ch 27 lower respiratory Flashcards

(512 cards)

1
Q

is a self-limiting inflammation of the bronchi in the lower respiratory tract.

A

Acute bronchitis

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2
Q

by viruses

A

Most acute bronchial infections are caused

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3
Q

Air pollution, dust, inhalation of chemicals, smoking, chronic sinusitis, and asthma are other triggers.

A

other causes of acute bronchial infections

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4
Q

may last for up to 3 weeks

A

Cough, which is the most common symptom(Acute bronchitis)

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5
Q

Clear sputum is often present, although some patients have purulent sputum. The presence of colored (e.g., green) sputum is not a reliable indicator of bacterial infection. Other symptoms may include headache, fever, malaise, hoarseness, myalgias, dyspnea, and chest pain.

A

other symp of Acute bronchitis

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6
Q

normal breath sounds or crackles or wheezes, usually on expiration and with exertion. Consolidation (which occurs when fluid accumulates in the lungs), suggestive of pneumonia, is absent with bronchitis

A

Assessment may reveal of Acute bronchitis

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7
Q

cough suppressants (e.g., dextromethorphan), encouraging oral fluid intake, and using a humidifier. Throat lozenges, hot tea, and honey may help relieve cough. β2-Agonist (bronchodilator) inhalers are useful for patients with wheezes or underlying pulmonary conditions. Antibiotics are not prescribed for viral infections because they have side effects and promote antibiotic resistance.

A

treatment for Acute bronchitis

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8
Q

is a highly contagious infection of the respiratory tract caused by the gram-negative bacillus Bordetella pertussis.

A

Pertussis

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9
Q

bacteria attach to the cilia of the respiratory tract and release toxins that damage the cilia, causing inflammation and swelling.

A

Pertussis pathophysiology

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10
Q

tetanus, diphtheria, and pertussis vaccine (Tdap) vaccination may decrease over time, allowing a milder (but still contagious) infection.

A

immunity from childhood for Pertussis

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11
Q

lasting 1 to 2 weeks, manifests as a mild upper respiratory tract infection (URI) with a low-grade or no fever, runny nose, watery eyes, generalized malaise, and mild, nonproductive cough.

A

Manifestations of pertussis occur in stages- first stage,

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12
Q

, from the second to tenth week of infection, is characterized by paroxysms of cough.

A

second stage pertussis

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13
Q

lasts 2 to 3 weeks. It is characterized by a less severe cough and weakness.

A

The last stage pertussis

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14
Q

is uncontrollable, violent coughing. Inspiration after each cough produces the typical “whooping” sound as the patient tries to breathe in air against an obstructed glottis.

A

hallmark characteristic of pertussis

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15
Q

Like acute bronchitis, the coughing is more frequent at night. Vomiting may occur with coughing. Unlike acute bronchitis, the cough with pertussis may last from 6 to 10 weeks.

A

acute bronchitis vs pertusis

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16
Q

nasopharyngeal cultures, polymerase chain reaction (PCR) of nasopharyngeal secretions, or serology testing

A

diagnosis of pertussis

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17
Q

is macrolide (erythromycin, azithromycin [Zithromax]) antibiotics to minimize symptoms and prevent spread of the disease. For the patient who cannot take macrolides, trimethoprim/sulfamethoxazole is used

A

treatment for pertussis

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18
Q

from the beginning of the first stage through the third week after onset of symptoms or until 5 days after antibiotic therapy has been started. Routine and droplet precautions are required for hospitalized patients.

A

patient is infectious (duration) for pertussis

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19
Q

Patients should not use cough suppressants and antihistamines as they are ineffective and may induce coughing episodes. Corticosteroids and bronchodilators are also not helpful. The CDC recommends postexposure antibiotics to those who have had close contact with the patient.

A

Medications NOT used for pertussis

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20
Q

from inhaled dust or chemicals

A

Environmental or occupational lung diseases result

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21
Q

the toxicity of the inhaled substance, amount and duration of exposure, and individual susceptibility

A

extent of lung damage is influenced by

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22
Q

pneumoconiosis, chemical pneumonitis, and hypersensitivity pneumonitis.

A

Environmentally induced lung disease includes

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23
Q

s a general term for a group of lung diseases caused by inhalation and retention of mineral or metal dust particles.

A

Pneumoconiosis

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24
Q

(e.g., silicosis, asbestosis, berylliosis)

A

Pneumoconiosis classified diseases according to the origin of the dust

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25
inhaling silica from sand and rock.
silicosis occurs from
26
inhaling large amounts of coal dust
Coal worker’s pneumoconiosis (CWP), also known as black lung, is caused by
27
occurs from tissue repair after inflammation. Breathing problems become evident after many years of repeated exposure, resulting in diffuse pulmonary fibrosis (excess connective tissue).
Fibrosis
28
Breathing problems become evident after many years of repeated exposure=
pulmonary fibrosis (excess connective tissue).
29
is a group of minerals composed of microscopic fibers
Asbestos
30
Lung cancer, either squamous cell carcinoma or adenocarcinoma, is the .
most frequent cancer associated with asbestos exposure
31
both pleural and peritoneal, is associated with asbestos exposure.
Mesothelioma,
32
= from exposures to toxic chemical fumes
Chemical pneumonitis results
33
acute and chronic.
2 types of chemical pneumonitis:
34
, there is diffuse lung injury characterized by pulmonary edema.
Acutely chemical pneumonitis:
35
the clinical picture is that of bronchiolitis obliterans (obstruction of the bronchioles due to inflammation and fibrosis). It is usually associated with a normal chest x-ray or one that shows hyperinflation.
Chronically chemical pneumonitis:
36
is a form of parenchymal lung disease seen when a person inhales antigens to which they are allergic.
Hypersensitivity pneumonitis, or extrinsic allergic alveolitis,
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There are acute, subacute, and chronic forms
Hypersensitivity pneumonitis, or extrinsic allergic alveolitis,
38
(exposure to particles in feathers and droppings of birds), and
Hypersensitivity pneumonitis, or extrinsic allergic alveolitis, ex: include bird fancier’s lung
39
(inhalation of hay dust particles).
Hypersensitivity pneumonitis, or extrinsic allergic alveolitis, ex: farmer’s lung
40
may not occur until at least 10 to 15 years after the initial exposure to the inhaled irritant
Symptoms of many environmental lung diseases (occurrence)
41
dyspnea, cough, wheezing, and weight loss.
Manifestations common to all pneumoconioses include
42
often show reduced vital capacity. A chest x-ray often reveals lung involvement specific to the primary problem. CT scans have been useful in detecting early lung involvement.
Pulmonary function studies pneumoconioses include
43
, a condition in which the right side of the heart fails, is a late complication, especially in conditions characterized by diffuse pulmonary fibrosis.
Cor pulmonale
44
Other associated disorders include acute pulmonary edema, lung cancer, mesothelioma, and TB.
COPD is the most common complication of environmental lung disease.
45
is responsible for workplace safety and health regulations in the United States.
NIOSH
46
Strategies may include O2 therapy, IV fluid, inhaled bronchodilators, corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), intubation and mechanical ventilation, percussion therapy, and pulmonary rehabilitation. Patients should be immunized against pneumococcal pneumonia and influenza
treatment for environmental lung disease.
47
is the leading cause of cancer-related deaths in the United States
Lung cancer
48
changes in the bronchial epithelium, which usually returns to normal with smoking cessation
Exposure to tobacco smoke causes
49
high levels of pollution, radiation (especially radon exposure), and asbestos
Other common causes of lung cancer include
50
Heavy or prolonged exposure to industrial agents, such as ionizing radiation, coal dust, nickel, uranium, chromium, formaldehyde, and arsenic, can
increase the risk for lung cancer, especially in smokers
51
are believed to arise from mutated epithelial cells.
Most primary lung tumors caused(pathophysiology)
52
carcinogens, is influenced by various genetic factors.
growth of mutations, which are caused by
53
cells grow slowly, taking 8 to 10 years for a tumor to reach 1 cm in size, the smallest lesion detectable on x-ray.
cells growth in cancer duration
54
in the segmental bronchi or beyond and usually occur in the upper lobes of the lungs
Lung cancers occur primarily (location in lung)
55
1. non–small cell lung cancer (NSCLC) (85%) 2. small cell lung cancer (SCLC) (15%)
Primary lung cancers are categorized into 2 broad subtypes
56
direct extension and through the blood and lymph system.
Lung cancers metastasize primarily by
57
lymph nodes, liver, brain, bones, and adrenal glands.
The common sites for metastasis are
58
paraneoplastic syndrome
Lung cancers can cause
59
may be caused by hormones, cytokines, enzymes (secreted by tumor cells) or antibodies (made by the body in response to the tumor) that destroy healthy cells.
Paraneoplastic syndrome
60
hypercalcemia, syndrome of inappropriate antidiuretic hormone secretion (SIADH), adrenal hypersecretion, polycythemia, and Cushing syndrome.
Examples of paraneoplastic syndrome include
61
may lead to pericardial effusion, cardiac tamponade, and dysrhythmias.
Mediastinal involvement
62
done for patients with suspected lung cancer.
chest x-ray is the first diagnostic test (cancer)
63
x-ray may be normal or identify a lung mass or infiltrate (Fig. 27.4). Evidence of metastasis to the ribs or vertebrae and a pleural effusion may be seen on chest x-ray
chest x ray in cancer pt shows
64
is used to further evaluate the lung mass. CT scans can identify the location and extent of masses in the chest, any mediastinal involvement, and lymph node enlargement.
CT scanning in cancer pt shows
65
cancer cells, but sputum samples are rarely used in diagnosing lung cancer because cancer cells are not always present in the sputum
Sputum cytologic studies can identify
66
Bone scans and CT scans of the brain, pelvis, and abdomen are
used to determine if metastatic disease is present
67
with A or B subtypes
TNM system, cancer is grouped into 4 stages
68
by TNM has not been useful because this cancer is aggressive and is always considered systemic. The stages of SCLC are limited and extensive.
Staging of SCLC
69
that the tumor is only on 1 side of the chest and regional lymph nodes.
Limited means
70
that the cancer extends beyond the limited stage.
Extensive SCLC means
71
extensive disease at time of diagnosis.
Most patients with SCLC have
72
Adults ages 55 to 77 with a history of smoking (30 pack-year smoking history or currently smoke) or who quit smoking but less than 15 years ago should have annual screening for lung cancer.
screening for high-risk patients lung cancer
73
NSCLC stages I to IIIA without mediastinal involvement.
Surgical resection is the treatment of choice in
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(removal of 1 or more lobes of the lung), or
lobectomy
75
(removal of 1 entire lung).
pneumonectomy
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may be used to treat lung cancers near the outside of the lung.
VATS
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because of its rapid growth and dissemination at the time of diagnosis.
Surgery is generally not done for SCLC
78
Pulmonary function studies, ABGs, and anesthesia and critical care consults are often
done before surgery to assess the patient’s cardiopulmonary status.
79
may be used as treatment for both NSCLC and SCLC
Radiation therapy
80
curative therapy, palliative therapy (to relieve symptoms), or adjuvant therapy in combination with surgery, chemotherapy, or targeted therapy.
Radiation therapy may be given as
81
is unable to tolerate surgical resection because of co-morbidities
Radiation therapy may be used as primary therapy in the person who
82
dyspnea and hemoptysis from bronchial obstructive tumors and treats superior vena cava syndrome. It can treat pain from metastatic bone lesions or brain metastasis. Radiation before surgery can reduce the tumor mass before surgical resection.
Radiation therapy relieves symptoms of
83
include esophagitis, skin irritation, nausea and vomiting, anorexia, and radiation pneumonitis
Complications of radiation therapy
84
, is a newer lung cancer treatment
Stereotactic body radiotherapy (SBRT), also called stereotactic radiosurgery (SRS)
85
type of radiation therapy that uses high doses of radiation delivered to tumors outside the CNS.
Stereotactic body radiotherapy (SBRT)
86
uses special positioning procedures and radiology techniques to deliver a higher dose of radiation to the tumor and expose only a small part of healthy lung.
Stereotactic body radiotherapy (SBRT) (process)
87
It does not destroy the tumor, but damages tumor DNA. Therapy is given over 1 to 3 days. SBRT provides an option for patients with early-stage lung cancers who are not surgical candidates for other medical reasons
Stereotactic body radiotherapy (SBRT) (how it works)
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or SCLC
Chemotherapy is the main treatment
89
nonresectable tumors or as adjuvant therapy to surgery.
NSCLC, chemotherapy may be used in the treatment of
90
etoposide (VP-16), carboplatin, cisplatin, paclitaxel (Taxol), vinorelbine (Navelbine), docetaxel (Taxotere), gemcitabine (Gemzar), and pemetrexed (Alimta)
Chemotherapy for lung cancer typically consists of combinations of 2 of the following drugs:
91
uses drugs that block the growth of molecules involved in specific aspects of tumor growth
Targeted therapy
92
Because this type of therapy inhibits growth rather than directly killing cancer cells,
targeted therapy may be less toxic than chemotherapy. bc
93
inhibits tyrosine kinase, an enzyme associated with speeding up molecular reactions
One type of targeted therapy for patients with NSCLC
94
which block signals for growth in the cancer cells, include cetuximab (Erbitux), erlotinib (Tarceva), afatinib (Gilotrif), gefitinib (Iressa), osimertinib (Tagrisso), and necitumumab (Portrazza).
Tyrosine kinase inhibitors,
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Drugs in this class include crizotinib (Xalkori), brigatinib (Alunbrig), and ceritinib (Zykadia). These drugs directly inhibit the kinase protein made by the ALK gene that is responsible for cancer development and growth.
Another type of kinase inhibitor is used to treat patients with NSCLC who have an abnormal anaplastic lymphoma kinase (ALK) gene.
96
by targeting vascular endothelial growth factor. Bevacizumab (Avastin) is an angiogenesis inhibitor.
Another type of targeted therapy used to treat lung cancer inhibits the growth of new blood vessels (angiogenesis)
97
a protein on T cells that normally helps keep these cells from attacking other cells in the body.
Nivolumab (Opdivo), atezolizumab (Tecentriq), and pembrolizumab (Keytruda) are drugs that target PD-1,
98
=boost the immune response against cancer cells. This can shrink some tumors or slow their growth.
By blocking PD-1, these drugs
99
whose cancer has progressed after other treatments and with tumors that express PD-1.
Nivolumab and pembrolizumab can be used in people with metastatic NSCLC
100
, especially to the CNS.
Patients with SCLC have early metastases
101
can decrease the incidence of brain metastases and may improve survival rates in patients with limited SCLC
Prophylactic radiation
102
makes it possible to remove obstructing bronchial lesions.
Bronchoscopic laser therapy
103
makes it possible to remove obstructing bronchial lesions.
Bronchoscopic laser therapy
104
laser’s thermal energy is transmitted to the target tissue. It is a safe and effective treatment of endobronchial obstructions from tumors. Symptoms of airway obstruction are relieved due to thermal necrosis and shrinkage of the tumor.
Bronchoscopic laser therapy laser’s thermal energy (how it works in body)
105
is a form of treatment for early-stage lung cancers that uses a combination of a drug and a specific type of light.
Photodynamic therapy (PDT)
106
the drug, known as a photosynthesizer, is exposed to a specific wavelength of light.
Photodynamic therapy (PDT): Cancer cells are killed when
107
is the most used photosynthesize
Porfimer (Photofrin)
108
are used alone or in combination with other techniques for relief of dyspnea, cough, or respiratory insufficiency
Stents
109
is inserted during a bronchoscopy. The advantage of an airway stent is that it supports the airway wall against collapse or external compression and can delay extension of tumor into the airway lumen
stent process
110
is an acute infection of the lung parenchyma
Pneumonia
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air filtration, epiglottis closure over the trachea, cough reflex, mucociliary escalator mechanism, and reflex bronchoconstriction
Mechanisms that create a mechanical barrier to microorganisms entering the tracheobronchial tree include
112
when defense mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents.
Pneumonia is more likely to occur
113
Tracheal intubation bypasses normal filtration processes and interferes with the cough reflex and mucociliary escalator mechanism.
Tracheal intubation defense mechanism corrupts by
114
Air pollution, cigarette smoking, viral URIs, and normal changes that occur with
aging can impair the mucociliary mechanism.
115
can suppress the immune system’s ability to inhibit bacterial growth
Chronic diseases affect defense mechanism
116
Aspiration of normal flora from the nasopharynx or oropharynx. Many organisms that cause pneumonia are normal inhabitants of the pharynx in healthy adults.
Pathogens that cause pneumonia reach the lung in 3 ways: (aspiration)
117
Inhalation of microbes present in the air. Examples include Mycoplasma pneumoniae and fungal pneumonias.
Pathogens that cause pneumonia reach the lung in 3 ways: (Inhalation )
118
hematogenous spread from a primary infection elsewhere in the body. Examples are streptococci and Staphylococcus aureus from infective endocarditis.
Pathogens that cause pneumonia reach the lung in 3 ways: (hematogenous )
119
the causative pathogens (e.g., bacterial, viral, fungal, etc.),
classifying pneumonia according to
120
is as either community-acquired or hospital-acquired pneumonia.
most widely recognized and effective way to classify pneumonia
121
most likely cause and the choice of antimicrobial therapy.
classification helps the HCP identify (pneumonia)
122
is an acute infection of the lung occurring in patients who have not been hospitalized or lived in a long-term care facility within 14 days of the onset of symptoms
Community-acquired pneumonia (CAP)
123
decision to treat the patient at home or admit to hospital is based on several factors. These include the patient’s age, vital signs, mental status, presence of co-morbid conditions, and current physiologic condition
CURB-65 MNEUMONIC (pneumonia acquired long-term care/community)
124
is pneumonia in a nonintubated patient that begins 48 hours or longer after admission to hospital and was not present at the time of admission.
Hospital-acquired pneumonia (HAP), also known as nosocomial pneumonia,
125
refers to pneumonia that occurs more than 48 hours after endotracheal intubation
Ventilator-associated pneumonia (VAP), a type of HAP,
126
longer hospital stays, increased associated costs, sicker patients, and increased risk for morbidity and mortality
HAP and VAP are associated with
127
treatment is started based on known risk factors, early versus late onset, presentation, underlying medical conditions, hemodynamic stability, and the likely causative pathogen
Once the diagnosis of CAP, HAP, or VAP is made,
128
the initiation of treatment before a definitive diagnosis or causative agent is confirmed, should be started as soon as pneumonia is suspected.
Empiric antibiotic therapy,(indication)
129
is based on the knowledge of drugs known to be effective for the likely cause.
Empiric antibiotic therapy (definition)
130
once the results of sputum cultures identify the exact pathoge
Antibiotic therapy can be adjusted
131
is the most common type of pneumonia -mild and self-limiting or cause potentially life-threatening problems, such as acute respiratory failure in influenza.
Viral pneumonia
132
may be extremely unwell and need hospital admission.
bacterial pneumonia
133
, which has traits of both bacteria and viruses, is often referred to as “atypical” pneumonia. It is mild and occurs in persons younger than 40 years of age.
Mycoplasma pneumonia
134
results from the abnormal entry of material from the mouth or stomach into the trachea and lungs
Aspiration pneumonia
135
decreased level of consciousness (e.g., seizure, anesthesia, head injury, stroke, alcohol intake), difficulty swallowing, and insertion of nasogastric (NG) tubes with or without enteral feeding.
Conditions that increase the risk for aspiration include
136
the gag and cough reflexes are depressed and aspiration is more likely to occur.
With loss of consciousness, at risk bc
137
an inflammatory response.
aspirated material (food, water, vomitus, oropharyngeal secretions) triggers
138
is a primary bacterial infection.
The most common form of aspiration pneumonia
139
aerobes and anaerobes, since they both make up the flora of the oropharynx.
Typically, the sputum culture shows more than 1 organism, (in aspiration pneumonia = bacterial infection)
140
an assessment of probable cause, severity of illness, and patient factors (e.g., malnutrition, current use of antibiotic therapy).
initial antibiotic therapy is based on (aspiration pneumonia)
141
both gram-negative organisms and methicillin-resistant Staphylococcus aureus (MRSA).
patients who aspirate in hospitals, antibiotic coverage should include
142
chemical (noninfectious) pneumonitis, which may not need antibiotic therapy. However, secondary bacterial infection can occur 48 to 72 hours later.
Aspiration of acidic gastric contents causes
143
is a rare complication of bacterial lung infection
Necrotizing pneumonia
144
causes the lung tissue to turn into a thick, liquid mass. In some situations, cavitation occurs. This often happens with CAP.
Necrotizing pneumonia effect on lung
145
Staphylococcus, Klebsiella, and Streptococcus. Lung abscesses often occur.
Necrotizing pneumonia causative organisms include
146
immediate respiratory insufficiency and/or failure, leukopenia, and bleeding into the airways.
Necrotizing pneumonia Signs and symptoms include
147
includes long-term antibiotic therapy and possible surgery.
Necrotizing pneumonia Treatment
148
is inflammation and infection of the lower respiratory tract in immunocompromised patients. Persons at risk include those with altered immune responses.
Opportunistic pneumonia (define)
149
include people with severe protein-calorie malnutrition or immunodeficiencies (e.g., human immunodeficiency virus [HIV] infection) and those receiving radiation therapy, chemotherapy, and any immunosuppressive therapy, including long-term corticosteroid therapy. In addition to the risk for bacterial and viral pneumonia, the immunocompromised person may develop an infection from organisms that do not normally cause disease, such as Pneumocystis jiroveci (formerly carinii) or cytomegalovirus (CMV).
Opportunistic pneumonia at risk
150
rarely occurs in the healthy person. It is the most common form of pneumonia in people with HIV disease.
P. jiroveci pneumonia (PJP) (Opportunistic pneumonia)
151
onset is slow and subtle with symptoms of fever, tachypnea, tachycardia, dyspnea, nonproductive cough, and hypoxemia. The chest x-ray usually shows diffuse bilateral infiltrates. In widespread disease, the lungs have massive consolidation. PJP can be life-threatening, causing acute respiratory failure and death. Infection can spread to other organs, including the liver, bone marrow, lymph nodes, spleen, and thyroid.
P. jiroveci pneumonia (PJP) signs /symp (Opportunistic pneumonia)
152
Bacterial and viral pneumonias first must be ruled out because of the vague presentation of PJP. Although the causative agent is fungal, PJP does not respond to antifungal agents.
causative agent is fungal for PJP (Opportunistic pneumonia)
153
of a course of trimethoprim/sulfamethoxazole (Bactrim, Septra) either IV or orally depending on the severity of disease and the patient’s response. ***does not respond to antifungal agents.
fungal for PJP (Opportunistic pneumonia)Treatment consists
154
, a herpesvirus, can cause viral pneumonia. Most CMV infections are asymptomatic or mild.
CMV (cytomegalovirus)/(Opportunistic pneumonia)
155
complications after hematopoietic stem cell transplantation.
CMV is one of the most important life-threatening infectious
156
Antiviral medications (e.g., ganciclovir [Cytovene], foscarnet [Foscavir], cidofovir) and high-dose immunoglobulin are used for treatment.
treatment. for CMV (cytomegalovirus)/(Opportunistic pneumonia)
157
Inflammation, characterized by an increase in blood flow and vascular permeability, activates neutrophils to engulf and kill the offending pathogens. As a result, the inflammatory process attracts more neutrophils, edema of the airways occurs, and fluid leaks from the capillaries and tissues into alveoli. Normal O2 transport is affected, leading to manifestations of hypoxia (e.g., tachypnea, dyspnea, tachycardia).
pathophysiology of pneumonia
158
, the absence of gas or air in 1 or more areas of the lung, may occur with pneumonia.
Atelectasis (occur w/ pneumonia)
159
, a feature typical of bacterial pneumonia, occurs when the normally air-filled alveoli become filled with water, fluid, and/or debris
consolidation (occur w/ pneumonia)
160
are cough, fever, chills, dyspnea, tachypnea, and pleuritic chest pain -cough may or may not be productive. -Sputum may be green, yellow, or even rust colored (bloody)
most common presenting symptoms of pneumonia
161
may initially be seen as influenza, with respiratory symptoms appearing and/or worsening 12 to 36 hours after onset.
Viral pneumonia sign/symp
162
Confusion or stupor (possibly related to hypoxia) may be the only finding. Hypothermia, rather than fever, also may be seen in the older adult. Nonspecific manifestations include diaphoresis, anorexia, fatigue, myalgias, and headache.
elderly does NOT have classic symp of pneumonia instead
163
fine or coarse crackles may be auscultated over the affected region. If consolidation is present, bronchial breath sounds, egophony (an increase in the sound of the patient’s voice), and increased fremitus (vibration of the chest wall made by vocalization) may be present. Patients with pleural effusion may have dullness to percussion over the affected area
elderly does NOT have classic symp of pneumonia instead (on assessment)
164
. Common culprits include MRSA and gram-negative bacilli
major problem today is pneumonia caused by multidrug-resistant (MDR) pathogens
165
advanced age, immunosuppression, history of antibiotic use, and prolonged mechanical ventilation.
Risk factors for MDR (multidrug-resistant) pneumonia include
166
can identify MDR pathogens.
Antibiotic susceptibility tests
167
Atelectasis, pleurisy, pleural effusion, bacteremia, pneumothorax, acute respiratory failure, sepsis shock, multiple organ dysfunction syndrome
Other complications from pneumonia develop more often in older adults and those with underlying chronic diseases. These include:
168
Lung abscess is
not a common complication of pneumonia
169
it may occur with pneumonia caused by S. aureus and gram-negative organisms.
Lung abscess (puss built up in tissue)
170
, the accumulation of purulent exudate in the pleural cavity, occurs in less than 5% of cases.
Empyema
171
requires antibiotic therapy and drainage of the exudate by a chest tube or open surgical drainage.
Empyema treatment
172
History, physical examination, and chest x-ray often give enough information to make immediate decisions about early treatment. Chest x-ray often shows patterns characteristic of the infecting pathogen -X-ray may also show pleural effusions. A thoracentesis and/or bronchoscopy with washings may be used to obtain fluid samples from patients not responding to initial therapy. -Arterial blood gases (ABGs) may be obtained to assess for hypoxemia (partial pressure of O2 in arterial blood [PaO2] less than 80 mm Hg), hypercapnia (partial pressure of carbon dioxide in arterial blood [PaCO2] greater than 45 mm Hg), and acidosis (pH less than 7.35). -Leukocytosis occurs in most patients with bacterial pneumonia. The white blood cell (WBC) count is usually greater than 15,000/μL (15 × 109/L) with the presence of bands (immature neutrophils).
common diagnostic procedures for pneumonia
173
beginning antibiotic therapy. However, antibiotic administration should not be delayed if a specimen cannot be obtained. Delays in antibiotic therapy can increase the risk for morbidity and mortality. Blood cultures are done for patients who are seriously ill.
sputum specimen for culture and Gram stain to identify the organism is obtained before (pneumonia)
174
• Increased fluid intake (at least 3 L/day), IV fluids • Balance between activity and rest • O2 therapy • Physiotherapy • VTE prophylaxis • Critical care management, with mechanical ventilation as needed
management for pneumonia
175
Appropriate antibiotic therapy (Table 27.6) • Antipyretics • Analgesics • Nonsteroidal antiinflammatory drugs (if no contraindications)
Drug treatment for pneumonia
176
both bacterial and mycoplasma pneumonia
Antibiotics are highly effective for
177
is used to prevent S. pneumoniae infection - Prompt treatment with the appropriate antibiotic is essential. - Antibiotics are highly effective for both bacterial and mycoplasma pneumonia. In uncomplicated cases, the patient responds to drug therapy within 48 to 72 hours
Pneumococcal vaccine
178
decreased temperature, improved breathing, and reduced chest discomfort.
Signs of improvement include(pneumonia)
179
than 7 days. A repeat chest x-ray may be done in 6 to 8 weeks to assess for resolution.
Abnormal physical findings can last more
180
include O2 therapy to treat hypoxemia, analgesics to relieve chest pain, and antipyretics (e.g., aspirin, acetaminophen) for fever. Although cough suppressants, mucolytics, bronchodilators, and corticosteroids are often prescribed as adjunctive therapy, the use of these drugs is debatable. However, they may be prescribed for patients with underlying chronic conditions.
management pneumonic part 2
181
no definitive treatment exists -self-limiting and will often resolve in 3 to 4 days. Antiviral therapy may be used to treat pneumonia caused by influenza (e.g., oseltamivir, zanamivir) or a few other viruses (e.g., acyclovir [Zovirax] for herpes simplex virus).11
viral pneumonias treatment
182
empiric therapy based on the likely pathogen
Once the pneumonia is classified, the HCP selects
183
whether the patient has risk factors for MDR pathogens.
empiric antibiotic therapy is based on
184
must be adapted to local patterns of antibiotic resistance. Multiple regimens exist, but all should initially include antibiotics that are effective against both resistant gram-negative and resistant gram-positive organisms.
antibiotic regimen
185
• All children <2 yrs • All adults ≥65 yrs • Anyone 2–64 yrs old with certain medical conditions (e.g., sickle cell disease, asplenia, immunodeficiencies, HIV infection, chronic renal failure, leukemia, cancer, long-term immunosuppressive therapy, CSF leaks, cochlear implant[s])
Pneumococcal conjugate vaccine (PCV13, Prevnar 13)
186
All adults ≥65 yrs • Anyone 2–64 yrs old with certain long-term health problems (e.g., heart disease, lung disease, diabetes, alcoholism, cirrhosis, sickle cell disease, CSF leaks, cochlear implant) • Anyone 2–64 yrs with a disease or condition that weakens the immune system or taking drugs that lower the body’s resistance to infection (e.g., HIV infection; lymphoma or leukemia; kidney failure; damaged or no spleen; multiple myeloma; receiving immunosuppressive chemotherapy, radiation therapy, or long-term corticosteroids; after organ or bone marrow transplantation) • Adults 19–64 yrs who smoke cigarettes or have asthma
Pneumococcal polysaccharide vaccine (PPSV23, Pneumovax 23)†
187
should be a minimum of 5 days. The patient should be afebrile for 48 to 72 hours before stopping treatment.
Total treatment time for patients with CAP
188
(e.g., side-lying, upright) that will prevent or minimize the risk for aspiration
altered consciousness in positions (aspiration pneumonia)
189
but not in the exact same location. The vaccines cannot be mixed into 1 injection.
Patients can receive the pneumococcal vaccine and influenza vaccine at the same time
190
is an infectious disease caused by Mycobacterium tuberculosis
Tuberculosis (TB)
191
It usually involves the lungs, but can infect any organ, including the brain, kidneys, and bones.
Tuberculosis (TB) infect
192
attributed to HIV disease and the emergence of drug-resistant strains of M. tuberculosis.
Tuberculosis (TB) infect mainly
193
the homeless, residents of inner-city neighborhoods, foreign-born people, those living or working in institutions (long-term care facilities, prisons, shelters, hospitals), IV injecting drug users, overcrowded living conditions, less than optimal sanitation, and those with poor access to health care. Immunosuppression from any cause (e.g., HIV infection, cancer, long-term corticosteroid use) increases the risk for active TB infection.
People most at risk TB include
194
Once a strain of M. tuberculosis develops resistance to the most potent first-line antitubercular drugs (isoniazid [INH] and rifampin [Rifadin]), it is defined as
multidrug-resistant tuberculosis (MDR-TB)
195
occurs when the organism is also resistant to any of the fluoroquinolones plus any injectable antibiotic agent
Extensively drug-resistant TB (XDR-TB)
196
several problems, including incorrect prescribing, lack of public health case management, patient nonadherence to the prescribed regimen, and lack of funding for education and prevention.
Resistance results from
197
is a gram-positive, aerobic, acid-fast bacillus (AFB). It is usually spread from person to person by airborne droplets expectorated when breathing, talking, singing, sneezing, and coughing
M. tuberculosis
198
. TB is not highly infectious, as transmission usually requires close contact and frequent or prolonged exposure.
Humans are the only known reservoir for TB
199
touching, sharing food utensils, kissing, or any other type of physical contact.
TB disease cannot be spread by
200
usually spread from person to person by airborne droplets expectorated when breathing, talking, singing, sneezing, and coughing. A process of evaporation leaves small droplet nuclei, 1 to 5 μm in size, suspended in the air for minutes to hours. Another person then inhales the bacteria. -Once inhaled, these small droplets lodge in bronchioles and alveoli.
process of how TB spreads
201
(1) number of organisms expelled into the air, (2) concentration of organisms (small spaces with limited ventilation would mean higher concentration), (3) length of time of exposure, and (4) immune system of the exposed person.
Factors that influence TB transmission include the
202
local inflammatory reaction occurs, and the focus of infection is established. This is called the
Ghon lesion or focus.
203
represents a calcified TB granuloma, the.
hallmark of a primary TB infection
204
defense mechanism aimed at walling off the infection and preventing further spread. Replication of the bacillus is inhibited, and the infection is stopped.
The formation of a granuloma is a
205
through the lymphatic system and find favorable environments for growth in other organs. These include the cerebral cortex, spine, epiphyses of the bone, liver, kidneys, lymph nodes, and adrenal glands.
M. tuberculosis is aerophilic (O2 loving) and has an affinity for the lungs, the infection can spread
206
(1) its presentation (primary, latent, or reactivated) and (2) whether it is pulmonary or extrapulmonary.
TB also can be classified according to
207
when the bacteria are inhaled and start an inflammatory reaction.
Primary TB infection occurs
208
When active disease develops within the first 2 years of infection, it is called
primary TB
209
As a result, the bacteria replicate
active TB disease results.
210
People co-infected with HIV are at
greatest risk for developing active TB.
211
TB disease occurring 2 or more years after the initial infection.
Post-primary TB, or reactivation TB, is defined as
212
the person is infectious and can transmit the disease to others.
If the site of TB is pulmonary or laryngeal,
213
occurs in a person who does not have active TB disease -People with LTBI have a positive skin test but are asymptomatic. They cannot transmit the TB bacteria to others but can develop active TB disease at some point.
Latent TB infection (LTBI)
214
Immunosuppression, diabetes, poor nutrition, aging, pregnancy, stress
chronic disease can reactivate the disease ex:
215
usually do not develop until 2 to 3 weeks after infection or reactivation. The primary manifestation is an initial dry cough that often becomes productive with mucoid or mucopurulent sputum. Active TB disease may initially present with constitutional symptoms (e.g., fatigue, malaise, anorexia, unexplained weight loss, low-grade fevers, night sweats). Dyspnea is a late symptom that may signify considerable pulmonary disease or a pleural effusion. Hemoptysis, is also a late symptom.
Symptoms of pulmonary TB (infectious)
216
more acute, sudden presentation. The patient may have a high fever, chills, generalized flu-like symptoms, pleuritic pain, a productive cough, and acute respiratory failure. Auscultation of the lungs may be normal or reveal adventitious sounds, such as crackles.
Symptoms TB disease
217
fever and other signs of an infection
Immunosuppressed (e.g., HIV-infected) people and older adults are less likely to have
218
such as fever, cough, and weight loss, may be wrongly attributed to PJP or other HIV-associated opportunistic diseases.
patients with HIV, classic manifestations of TB,
219
change in cognitive function may be the
only initial presenting sign of TB in an older person
220
depend on the organs infected. For example, renal TB can cause dysuria and hematuria. Bone and joint TB may cause severe pain. Headaches, vomiting, and lymphadenopathy may be present with TB meningitis.
manifestations of extrapulmonary TB
221
heals without complications, except for scarring and residual cavitation within the lung. Significant pulmonary damage, although rare, can occur in patients who are poorly treated or who do not respond to TB treatment.
pulmonary TB typically healing
222
is widespread dissemination of the mycobacterium. The bacteria spread through the bloodstream to several distant organs. The infection is characterized by a large amount of TB bacilli and may be fatal if untreated.
Miliary TB can occur with primary disease or reactivation of LTBI.
223
slowly progress over a period of days, weeks, or even months. Symptoms vary depending on the organs that are affected. Fever, cough, and lymphadenopathy are present. Hepatomegaly and splenomegaly may occur.
Manifestations Miliary TB
224
, a specific type of extrapulmonary TB, can result from either primary disease or reactivation of a latent infection.
Pleural TB
225
Chest pain, fever, cough, and presence of a unilateral pleural effusion are common.
Pleural TB sign/symp
226
bacteria in the pleural space, which trigger an inflammatory reaction and a pleural exudate of protein-rich fluid.
pleural effusion is caused by
227
from large numbers of tubercular organisms in the pleural space
Empyema is less common than effusion but may occur
228
AFB cultures and a pleural biopsy.
Diagnosis is confirmed by
229
can lead to destruction of the intervertebral disc and adjacent vertebrae.
TB in the spine (Pott’s disease)
230
can cause severe bacterial meningitis.
Central nervous system (CNS) TB
231
can lead to peritonitis, especially in HIV-positive patients.
Abdominal TB
232
using purified protein derivative (PPD) is the standard method to screen people for M. tuberculosis.
tuberculin skin test (TST) (Mantoux test)
233
The test is read by inspection and palpation 48 to 72 hours later for the presence or absence of induration.
tuberculin skin test read by
234
Induration, a palpable, raised, hardened area or swelling (not redness) at the injection site means the person has been exposed to TB and has developed antibodies.1 -Antibody formation occurs 2 to 12 weeks after initial exposure to the bacteria.
positive TB skin test
235
Because the immunocompromised patient may have a decreased response to TST, smaller induration reactions (5 mm or larger) are considered positive.
Immunocompromised positive TB size
236
have a false negative result with the first TST
people with LTBI or who were previously infected with TB may
237
could be a new infection or the result of the boosted reaction to an old infection.
positive reaction to a subsequent test
238
that any future positive results can be accurately interpreted as being caused by a new infection.
A previously negative 2-step TST ensures
239
are another screening tool for TB
Interferon-γ (INF-γ) release assays (IGRAs)
240
are blood tests that detect INF-γ release from T cells in response to M. tuberculosis.
IGRAs
241
QuantiFERON-TB Gold In-Tube test (QFT-GIT) and the T-SPOT.TB test. Test results are available in a few hours.
Examples of IGRAs include
242
in that they require only 1 patient visit, are not subject to reader bias, have no booster phenomenon, and are not affected by prior bacillus Calmette-Guérin (BCG) vaccination.
IGRAs offer several advantages over the TST
243
Culture is the
gold standard for diagnosing TB
244
, each collected at 8- to 24-hour intervals, with at least 1 early morning specimen.
Three consecutive sputum specimens are needed
245
a microscopic examination of stained sputum smears for AFB. A definitive diagnosis of TB requires mycobacterial growth, which can take up to 6 weeks.
initial TB test involves
246
are considered infectious for the first 2 weeks after starting treatment.
Patients with sputum smear–positive TB
247
is drug therapy (Promoting and monitoring adherence are critical for treatment to be successful
mainstay of TB treatment
248
initial and continuation
Drug therapy for TB is divided into 2 phases:
249
a 3-month initial phase with 4 drugs (isoniazid, rifampin, pyrazinamide, and ethambutol) -if effective= ethambutol may be stopped
treatment regimen for patients with previously untreated TB consists of
250
, other drugs can be used, including rifabutin and rifapentine (Priftin)
If the patient develops a toxic reaction to the primary drugs
251
the remaining 3 drugs are used for the initial phase.
If pyrazinamide cannot be included in the initial phase (because of liver disease, pregnancy, etc.),
252
in the initial phase typically includes 5 drugs: 1or 2 first-line agents, a fluoroquinolone, an injectable antibiotic, and 1 or more second-line agents, for at least 6 months after sputum culture is negative
MDR-TB therapy
253
Two newer drugs, bedaquiline (Sirturo) and Delamanid (Deltyba), are
used in combination with other drugs to treat MDR-TB and XDR-TB.
254
involves providing the antitubercular drugs directly to patients and watching as they swallow the medications.
Directly observed therapy (DOT)
255
once-weekly isoniazid plus rifapentine continuation dosing or twice-weekly isoniazid plus rifampin or rifabutin, should not be used if CD4+ counts are less than 100/μL.
alternative regimens in any HIV-infected patient that include
256
nonviral hepatitis. Baseline liver function tests (LFTs) are done at the start of treatment and monitored closely (e.g., every 2 to 4 weeks), especially if results are abnormal.
major side effect of isoniazid, rifampin, and pyrazinamide is
257
is 9 months of daily isoniazid. -adherence issues may make a 6-month regimen
standard treatment regimen for LTBI
258
or otherwise healthy patients who are not presumed to be infected with MDR bacilli.
alternative 3-month regimen of isoniazid and rifapentine may be used f
259
resistant to isoniazid. Because of severe liver injury
Four-month therapy with rifampin may be indicated if the patient is
260
is a live, attenuated strain of Mycobacterium bovis. The vaccine is given to infants in parts of the world with a high prevalence of TB. I
Bacille Calmette-Guérin (BCG) vaccine
261
not used because of the low risk for infection, the vaccine’s variable effectiveness against adult pulmonary TB, and potential interference with TB skin test reactivity.
Bacille Calmette-Guérin (BCG) vaccine not used because
262
(e.g., health care workers who are continually exposed to patients with MDR-TB and when infection control precautions are not successful).
BCG vaccine should be considered only for select persons who meet specific criteria
263
isolation of patients infected with organisms spread by the airborne route. Patients are in a single-occupancy room with negative pressure and airflow of 6 to 12 exchanges per hour.
Airborne infection isolation refers to (TB PT)
264
teaching and counseling, reminder systems, incentives or rewards, contracts, and DOT.
Strategies to improve adherence include
265
pulmonary disease, lymphadenitis, skin or soft tissue disease, or disseminated disease.
There are more than 30 varieties of acid-fast mycobacteria that do not cause TB but cause
266
are not airborne or transmitted by droplets. They can be found in tap water, soil, bird feces, and house dust.
Atypical mycobacteria
267
Pulmonary symptoms include cough, shortness of breath, weight loss, fatigue, and blood-tinged sputum.
Atypical mycobacteria symptoms
268
endemic (native and common) or opportunistic fungi
Pulmonary fungal pneumonia is an infectious process in the lungs caused by
269
infection in healthy people and in immunocompromised people in certain geographic locations in the United States.
Endemic fungal pathogens cause
270
coccidioidomycosis, is a fungus found in the soil of dry, low-rainfall areas.
Coccidioides, which causes (endemic fungi)
271
in immunocompromised patients (e.g., those receiving chemotherapy, immunosuppressive drugs) and in patients with HIV and cystic fibrosis. These pulmonary fungal infections can be life-threatening.
Opportunistic fungal infections occur
272
by inhaling spores. -They are not transmitted from person to person. The patient does not have to be placed in isolation.
Pulmonary fungal infections are acquired
273
are like those of bacterial pneumonia
manifestations Pulmonary fungal
274
Skin testing, serology, and biopsy
methods aid in identifying the infecting organism Pulmonary fungal
275
is the standard therapy for treating serious systemic fungal infections. It must be given IV
Amphotericin B
276
ketoconazole, fluconazole (Diflucan), voriconazole (Vfend), and itraconazole (Sporanox).
Less serious infections can be treated with oral antifungals, such as (Pulmonary fungal infection)
277
, the most common benign tumor, is a slow-growing congenital tumor composed of fibrous tissue, fat, and blood vessels.
Hamartomas
278
is a benign tumor arising in the bronchi that consists of columnar cystic spaces.
Mucous gland adenoma
279
are either malignant or benign and start in the visceral pleura. Malignant mesotheliomas are associated with exposure to asbestos. Benign mesotheliomas are localized lesions.
Mesotheliomas
280
as either blunt trauma or penetrating trauma.
primary mechanisms of injury responsible for chest trauma
281
occurs when the chest strikes or is struck by an object. The impact can cause shearing and compression of chest structures.
Blunt trauma
282
laceration or tearing of the aorta.
high-velocity impact, shearing forces can result in
283
contusion, crush injury, and organ rupture.
Compression of the chest may result in
284
is an injury in which a foreign object impales or passes through the body tissues, creating an open wound.
Penetrating trauma
285
are the most common type of chest injury from blunt trauma
Rib fractures
286
fractured because they are the least protected by chest muscles.
Ribs 5 through 9 are most often
287
pain at the site of injury, especially during inspiration and with coughing -Atelectasis and pneumonia may develop because of decreased chest wall movement and retained secretions.
Manifestations of fractured ribs include
288
NSAIDs, opioids, and thoracic nerve blocks can be used to reduce pain and assist with deep breathing and coughing. Patient teaching should emphasize deep breathing, coughing, incentive spirometry, and appropriate use of pain medications.
treatment of fractured ribs include
289
from the fracture of 3 or more consecutive ribs, in 2 or more separate places, causing an unstable segment
Flail chest results
290
also can be caused by fracture of the sternum and several consecutive ribs. -On expiration, the flail section bulges outward with mediastinal shift to the injured side.
Flail chest caused by
291
in the opposite direction with respect to the intact part of the chest. During inspiration, the affected part is sucked in, and during expiration, it bulges out
affected (flail) area moves
292
by air entering the pleural cavity.
pneumothorax is caused
293
Normally, negative (subatmospheric) pressure exists between the visceral pleura (surrounding the lung) and parietal pleura (lining the chest cavity), known as the =
pleural space
294
pleural space has a few milliliters of lubricating fluid to reduce friction when the tissues move. When air enters this space, the change to positive pressure
causes a partial or complete lung collapse (pneumothorax)
295
open (air entering through an opening in the chest wall) or closed (no external wound).
Pneumothorax can be classified as
296
penetrating chest wound may be referred to as a sucking chest wound, since air enters the pleural space through the chest wall during inspiration
sucking chest wound/ penetrating chest wound
297
breath sounds are absent over the affected area. Time permitting, a chest x-ray will show air or fluid in the pleural space and reduction in lung volume.
On auscultation, pneumothorax
298
typically occurs due to the rupture of small blebs (air-filled sacs) on the surface of the lung.
spontaneous pneumothorax
299
in healthy, young people or from lung disease, such as COPD, asthma, cystic fibrosis, and pneumonia
blebs can occur
300
can occur due to laceration or puncture of the lung during medical procedures.
Iatrogenic pneumothorax
301
example, transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, and transbronchial lung biopsy all have the potential to injure the lung.
causes of Iatrogenic pneumothorax
302
Barotrauma from excessive ventilatory pressure during manual or mechanical ventilation can rupture alveoli, =
Barotrauma creating a pneumothorax.
303
when air enters the pleural space but cannot escape.
Tension pneumothorax occurs
304
This results in compression of the lung on the affected side and pressure on the heart and great vessels, pushing them away from the affected side
Tension pneumothorax pathophysiology
305
, a flap may act as a one-way valve. Thus air can enter on inspiration but cannot escape
In an open chest wound
306
severe dyspnea, marked tachycardia, tracheal deviation, decreased or absent breath sounds on the affected side, neck vein distention, cyanosis, and profuse diaphoresis.
Manifestations Tension pneumothorax include
307
is an accumulation of blood in the pleural space from injury to the chest wall, diaphragm, lung, blood vessels, or mediastinum
Hemothorax
308
When hemothorax occurs with pneumothorax, it is called a
hemopneumothorax
309
needs immediate insertion of a chest tube for evacuation of the blood. Recovered blood can be reinfused for a short time after the injury.
traumatic hemothorax treatment
310
is the presence of lymphatic fluid in the pleural space
Chylothorax
311
thoracic duct is disrupted either traumatically or from cancer, allowing lymphatic fluid to fill the pleural space.
chylothorax definition pathology
312
cases heal with conservative treatment (chest drainage, bowel rest, dietary modifications). Octreotide may reduce the flow of lymphatic fluid. Surgery (thoracic duct ligation) and pleurodesis (the artificial production of adhesions between the parietal and visceral pleura) are options for refractory cases.
Chylothorax Treatment
313
If the patient is stable and has minimal air and/or fluid accumulated in the intrapleural space, no treatment may be needed since the condition may resolve spontaneously.
Treatment of a pneumothorax if pt is stable
314
Emergency treatment consists of covering the wound with an occlusive dressing that is secured on 3 sides (vent dressing).
Treatment of a pneumothorax Emergency treatment
315
is to insert a chest tube and connect it to water-seal drainage.
most definitive and common treatment of pneumothorax and hemothorax
316
with a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another.
Repeated spontaneous pneumothorax may need surgical treatment
317
are used to drain blood, and small
Large (36F to 40F) tubes (chest tube)
318
are used to drain fluid,
medium (24F to 36F) tubes (chest tube)
319
are used to drain air
(12F to 24F) tubes (chest tube)
320
with a curly end designed to keep them in place. Pigtail tubes are a safe and effective alternative to larger-bore chest tubes for treatment of pneumothorax
Pigtail tubes are very small (10F to 14F) tubes
321
is used to remove air from the pleural space
flutter valve (also called the Heimlich valve)
322
is usually attached to a drainage device or chamber to collect fluid, air, and/or blood from the chest cavity.
chest tube
323
receives fluid and air from the pleural space.
first compartment, or collection chamber,
324
the water-seal chamber, contains 2 cm of water, which acts as a one-way valve
second compartment,
325
, coughing, or sneezing (when the patient’s intrathoracic pressure is increased) may be seen as long as there is air in the pleural space.
Intermittent bubbling during exhalation
326
of air often occurs in this chamber when a pneumothorax is first evacuated
Brisk bubbling
327
Normal fluctuation of the water within the water-seal chamber is called
tidaling.
328
his may signify an occluded chest tube. As the lung reexpands, tidaling gradually slows then eventually stops.
If tidaling stops suddenly, assess the chest tube as t
329
the suction control chamber, applies suction to the chest drainage unit.
third compartment,
330
water and dry.
2 main types of suction control:
331
a column of water to control the amount of suction from the wall regulator.
water suction control chamber uses
332
is no longer advocated. -immediate priority is to reestablish the water-seal system.
Clamping of chest tubes during transport or when the tube is accidentally disconnected
333
to change the drainage apparatus or to check for air leaks
Chest tubes may be momentarily clamped if
334
reexpansion pulmonary edema or severe, symptomatic hypotension can occur.
If volumes from 1 to 1.5 L of fluid and/or blood are removed rapidly, from chest tube
335
can occur from air leaking into the tissue surrounding the chest tube insertion site
Subcutaneous emphysema (chest tube)
336
, development of subcutaneous emphysema, or any signs and symptoms of respiratory distress should be reported to the HCP at once.
Drainage greater than 200 mL in the first hour (chest tube emergency)
337
is a surgical incision into the chest to gain access to the heart, lungs, esophagus, thoracic aorta, or anterior spine.
thoracotomy
338
are the median sternotomy and lateral thoracotomy
Two common approaches to a thoracotomy
339
splitting the sternum. It is primarily used for surgery involving the heart
median sternotomy involves (thoracotomy)
340
can be done using a posterolateral or anterolateral incision.
lateral thoracotomy incision (thoracotomy)
341
is used for most surgeries involving the lung. -incision is made from front to back at the level of the 4th, 5th, or 6th intercostal space.
posterolateral incision (thoracotomy)
342
is made in the 4th or 5th intercostal space from the sternal border to the midaxillary line. This procedure is often done for surgery or trauma victims, mediastinal operations, and wedge resections of the upper and middle lobes of the lung.
anterolateral incision (thoracotomy)
343
Removal or stripping of thick, fibrous membrane from visceral pleura
Decortication
344
Incision into thorax to look for injured or bleeding tissues
Exploratory Thoracotomy
345
Removal of 1 lobe of lung
Lobectomy
346
Bronchoscopic procedure
Lung Volume Reduction Surgery
347
Open surgical procedure -multiple wedge excisions or VATS
Lung Volume Reduction Surgery
348
Removal of entire lung (lung cancer) -Position patient on operative side to promote expansion of remaining lung
Pneumonectomy
349
Removal of 1 or more lung segments
Segmental Resection
350
Incision into thorax for surgery on other organs -Hiatal hernia repair, open heart surgery, esophageal surgery, tracheal resection, thoracic aorta repair
Thoracotomy (Not Involving Lungs)
351
Video-assisted technique with a rigid scope with a distal lens inserted into pleura and image shown on a monitor screen
Video-Assisted Thoracic Surgery
352
Allows HCP to manipulate instruments passed into pleural space through separate small intercostal incisions
Video-Assisted Thoracic Surgery (reasoning)
353
Removal of small, localized lesion that occupies only part of a segment -Lung biopsy, excision of small nodules
Wedge Resection
354
used for diagnosis and treatment of diseases of the pleura, pulmonary masses and nodules, mediastinal masses, and interstitial lung disease.
Video-Assisted Thoracic Surgery (reasoning)
355
patients with chest trauma. The HCP can examine, diagnose, and manage injuries in both blunt and penetrating trauma, including injuries to the diaphragm.
VATS is increasingly being used for
356
less discomfort, faster return to normal activity level, reduced length of hospital stay, lower postoperative morbidity risk, and fewer complications.
advantages of VATS include
357
Patients who have marginal respiratory reserve or are too debilitated to tolerate an open thoracotomy approach may benefit from the VATS procedure.
Patients who benefit from VATS include
358
may include chest x-ray, electrocardiogram (ECG), ABGs, pulmonary function studies, blood urea nitrogen (BUN), serum creatinine, blood glucose, serum electrolytes, prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), and CBC.
Diagnostic studies preop pneumonectomy
359
to prevent respiratory compromise. The use of PCA, epidural infusions, and intercostal nerve blocks allows patients to breathe deeply, cough, and move the arm and shoulder on the operative side.
Adequate pain management is a priority (pneumoectomy)
360
is aspiration of intrapleural fluid for diagnostic and therapeutic purposes
Thoracentesis
361
the patient may sit on the edge of a bed and lean forward over a bedside table
thoracentesis, (how to sit pt)
362
chest x-ray or ultrasound images are
used to determine the optimal puncture site. in thoracentesis
363
skin is cleansed with an antiseptic solution and injected with a local anesthetic.
how skin cleaned during thoracentesis
364
Fluid is aspirated with a syringe, or tubing is connected to the needle to allow fluid to drain into a sterile container. After the fluid is removed, the needle is withdrawn, and a bandage is applied over the insertion site. -Usually no more than 1000 to 1200 mL of pleural fluid is removed at one time.
thoracentesis (process of aspiration)
365
-Usually no more than 1000 to 1200 mL of pleural fluid is removed at one time. -Rapid removal of a large volume can result in hypotension, hypoxemia, or reexpansion pulmonary edema.
thoracentesis (remove of fluid)
366
to assess for complications, such as pneumothorax
chest x-ray may be done after the procedure of thoracentesis
367
Disorders that impair the ability of the chest wall and diaphragm to move with respiration are called
restrictive respiratory disorders
368
1.extrapulmonary conditions 2.intrapulmonary conditions,
restrictive respiratory disorders 2 categories: extrapulmonary conditions, in which the lung tissue is normal, and intrapulmonary conditions, in which the cause is the lung or pleura.
369
in which the lung tissue is normal,
extrapulmonary conditions,(restrictive respiratory disorders)
370
, in which the cause is the lung or pleura.
intrapulmonary conditions (restrictive respiratory disorders)
371
between restrictive and obstructive respiratory disorders.
Pulmonary function tests are the best means of distinguishing
372
is a reduced total lung capacity (TLC). -ex:pulmonary fibrosis
hallmark characteristic of a restrictive lung disorder
373
is reduced forced expiratory volume (FEV1). -ex: asthma
The hallmark characteristic of an obstructive disorder
374
amount oxygen in lungs -ex: pulmonary fibrosis
TLC (restrictive lung disorder)
375
amount of oxygen exhaled out lungs -ex: asthma
(FEV1).obstructive disorder
376
a patient may have both asthma (an obstructive problem) and pulmonary fibrosis (a restrictive problem).
Mixed obstructive and restrictive disorders sometimes occur together example
377
• Pleural effusion • Pleurisy (pleuritis) • Pneumothorax
Intrapulmonary Causes Pleural Disorders (common cause restrictive respiratory disorder)
378
• Acute respiratory distress syndrome (ARDS) • Atelectasis • Interstitial lung diseases • Pneumonia
Parenchymal Disorders (common cause restrictive respiratory disorder)
379
• Head injury, central nervous system lesion (e.g., tumor, stroke) • Opioid and barbiturate overdose
Extrapulmonary Causes Central Nervous System (common cause restrictive respiratory disorder)
380
• Amyotrophic lateral sclerosis • Guillain-Barré syndrome • Muscular dystrophy • Myasthenia gravis
Neuromuscular System (common cause restrictive respiratory disorder)
381
• Kyphoscoliosis • Obesity-hypoventilation syndrome (Pickwickian syndrome)
Chest Wall (common cause restrictive respiratory disorder)
382
is a lung condition characterized by collapsed, airless alveoli
Atelectasis
383
decreased or absent breath sounds and dullness to percussion over the affected area
Atelectasis breath sounds
384
is obstruction of the small airways with secretions.
most common cause of atelectasis
385
bedridden patients and in postoperative abdominal and chest surgery patients.
Atelectasis common in pts that
386
is an inflammation of the pleura
Pleurisy (pleuritis)
387
caused by infectious diseases, cancer, autoimmune disorders, chest trauma, GI disease, and certain medications.
causes of Pleurisy (pleuritis)
388
inflammation usually subsides with adequate treatment of the primary disease
Pleurisy (pleuritis) process of healing
389
pain of pleurisy is typically abrupt, sharp in onset, and worse with inspiration. -breathing is shallow and rapid ( avoid unnecessary movement of the pleura and chest wall) -pleural friction rub ( sound heard bc inflamed visceral pleura and parietal pleura rub over one another during inspiration) =sound, like a squeaking door, is usually loudest at peak inspiration.
sign/ symp of pleurisy
390
is aimed at treating the underlying disease and providing pain relief. Teach the patient to splint the rib cage when coughing. If the pain is severe, intercostal nerve blocks may be considered.
Treatment of pleurisy
391
to more than 200 lung disorders in which the tissue between the air sacs of the lungs (the interstitium) is affected by inflammation or scarring (fibrosis)
Interstitial lung disease (ILD), also called diffuse parenchymal lung disease, refers
392
idiopathic pulmonary fibrosis and sarcoidosis. -Other ILDs are caused by inhalation of occupational and environmental toxins, certain medications, radiation therapy, connective tissue disorders, cancer, and infection
Two common ILDs of unknown cause are
393
is aimed at reducing exposure to the causative agent and/or treating the underlying disease process. - Although scarring is irreversible, treatment with corticosteroids and immunosuppressant drugs can minimize progression. -A lung transplant may be an option for some patients.
Treatment Interstitial lung disease (ILD)
394
is a chronic, progressive disorder characterized by chronic inflammation and formation of scar tissue in the connective tissue
Idiopathic pulmonary fibrosis (IPF)// (cause Interstitial lung disease)
395
a history of cigarette smoking and exposure to wood and metal dust. -appears bw age 50-70
Risk factors Idiopathic pulmonary fibrosis (IPF) include
396
no known cure for IPF.
Treatment for Idiopathic pulmonary fibrosis (IPF)
397
exertional dyspnea; dry, nonproductive cough; clubbing of the fingers; and inspiratory crackles. Fatigue, weakness, anorexia, and weight loss may occur as the disease progresses
Manifestations Idiopathic pulmonary fibrosis (IPF) include
398
Chest x-ray findings are generally nonspecific. Pulmonary function tests may be abnormal, with evidence of restriction (reduced vital capacity) and impaired gas exchange. Open lung biopsy using VATS often helps to confirm the pathology and is considered the gold standard for diagnosis.
Diagnosis for Idiopathic pulmonary fibrosis (IPF)
399
with a corticosteroid (prednisone), sometimes in combination with other drugs that suppress the immune system (e.g., methotrexate, cyclosporine). Kinase inhibitor drugs, which block multiple pathways that involved with scarring, include nintedanib (Ofev) and pirfenidone (Esbriet). O2 therapy and pulmonary rehabilitation should be prescribed for all patients. Lung transplantation may be an option for those who meet the criteria
IPF are first treated
400
is a chronic, multisystem granulomatous disease of unknown cause that primarily affects the lungs
Sarcoidosis (cause Interstitial lung disease)
401
disease may also involve the skin, eyes, liver, kidney, heart, and lymph nodes.
Sarcoidosis involve (cause Interstitial lung disease)
402
Signs and symptoms vary depending on what organs are affected. Pulmonary symptoms include dyspnea, cough, and chest pain. Many patients do not have symptoms.
Signs and symptoms Sarcoidosis
403
-is aimed at suppressing the inflammatory response. -Patients are followed every 3 to 6 months with pulmonary function tests, chest x-ray, and CT scan to monitor disease progression.
Treatment Sarcoidosis
404
10 to 20 mL of fluid that acts as a lubricant between the chest wall (parietal pleura) and lungs (visceral pleura).
pleural space normally holds
405
is an abnormal collection of fluid in this space. It is not a disease but a sign of disease.
Pleural effusion (sign of disease)
406
balance among hydrostatic pressure, oncotic pressure, and capillary membrane permeability governs movement of fluid in and out of the pleural space.
Keeps FLuid stable in pleural effusion
407
increased pulmonary capillary pressure, decreased oncotic pressure, increased pleural membrane permeability, or obstruction of lymphatic flow.
Fluid accumulation in pleural effusion can be due to
408
transudative or exudative depending on the protein content
classify pleural effusions as
409
occurs primarily in noninflammatory conditions. It is an accumulation of protein-poor, cell-poor fluid. The fluid is clear, pale yellow.
transudate (classification of pleural effusion)
410
(1) increased hydrostatic pressure found in HF or (2) decreased oncotic pressure (from hypoalbuminemia) found in chronic liver or renal disease.
effusions are caused by (transudate)
411
increased capillary permeability due to an inflammatory reaction. They most often occur with an infection or cancer (called a malignant effusion).
exudative effusion results from (classification of pleural effusion)
412
is the collection of purulent fluid in the pleural space. It is often caused by pneumonia, TB, lung abscess, and infected surgical wounds of the chest
empyema (pleural effusion)
413
antibiotic therapy (to eradicate the causative organism), percutaneous drainage, chest tube insertion, VATS, intrapleural fibrinolytic therapy (instilled through the chest tube) to dissolve fibrous adhesions, decortication, and open window thoracostomy.
Treatment empyema options include
414
dyspnea, cough, and occasional sharp, non-radiating chest pain that is worse on inhalation. Physical examination of the chest may show decreased movement of the chest on the affected side, dullness to percussion, and decreased breath sounds over the affected area
Common manifestations of pleural effusion are
415
as well as fever, night sweats, cough, and weight loss.
Indications of an empyema include the manifestations of pleural effusion
416
chest x-ray and CT reveal the volume and location of the effusion.
Diagnosis of pleural effusion
417
is to treat the underlying cause. -For example, adequate treatment of HF with diuretics and sodium restriction may result in a decreased incidence of pleural effusion. The treatment of malignant effusions is more difficult. These effusions often reoccur and reaccumulate quickly after thoracentesis.
management/ Tx of pleural effusions
418
is more difficult. These effusions often reoccur and reaccumulate quickly after thoracentesis.
treatment of malignant effusions (plural effusion)
419
is done to obliterate the pleural space and prevent reaccumulation of effusion fluid. -Talc is the most effective agent for pleurodesis -Other agents that can be used include doxycycline and bleomycin.
Chemical pleurodesis ( Tx pleural effusion)
420
chest tube is clamped for 8 hours while the patient is turned in different positions to allow the chemical to contact the entire pleural space. After 8 hours the chest tube is unclamped and attached to a drainage unit. -Chest tubes are left in place until fluid drainage is less than 150 mL/day and no air leaks are noted. Fever and chest pain are the most common side effects associated with pleurodesis.
Chemical pleurodesis ( Tx pleural effusion)
421
is an abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs.
Pulmonary edema
422
left-sided HF.
most common cause of pulmonary edema is
423
is the blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue -lower lobes of the lung are most often affected.
Pulmonary embolism (PE)
424
are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system
Emboli
425
n the deep veins of the legs.
Most PEs arise from deep vein thrombosis (DVT) i
426
is the preferred term to describe the spectrum of pathologic conditions from DVT to PE
Venous thromboembolism (VTE)
427
femoral or iliac veins, right side of the heart (atrial fibrillation), and pelvic veins (especially after surgery or childbirth).
Other sites of origin of PE include
428
in the presence of central venous catheters or arterial lines. These cases may resolve with the removal of the catheter.
Upper extremity DVT sometimes occurs
429
to a large thrombus lodged at an arterial bifurcation.
saddle embolus refers
430
fat emboli (from fractured long bones), air emboli (from improperly administered IV therapy), bacterial vegetation on heart valves, amniotic fluid, and cancer.
Less common causes PE include
431
immobility or reduced mobility, surgery within the last 3 months (especially pelvic and lower extremity surgery), history of VTE, cancer, obesity, oral contraceptives, hormone therapy, cigarette smoking, prolonged air travel, HF, pregnancy, and clotting disorders
Risk factors for PE include
432
Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE. Mild to moderate hypoxemia may occur. Other manifestations include tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, accentuation of pulmonic heart sound, tachycardia, and syncope. Massive PE may cause a sudden change in mental status, hypotension, and feelings of impending doom.
sign/symp of PE
433
include pulmonary infarction and pulmonary hypertension.
Complications of PE
434
(1) occlusion of a large or medium-sized pulmonary vessel (more than 2 mm in diameter), (2) insufficient collateral blood flow from the bronchial circulation, or (3) preexisting lung disease. ***Infarction results in alveolar necrosis and hemorrhage.
Pulmonary infarction (death of lung tissue) is most likely when there is:
435
from hypoxemia or from involvement of more than 50% of the area of the normal pulmonary bed
Pulmonary hypertension results
436
Dilation and hypertrophy of the right ventricle
can develop due to pulmonary hypertension
437
is a laboratory test that measures the amount of cross-linked fibrin fragments. These fragments are the result of clot degradation
D-dimer
438
is that it is neither specific (many other conditions cause elevation) nor sensitive, because up to 50% of patients with a small PE have normal results.
disadvantage of D-dimer testing
439
spiral CT or lung scan.
Patients with suspected PE and an elevated D-dimer level but normal venous ultrasound may need a
440
is the most common test to diagnose PE. - Computer software reconstructs the data to give a 3-dimensional picture and assist in seeing PEs.
spiral (helical) CT scan (also known as CT angiography or CTA)
441
a ventilation-perfusion (V/Q) scan is done.
If a patient cannot have contrast media, (PE diagnosis)
442
1. Perfusion scanning involves IV injection of a radioisotope. 2. Ventilation scanning involves inhalation of a radioactive gas, such as xenon.
he V/Q scan has 2 parts
443
IV injection of a radioisotope. A scanning device images the pulmonary circulation.
1. Perfusion scanning involves ( V/Q scan has 2 parts)
444
inhalation of a radioactive gas, such as xenon. Scanning reflects the distribution of gas through the lung. The ventilation portion requires the patient’s cooperation. It may not be possible to perform in the critically ill patient, especially if the patient is intubated.
Ventilation scanning involves ( V/Q scan has 2 parts)
445
The PaO2 may be low because of inadequate oxygenation from occluded pulmonary vasculature preventing matching of perfusion to ventilation.
ABG analysis is important but not diagnostic. (PE)
446
Subcutaneous administration of low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox]) or fragmin [Dalteparin] or fondaparinux) is the recommended treatment for patients with acute PE
Treatment for PE
447
LMWH is safer and more effective than unfractionated heparin. -Advantages of LMWH over unfractionated heparin include greater bioavailability, subcutaneous administration, once daily dosing, and longer duration of therapeutic effect. Monitoring the aPTT is not necessary or useful with LMWH. Unfractionated IV heparin can be as effective but is hard to titrate to therapeutic levels.
LMWH VS. UNFRACTIONATED HEPARIN
448
Warfarin (Coumadin), an oral anticoagulant, should also be started at the time of diagnosis -given for at least 3 months and then reevaluated -Alternatives to warfarin include apixaban (Eliquis), dabigatran (Pradaxa), and edoxaban (Savaysa). -Some HCPs use direct thrombin inhibitors (help dissolve the PE and the source of the thrombus in the pelvis or deep leg veins, thereby decreasing the risk for recurrent emboli. )
Tx for PE
449
the patient has complicating factors, such as liver problems causing changes in the clotting, overt bleeding, a history of hemorrhagic stroke, heparin-induced thrombocytopenia (HIT), or other blood dyscrasias.
Anticoagulant therapy may be contraindicated if
450
Hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated may be
candidates for pulmonary embolectomy.
451
the removal of emboli, can be achieved through a diagnostic imaging (vascular catheter) or surgical approach
Embolectomy,
452
are newer, moderately invasive procedures for PE
Percutaneous catheter embolectomy or endovascular ultrasound delivered thrombolysis
453
patients who are at high risk and patients for whom anticoagulation is contraindicated, an
inferior vena cava (IVC) filter may be the treatment of choice.
454
inserted percutaneously through the femoral vein, is placed at the level of the renal veins in the inferior vena cava. Once inserted, the filter expands and prevents migration of large clots into the pulmonary system. -Complications associated with this device are rare but include misplacement, migration, and perforation.
inferior vena cava (IVC) filter process
455
is characterized by elevated pulmonary artery pressure from an increase in resistance to blood flow through the pulmonary circulation.
Pulmonary hypertension
456
by low resistance and low pressure. I
pulmonary circulation is characterized
457
high, with the mean pulmonary artery pressure greater than 25 mm Hg at rest (normal is 12 to 16 mm Hg) or greater than 30 mm Hg with exercise.
pulmonary hypertension the pulmonary pressures are
458
Group 1: Attributed to medication, specific diseases, genetic (inherited) link, or idiopathic Group 2: Related to left-sided HF Group 3: Related to the lungs and hypoxemia Group 4: Related to the cardiovascular system and thromboembolic occlusion Group 5: Multifactorial (and often unclear) origins with hematologic or metabolic involvement
World Health Organization (WHO) has identified 5 classes of pulmonary hypertension.35 Each group is based on cause of the disorder.
459
as a primary disease (idiopathic pulmonary arterial hypertension) or as a secondary complication of a respiratory, heart, autoimmune, liver, or connective tissue disorder (secondary pulmonary arterial hypertension).
Pulmonary hypertension can occur
460
(idiopathic pulmonary arterial hypertension)
primary disease Pulmonary hypertension
461
secondary complication of a respiratory, heart, autoimmune, liver, or connective tissue disorder
secondary pulmonary arterial hypertension
462
is pulmonary hypertension that occurs without an apparent cause. -causing right-sided HF
Idiopathic pulmonary arterial hypertension (IPAH) Aka primary pulmonary hypertension (PPH)
463
is unknown. It is related to connective tissue diseases, cirrhosis, and HIV.
cause of IPAH
464
are dyspnea on exertion and fatigue. Exertional chest pain, dizziness, and syncope may occur. Abnormal heart sounds may be heard, including an S3. --as the disease progresses, dyspnea occurs at rest. Pulmonary hypertension increases the workload of the right ventricle and causes right ventricular hypertrophy (a condition called cor pulmonale) and eventually HF.
classic symptoms of idiopathic pulmonary HTN
465
Right-sided cardiac catheterization is the
definitive test to diagnose any type of pulmonary hypertension
466
of agents that promote vasodilation of the pulmonary blood vessels, reduce right ventricular overload, and reverse remodeling
Drug therapy consists for idiopathic pulmonary HTN
467
Diuretics are used to manage peripheral edema. Anticoagulants are beneficial in pulmonary complications related to thrombus formation. Because hypoxia is a potent pulmonary vasoconstrictor, low-flow O2 gives symptomatic relief. -Surgical interventions include pulmonary thromboendarterectomy (PTE), in which clots are removed from the pulmonary arteries -Atrial septostomy (AS) is a palliative procedure that involves the creation of an intraatrial right-to-left shunt to decompress the right ventricle. It is used for a select group of patients awaiting lung transplantation. -Lung transplantation is an option
idiopathic pulmonary HTN Treatment
468
when another disease causes a chronic increase in pulmonary artery pressures.
Secondary pulmonary arterial hypertension (SPAH) occurs
469
develop due to parenchymal lung disease, left ventricular dysfunction, intracardiac shunts, chronic PE, or systemic connective tissue disease.
causes Secondary pulmonary arterial hypertension (SPAH)
470
including dyspnea, fatigue, lethargy, and chest pain. right ventricular hypertrophy and signs of right-sided HF (increased pulmonic heart sound, S4 heart sound, peripheral edema, hepatomegaly).
signs and symp Secondary pulmonary arterial hypertension (SPAH)
471
is like that of IPAH.
Diagnosis of SPAH
472
treating the underlying primary disorder. When irreversible pulmonary vascular damage has occurred, therapies used for IPAH are started. A PTE may offer a cure for patients with chronic pulmonary hypertension caused by PE.
Treatment of SPAH consists of
473
is enlargement of the right ventricle caused by a primary disorder of the respiratory system - Almost any disorder that affects the respiratory system can cause cor pulmonale.
Cor pulmonale
474
COPD
most common cause of Cor pulmonale
475
Pulmonary hypertension
preexisting condition in the person with cor pulmonale.
476
Manifestations are subtle and often masked by symptoms of the pulmonary condition. Common symptoms include exertional dyspnea, tachypnea, cough, and fatigue. Physical signs include evidence of right ventricular hypertrophy on ECG and an increase in intensity of S2. Chronic hypoxemia leads to polycythemia and increased total blood volume and viscosity of the blood. ****Polycythemia is often present in cor pulmonale from COPD.
signs and symp Cor pulmonale
477
peripheral edema, weight gain, distended neck veins, full, bounding pulse, and enlarged liver, may occur.
if HF accompanies cor pulmonale, manifestations, including
478
• Bronchodilators • Diuretics • Vasodilators (if indicated) • Calcium channel blockers (if indicated) • Inotropic agents -Long-ternm o2
Tx car pulmonale (depends on disease)
479
has become an important alternative option for patients with end-stage lung disease.
Lung transplantation
480
cancer within past 2 years (some types of skin cancer are excluded), chronic active hepatitis B or C, HIV, untreatable advanced dysfunction of another major organ system (e.g., liver or renal failure), current smoker, poor nutritional status, poor rehabilitation potential, and significant psychosocial problems. The patient and family must be able to cope with a complex postoperative regimen (e.g., strict adherence to immunosuppressive therapy, continuous monitoring for early signs of infection, prompt reporting of manifestations of infection).
Absolute contraindications for lung transplant include
481
to prioritize waiting list recipients based on the urgency of need and expected posttransplant survival expectations.
UNOS designates recipients of donor lungs based on a lung allocation score (LAS). The LAS helps
482
• α1-Antitrypsin deficiency • Chronic obstructive pulmonary disease (COPD) • Cystic fibrosis • Idiopathic pulmonary arterial hypertension • Idiopathic pulmonary fibrosis
common indications for lung transplant
483
single-lung transplantation, bilateral lung transplantation, heart-lung transplantation, and transplantation of lobes from a living-related donor.
Four types of transplant procedures are available:
484
a thoracotomy incision on the side of the chest. The opposite lung is ventilated while the diseased lung is excised and the donor lung implanted. -Three anastomoses are done: bronchus, pulmonary artery, and pulmonary veins.
Single-lung transplantation involves
485
the incision is made across the sternum and the donor lungs are implanted separately.
bilateral lung transplantation,
486
is used for a heart-lung transplant procedure
median sternotomy incision
487
from living donors is reserved for those who urgently need transplantation and are unlikely to survive until a donor becomes available.
Lobar transplantation
488
ventilatory support, hemodynamic management, IV fluid therapy, immunosuppression, nutritional support, detection of early rejection, and prevention or treatment of complications, including infection
Early postoperative care for lung transplant often includes
489
Infections are the leading cause of death at all time points after lung transplant. Bacterial bronchitis and pneumonia are the most common infections. CMV, fungi, viruses, and mycobacteria are also causative agents. Noninfectious issues may include VTE, diaphragmatic dysfunction, and cancer.
Complications after lung transplant
490
of tacrolimus, mycophenolate mofetil (CellCept), and prednisone
Immunosuppressive therapy usually includes a 3-drug regimen (after lung transplant)
491
in the first 5 to 10 days after surgery. Signs of rejection include low-grade fever, fatigue, dyspnea, dry cough, and O2 desaturation.
Acute rejection is fairly common in lung transplantation. It typically occurs & s/s
492
is by transtracheal biopsy.
Accurate diagnosis of lung transplant rejection
493
of high doses of IV corticosteroids for 3 days, followed by high doses of oral prednisone. In patients with persistent or recurrent acute rejection, antilymphocyte therapy may be useful.
Treatment rejection of lung transplant consists
494
is a manifestation of chronic rejection in lung transplant patients.
Bronchiolitis obliterans (BOS)
495
BOS is characterized by airflow obstruction that progresses over time.
Bronchiolitis obliterans (BOS) is characterized
496
onset is often subacute, with gradual development of exertional dyspnea, nonproductive cough, wheezing, and/or low-grade fever.
Bronchiolitis obliterans (BOS) sign/symp
497
bronchodilators and corticosteroid therapy
Airway obstruction is not responsive to
498
aerosolized bronchodilators, chest physiotherapy, and deep-breathing and coughing techniques, to help minimize complications. Home spirometry is useful in monitoring trends in lung function
Patients are taught pulmonary clearance measures, (lung transplant) including
499
is necrosis of lung tissue. It typically results from bacteria aspirated from the oral cavity in patients with periodontal disease
lung abscess
500
also result from IV drug use, cancer, pulmonary emboli, TB, and various parasitic and fungal diseases.
cause lung abscess
501
, beginning with an enlarging area of infection that becomes necrotic and eventually forms a cavity filled with purulent material.
abscess usually develops slowly
502
most often reflecting the anaerobic flora of the mouth.
Abscesses usually contain more than 1 type of microbe,
503
n is the posterior segment of the upper lobes -abscess may erode into the bronchial system, causing the production of foul-smelling or sour-tasting sputum -may grow toward the pleura and cause pleuritic pain.
area of the lung most often affected due to aspiratio (abscess)
504
Multiple small abscesses, sometimes referred to as
necrotizing pneumonia, can occur within the lung
505
especially if anaerobic organisms are the cause.
Manifestations usually occur slowly over a period of weeks to months,
506
develop more acutely and resemble bacterial pneumonia. The most common is cough-producing purulent sputum (often dark brown) that is foul smelling and foul tasting. Hemoptysis is common, especially when an abscess ruptures into a bronchus. -Other manifestations include fever, chills, prostration, night sweats, pleuritic pain, dyspnea, anorexia, and weight loss -Lung assessment reveals dullness to percussion and decreased breath sounds on auscultation over the involved segment of lung. -Bronchial breath sounds may be transmitted to the periphery if the communicating bronchus becomes patent and the segment begins to drain. Crackles may be present in the later stages as the abscess drains.
Symptoms of abscess caused by aerobic bacteria
507
Pulmonary abscess, bronchopleural fistula, bronchiectasis, and empyema from perforation of the abscess into the pleural cavity can occur
cause several possible complications lung abscess
508
chest x-ray is often the
only test needed to diagnose a lung abscess.
509
If there is drainage via the bronchus, sputum will contain the
microorganisms that are present in the abscess
510
(1) avoid oropharyngeal contamination, (2) collect a specimen if drainage is delayed, or (3) investigate for an underlying cancer.
Bronchoscopy may be used to
511
by lung infarction, pulmonary embolism, and sarcoidosis.
Necrotic pulmonary lesions also can be caused
512
Parenteral antibiotics are switched to oral antibiotics once the patient shows clinical and chest x-ray signs of improvement
Clindamycin is first-line therapy for its effectiveness against Staphylococcus and anaerobic organisms.