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NURS 428: Evolution > Common Respiratory Disorders > Flashcards

Common Respiratory Disorders Flashcards

Exam 1

1
Q

Pneumonia: What is it?

A

An infection involving the lower respiratory tract,

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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.

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3
Q

What is the leading cause of death worldwide?

A

Pneumonia is the leading cause of death worldwide in the United States.

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4
Q

What is the ninth leading cause of death?

A

Pneumonia combined with influenza is the ninth leading cause of death

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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)

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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

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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

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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

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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

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10
Q

Pneumonia—Etiology

What causes it?

A

Bacteria, viruses, mycoplasmas, fungi, and foreign material

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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.

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12
Q

Pneumonia—Etiology

Other pathogens that cause Pneumonia?

A

Others include Haemophilus influenzae, Staphylococcus aureus, and other Gram-negative bacilli.

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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.

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14
Q

Pneumonia—Etiology

What is typical pneumonia?

A

S. pneumoniae, S. pyrogenes, and S. aureus

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15
Q

Pneumonia—Etiology

What are atypical pneumonia?

A

Mycoplasma pneumoniae, C. pneumoniae, influenza virus, adenovirus, and Legionella species

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16
Q

Pneumonia—Assessment

What to look for in the history?

A

Risk Factors

Signs and symptoms

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17
Q

Pneumonia—Assessment

Physical findings

A

Hypoxemia, dyspnea, new onset respiratory symptoms (cough, sputum production, dyspnea, pleuritic chest pain, hemoptysis), fever, and chills

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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

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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

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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

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21
Q

Pneumonia—Management

A

Antibiotic therapy

Supportive therapy

Prevention

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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

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23
Q

Pneumonia—Management

Supportive therapy: What does it include?

A

Oxygen, mechanical ventilation, pulmonary toilet, nutritional support

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24
Q

Pneumonia—Management

Prevention: What does it include?

A

Influenza and pneumococcal vaccine

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25
Q

Pleural Effusion—Pathophysiology

A

Caused by at least one of the five following mechanisms:

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26
Q

Pleural Effusion—Pathophysiology

Caused by at least one of the five following mechanisms:

An increase in…

A

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)

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27
Q

Pleural Effusion—Pathophysiology

Caused by at least one of the five following mechanisms:

An decrease in…

A

Decreased plasma osmotic pressure (eg, hypoalbuminemia, hypoproteinemia, cirrhosis)

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28
Q

Pleural Effusion—Pathophysiology

Caused by at least one of the five following mechanisms:

An impaired…

A

Impaired lymphatic drainage of the pleural space (eg, pleural malignancy or infection)

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29
Q

Pleural Effusion—Pathophysiology

What can pleural effusion be a complication of?

A

Pleural effusion is a complication of pneumonia.

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30
Q

Pleural Effusion—Pathophysiology

What is pleural effusion?

A

Accumulation of fluid in the pleural space.

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31
Q

Pleural Effusion—Assessment

What does it include?

A

History and physical findings

Subjective findings:

Objective findings:

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32
Q

Pleural Effusion—Assessment

What are subjective findings?

A

Subjective findings: shortness of breath and pleuritic chest pain, depending on the amount of fluid accumulation

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33
Q

Pleural Effusion—Assessment

What are Objective findings?

A

Objective findings:

tachypnea and hypoxemia if ventilation is impaired,

dullness to percussion,

and decreased breath sounds over the involved area

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34
Q

Pleural Effusion—Diagnostic Studies

What does it include?

A

Chest radiograph, ultrasound, or a CT scan

When physical exam and CXR confirm diagnosis pleural fluid exam via thoracentesis is performed.

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35
Q

Pleural Effusion—Diagnostic Studies

What does thoracentesis do?

A

Thoracentesis distinguishes transudate from exudate.

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36
Q

Pleural Effusion—Management: What is included?

A

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

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37
Q

Pleural Effusion—Management:

Chest tube placement or surgery may be indicated depending on what?

A

the etiology and size.

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38
Q

Pleural Effusion—Management:

Drainage of the pleural effusion by

A

thoracentesis

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39
Q

Pneumothorax:

What occurs in this? What does it produce?

A

Air enters the pleural space between the visceral and parietal pleurae, producing partial or complete lung collapse.

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40
Q

Pneumothorax:

Pathophysiology

A

Sudden communication of the pleural space with alveolar or external air

Pleural pressure rises and the elasticity of the lung causes collapse.

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41
Q

Pneumothorax:

What are the two types?

A

Spontaneous or traumatic

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42
Q

Pneumothorax:

Spontaneous

A

Any pneumothorax that develops without trauma.

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43
Q

Pneumothorax:

Traumatic:

A

From trauma.

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44
Q

Pneumothorax—Assessment

History and physical findings

A

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

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45
Q

Pneumothorax—Diagnostic Studies

A

Chest radiograph,

CT

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46
Q

Pneumothorax—Diagnostic Studies

Management:

A

Supplemental oxygen
Chest tube

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47
Q

Pneumothorax—Diagnostic Studies

Tension pneumothorax

A

—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
Q

Pneumothorax—Diagnostic Studies

Tension pneumothorax: Intervention

A

Large-bore (16- or 18-gauge) needle should be placed into the anterior second intercostal space.

49
Q

Tension pneumothorax: What is heard? What else?

A

Tension pneumothorax: breath sounds absent. You may also found distended neck vessels.

50
Q

Pulmonary Embolism: What is it?

A

Thrombus migrates to pulmonary arteries.

51
Q

Pulmonary Embolism: What does it include?

A

Venous thromboembolism includes pulmonary embolism and deep vein thrombosis

52
Q

Pulmonary Embolism: What is it called (the three things)

A

Virchow’s triad (venous stasis, hypercoagulability, vein wall damage)

53
Q

Pulmonary Embolism

Virchow’s triad (venous stasis, hypercoagulability, vein wall damage)

What contributes to this?

A

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
Q

Pulmonary Embolism—Assessment

What are PE’s called? Why?

A

PE called “the great masquerader” because of nonspecific signs and symptoms

55
Q

Pulmonary Embolism—Assessment

What are symptoms that are assessed?

A

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
Q

Pulmonary Embolism—Assessment

Diagnosis: Using what?

A

Computed pulmonary angiography

Ventilation–perfusion (VQ) scans

Transthoracic echocardiogram (TEE)

57
Q

Pulmonary Embolism—Management

Using what to treat?

A

Heparin and thrombolytics

Continue oral anticoagulants for 3 to 6 months.

58
Q

Pulmonary Embolism—Management

Heparin and thrombolytics: What types of heparin are used?

A

Subcutaneous LMWH,

unfractionated heparin IV,

subcutaneous fondaparinux and

adjusted-dose heparin

59
Q

Pulmonary Embolism—Management

How long should LMWH be continued?

A

LMWH should be continued for at least 5 days.

60
Q

Pulmonary Embolism—Management

How long should oral anticoagulants be continued?

A

Continue oral anticoagulants for 3 to 6 months.

61
Q

Pulmonary Embolism—Management

Prevention:

A

Prophylactic measures are based on the patient’s specific risk factors

62
Q

Chronic Obstructive Pulmonary Disease (COPD):
What is this disease characterized by?

A

Disease state characterized by airflow limitation that is not fully reversible

63
Q

Chronic Obstructive Pulmonary Disease (COPD)

Pathophysiology—changes occur in the following order:

A

Mucous hypersecretion

Ciliary dysfunction

Airflow limitation

Pulmonary hyperinflation

Gas exchange abnormalities

Pulmonary hypertension

Cor pulmonale

64
Q

COPD—Assessment

What is assessed?

A

Detailed medical history

65
Q

COPD—Assessment

Detailed medical history

A

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
Q

COPD—Physical Findings

Inspection: What are you inspecting for middle of body?

A

Central cyanosis, horizontal ribs, barrel-shaped chest, protruding abdomen

resting muscle activation

67
Q

COPD—Physical Findings

Inspection: What are you inspecting for lower part of body?

A

Ankle or lower leg edema

68
Q

COPD—Physical Findings

Inspection: What are you inspecting for breathing?

A

Flattening of hemidiaphragms, increased
resting respiratory rate, pursed-lip breathing

Supraclavicular wasting and nasal flaring;

69
Q

COPD—Physical Findings

What is not helpful for diagnosis?

A

Palpation and percussion—not helpful in diagnosis

70
Q

COPD—Physical Findings

Auscultation

A

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
Q

COPD—Diagnostic Studies

A

Spirometry

Diffusing capacity

Bronchodilator reversibility

Chest radiography

CT ABGs

a1-antitrypsin deficiency screening if <45 years old and strong family predisposition

Exercise testing

72
Q

COPD—Management

What types of therapy?

A

Nonpharmacologic therapy

Pharmacologic therapy

Oxygen therapy

73
Q

COPD—Management

Pharmacologic therapy like what?

A

Bronchodilators

Corticosteroids

Other (theophylline, phosphodiesterase-4 inhibitors)

74
Q

COPD—Management

Other kinds of management?

A

Pulmonary rehabilitation

Nutritional counseling

Smoking cessation

Pharmacologic therapy

Oxygen therapy

Surgery (lung volume reduction surgery, bullectomy, lung transplantation)

75
Q

COPD—Management

What kind of surgical management?

A

Surgery (lung volume reduction surgery,

bullectomy,

lung transplantation)

76
Q

Acute Asthma

Types of Asthma include:

A

Allergic asthma:

Nonallergic asthma:

Late onset asthma:

Asthma with fixed airflow limitation:

Asthma with obesity:

77
Q

Acute Asthma

What is the most common type of asthma?

A

Allergic asthma

78
Q

Acute Asthma

Allergic Asthma: What may it be associated with?

A

it may be associated with eczema, allergic rhinitis, or food or drug allergy.

79
Q

Acute Asthma

Nonallergic Asthma: What may it be associated with?

A

not associated with an allergen.

80
Q

Acute Asthma

Late onset Asthma: Who is it more common in? How does it usually present?

A

Late onset asthma: more common in women;

it usually presents in adulthood and is often the nonallergic type.

81
Q

Acute Asthma

Asthma with fixed airflow limitation:

A

Asthma with fixed airflow limitation: Patients with long-standing asthma can develop a fixed airflow limitation.

82
Q

Acute Asthma

Asthma with obesity:

A

Obese asthma patients have prominent respiratory symptoms that are not associated with eosinophilic airway inflammation

83
Q

Acute Asthma: What increases with age?

A

Risk of death from asthma increases with age.

84
Q

Assessment—Asthma

History and physical findings

A

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
Q

Asthma—Diagnostic Studies

A

Spirometry and pulmonary function testing

Allergy testing

Peak flow meters to monitor ongoing lung function

86
Q

Asthma—Diagnostic Studies

Peak flow meters to

A

Peak flow meters to monitor ongoing lung function

87
Q

Asthma—Diagnostic Studies

Management

A

Based on severity, age, compliance with treatment

Stepwise pharmacologic approach

Patient education and self-management

88
Q

Acute Respiratory Failure

What is it defined as?

A

Defined as the rapid onset of inadequate gas exchange demonstrated as hypoxemia.

89
Q

Acute Respiratory Failure

Pathophysiology: What are the PaO2, PaCO2 and arterial pH levels?

A

PaO2 55 mm Hg or less,

PaCO2 50 mm Hg or greater,

and arterial pH 7.35 or less.

90
Q

Acute Respiratory Failure

What may it result in?

A

May result from malfunction of the respiratory center,

abnormal respiratory neuromuscular system,

chest wall diseases,

airway obstruction, or

parenchymal lung disorders.

91
Q

Acute Respiratory Failure—Classification

What are the two groups?

A
  1. Acute hypoxemic respiratory failure
  2. Acute hypercapnic respiratory failure
92
Q

Acute Respiratory Failure—Classification

Acute hypoxemic respiratory failure: What abnormality occurs? What is there an inability to achieve?

A

Abnormal oxygen transport

Inability to achieve adequate oxygenation

93
Q

Acute Respiratory Failure—Classification

Acute hypoxemic respiratory failure: What is PaO2 levels?

A

PaO2 less than 55 mm Hg

94
Q

Acute Respiratory Failure—Classification

Acute hypercapnic respiratory failure: What occurs?

A

Inadequate alveolar ventilation

95
Q

Acute Respiratory Failure—Classification

Acute hypercapnic respiratory failure: What abnormal levels are there?

A

Marked elevation of carbon dioxide with relative preservation of oxygenation

96
Q

Acute Respiratory Failure—Assessment

Physical findings

A

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
Q

Acute Respiratory Failure—Assessment

What are cardinal symptoms of hypercapnia?

A

Dyspnea and headache are cardinal symptoms of hypercapnia.

98
Q

Acute Respiratory Failure—Assessment

What are other symptoms of hypercapnia?

A

Other symptoms of hypercapnia include peripheral and conjunctival hyperemia, hypertension, tachycardia, tachypnea, impaired consciousness, papilledema, and asterixis.

99
Q

Acute Respiratory Failure—Diagnostic Studies

A

ABG

CXR

Angiography

Ventilation–perfusion scanning

CT

Toxicology screen

Sputum examination

CBC

Serum electrolytes

Cytology

Urinalysis

Bronchoscopy

Electrocardiography

Thoracentesis

100
Q

Acute Respiratory Failure—Management

What must be established? Why?

A

Establish adequate airway; need for mechanical ventilation.

101
Q

Acute Respiratory Failure—Management

What must be established? Why?

A

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
Q

Acute Respiratory Distress Syndrome

Definition of ARDS: What is ARDS considered?

A

A complex clinical syndrome rather than a single disease process that carries a high risk of mortality.

103
Q

Acute Respiratory Distress Syndrome

Definition of ARDS: What causes ARDS?

A

May be precipitated by direct or indirect pulmonary injury

104
Q

Acute Respiratory Distress Syndrome

Definition of ARDS: How do symptoms appear?

A

Acute in onset, and symptoms typically develop over 4 to 48 hours after the inciting insult

105
Q

Acute Respiratory Distress Syndrome

Definition of ARDS: Pathologic changes affect what?

A

Pathologic changes affect pulmonary blood vessels, gas exchange, and lung and bronchial mechanics.

106
Q

Acute Respiratory Distress Syndrome

Definition of ARDS:

What happens to ventilation? Why?

A

Ventilation is impaired from a decrease in lung compliance and increase in airway resistance.

107
Q

Acute Respiratory Distress Syndrome

Definition of ARDS: What happens to surfactant? What does this result in?

A

Surfactant is lost, resulting in alveolar collapse.

Mediator-induced bronchoconstriction restricts air flow.

108
Q

Acute Respiratory Distress Syndrome

Physiologic Effects

A

Impaired oxygenation

Pulmonary vasoconstriction

Impaired ventilation

Decrease lung compliance and increase airway resistance

Fluid-filled alveoli

Alveolar collapse

Bronchoconstriction

109
Q

Acute Respiratory Distress Syndrome

Physiologic Effects: Pulmonary vasoconstriction

What does Pulmonary vasoconstriction lead to?

A

Pulmonary hypertension

Reduced blood flow

110
Q

SIRS CRITERIA: read slide 34

A
111
Q

ARDS: Physical Examination

A

Hypotension, tachycardia

Hyperthermia or hypothermia

Tachypnea, dyspnea

Restlessness and agitation

Hypoxia and decreases in oxygen saturation

Crackle

112
Q

ARDS: Physical Examination

What is an ominous sign?

A

Restlessness and agitation

113
Q

ARDS Management

A

Oxygenation and Mechanical Ventilation

Positioning

Pharmacologic Therapy

114
Q

ARDS Management

Positioning:

A

Frequent position changes

HOB elevated >30 degrees to prevent VAP

Prone positioning

115
Q

ARDS Management

Positioning: Why is prone positioning recommended?

A

Improves gas exchange

116
Q

ARDS Management

Pharmacologic Therapy

A

Antibiotics, if indicated

Bronchodilators and mucolytics

IV corticosteroids

Sedation

Neuromuscular blocking agents

NURS 428: Evolution (17 decks)

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