophylline, phosphodiesterase-4 inhibitors)
74
COPD—Management
Other kinds of management?
Pulmonary rehabilitation
Nutritional counseling
Smoking cessation
Pharmacologic therapy
Oxygen therapy
Surgery (lung volume reduction surgery, bullectomy, lung transplantation)
75
COPD—Management
What kind of surgical management?
Surgery (lung volume reduction surgery,
bullectomy,
lung transplantation)
76
Acute Asthma
Types of Asthma include:
Allergic asthma:
Nonallergic asthma:
Late onset asthma:
Asthma with fixed airflow limitation:
Asthma with obesity:
77
Acute Asthma
What is the most common type of asthma?
Allergic asthma
78
Acute Asthma
Allergic Asthma: What may it be associated with?
it may be associated with eczema, allergic rhinitis, or food or drug allergy.
79
Acute Asthma
Nonallergic Asthma: What may it be associated with?
not associated with an allergen.
80
Acute Asthma
Late onset Asthma: Who is it more common in? How does it usually present?
Late onset asthma: more common in women;
it usually presents in adulthood and is often the nonallergic type.
81
Acute Asthma
Asthma with fixed airflow limitation:
Asthma with fixed airflow limitation: Patients with long-standing asthma can develop a fixed airflow limitation.
82
Acute Asthma
Asthma with obesity:
Obese asthma patients have prominent respiratory symptoms that are not associated with eosinophilic airway inflammation
83
Acute Asthma: What increases with age?
Risk of death from asthma increases with age.
84
Assessment—Asthma
History and physical findings
Symptoms and symptom patterns
Precipitating and aggravating factors
Development of disease
Current treatment
Effect of symptoms on activities of daily living
Impact of asthma on the patient and family
Perceptions of the disease by the patient and family (parent, if appropriate)
85
Asthma—Diagnostic Studies
Spirometry and pulmonary function testing
Allergy testing
Peak flow meters to monitor ongoing lung function
86
Asthma—Diagnostic Studies
Peak flow meters to
Peak flow meters to monitor ongoing lung function
87
Asthma—Diagnostic Studies
Management
Based on severity, age, compliance with treatment
Stepwise pharmacologic approach
Patient education and self-management
88
Acute Respiratory Failure
What is it defined as?
Defined as the rapid onset of inadequate gas exchange demonstrated as hypoxemia.
89
Acute Respiratory Failure
Pathophysiology: What are the PaO2, PaCO2 and arterial pH levels?
PaO2 55 mm Hg or less,
PaCO2 50 mm Hg or greater,
and arterial pH 7.35 or less.
90
Acute Respiratory Failure
What may it result in?
May result from malfunction of the respiratory center,
abnormal respiratory neuromuscular system,
chest wall diseases,
airway obstruction, or
parenchymal lung disorders.
91
Acute Respiratory Failure—Classification
What are the two groups?
1. Acute hypoxemic respiratory failure
2. Acute hypercapnic respiratory failure
92
Acute Respiratory Failure—Classification
Acute hypoxemic respiratory failure: What abnormality occurs? What is there an inability to achieve?
Abnormal oxygen transport
Inability to achieve adequate oxygenation
93
Acute Respiratory Failure—Classification
Acute hypoxemic respiratory failure: What is PaO2 levels?
PaO2 less than 55 mm Hg
94
Acute Respiratory Failure—Classification
Acute hypercapnic respiratory failure: What occurs?
Inadequate alveolar ventilation
95
Acute Respiratory Failure—Classification
Acute hypercapnic respiratory failure: What abnormal levels are there?
Marked elevation of carbon dioxide with relative preservation of oxygenation
96
Acute Respiratory Failure—Assessment
Physical findings
Dyspnea, cyanosis, restlessness, confusion, anxiety, delirium, tachypnea, tachycardia, hypertension, cardiac dysrhythmia, tremor
Use of accessory muscles of respiration, intercostal or supraclavicular retraction, and paradoxical abdominal movement if diaphragmatic weakness or fatigue is present.
Dyspnea and headache are cardinal symptoms of hypercapnia.
97
Acute Respiratory Failure—Assessment
What are cardinal symptoms of hypercapnia?
Dyspnea and headache are cardinal symptoms of hypercapnia.
98
Acute Respiratory Failure—Assessment
What are other symptoms of hypercapnia?
Other symptoms of hypercapnia include peripheral and conjunctival hyperemia, hypertension, tachycardia, tachypnea, impaired consciousness, papilledema, and asterixis.
99
Acute Respiratory Failure—Diagnostic Studies
ABG
CXR
Angiography
Ventilation–perfusion scanning
CT
Toxicology screen
Sputum examination
CBC
Serum electrolytes
Cytology
Urinalysis
Bronchoscopy
Electrocardiography
Thoracentesis
100
Acute Respiratory Failure—Management
What must be established? Why?
Establish adequate airway; need for mechanical ventilation.
101
Acute Respiratory Failure—Management
What must be established? Why?
Oxygenation and continuous pulse oximetry
Correct acid-base disturbance
Restore fluid and electrolyte balance
Optimize cardiac function
Treat underlying condition and precipitating causes
Prevent complications
Nutritional support
102
Acute Respiratory Distress Syndrome
Definition of ARDS: What is ARDS considered?
A complex clinical syndrome rather than a single disease process that carries a high risk of mortality.
103
Acute Respiratory Distress Syndrome
Definition of ARDS: What causes ARDS?
May be precipitated by direct or indirect pulmonary injury
104
Acute Respiratory Distress Syndrome
Definition of ARDS: How do symptoms appear?
Acute in onset, and symptoms typically develop over 4 to 48 hours after the inciting insult
105
Acute Respiratory Distress Syndrome
Definition of ARDS: Pathologic changes affect what?
Pathologic changes affect pulmonary blood vessels, gas exchange, and lung and bronchial mechanics.
106
Acute Respiratory Distress Syndrome
Definition of ARDS:
What happens to ventilation? Why?
Ventilation is impaired from a decrease in lung compliance and increase in airway resistance.
107
Acute Respiratory Distress Syndrome
Definition of ARDS: What happens to surfactant? What does this result in?
Surfactant is lost, resulting in alveolar collapse.
Mediator-induced bronchoconstriction restricts air flow.
108
Acute Respiratory Distress Syndrome
Physiologic Effects
Impaired oxygenation
Pulmonary vasoconstriction
Impaired ventilation
Decrease lung compliance and increase airway resistance
Fluid-filled alveoli
Alveolar collapse
Bronchoconstriction
109
Acute Respiratory Distress Syndrome
Physiologic Effects: Pulmonary vasoconstriction
What does Pulmonary vasoconstriction lead to?
Pulmonary hypertension
Reduced blood flow
110
SIRS CRITERIA: read slide 34
111
ARDS: Physical Examination
Hypotension, tachycardia
Hyperthermia or hypothermia
Tachypnea, dyspnea
Restlessness and agitation
Hypoxia and decreases in oxygen saturation
Crackle
112
ARDS: Physical Examination
What is an ominous sign?
Restlessness and agitation
113
ARDS Management
Oxygenation and Mechanical Ventilation
Positioning
Pharmacologic Therapy
114
ARDS Management
Positioning:
Frequent position changes
HOB elevated >30 degrees to prevent VAP
Prone positioning
115
ARDS Management
Positioning: Why is prone positioning recommended?
Improves gas exchange
116
ARDS Management
Pharmacologic Therapy
Antibiotics, if indicated
Bronchodilators and mucolytics
IV corticosteroids
Sedation
Neuromuscular blocking agents
