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hlsc 222 > Ch. 27 > Flashcards

Ch. 27 Flashcards

1
Q

Ventilation

A

Movement of air in and out of lungs

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2
Q

Oxygenation

A

loading of oxygen molecules onto hemoglobin

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3
Q

Respiration

A

O2 and CO2 exchange of alveoli (external) and systemic capillaries (Internal)

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4
Q

Perfusion

A

Delivery of blood to a capillary bed in tissue

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5
Q

Dyspnea

A

Breathlessness
-Subjective experience of breathing difficulty
-Work of beathing>result

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6
Q

Dyspnea signs

A

-Flaring nostrils
-use of accessory muscles
-Head bobbing in children

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7
Q

Paroxysmal Nocturnal Dyspnea

A

Pulmonary condition that wakes you up gasping for breath in the middle of the night

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8
Q

Sputum

A

-Color provides information of progression of a disease
-Microscopic appearance allows microorganism identity

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9
Q

Hemoptysis

A

-Coughing up blood = usually indicates infection or inflammation of bronchiole
-Severe indicates cancer

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10
Q

Eupnea

A

Normal Breathing
-Rhythmic + effortless
-Short expiratory pause with each breath
-occasional deeper breath (Sigh)

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11
Q

Sigh

A

1.5 - 2x normal tidal volume

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12
Q

Abnormal Patterns of breathing

A

patterns of breathing automatically adjust to minimize WOB

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13
Q

Purpose of a sigh

A

-Twice the tidal volume:10x/h
-Helps maintain normal breathing
-Equals out oxygen consumption and carbon dioxide explusion

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14
Q

Hyperpnea: Kussmaul Respiration

A

Occurs with Strenuous activity
-Increased ventilation rate/ greatly increases tidal volume
-no pause at the end of expiration

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15
Q

Cheyne-Stokes respiration

A

-alternating deep/shallow breathing
-includes periods of apnea 15-60s
-followed by increased respirations when returned to normal triggers apnea again

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16
Q

Cheyne-Stokes Syndrome cause

A

-Reduced blood flow to brain
-reduced brain impulses to respiratory center

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17
Q

Hypo/hyperventilation determination

A

Blood gasses

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18
Q

HypOventilation

A

Inadequate ventilation

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19
Q

Hypoventilation issue

A

CO2removal doesn’t keep up with CO2 production

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20
Q

Hypoventilation Result

A

HypERcapnia

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21
Q

HypERcapnia

A

Increased CO2 in blood stream

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22
Q

HypERventilation

A

Alveolar ventilation exceeds needs

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23
Q

Hyperventilation issue

A

Removal of more CO2 then produced

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24
Q

Hyperventilation Result

A

HypOcapnia

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25
Q

HypOcapnia

A

reduced CO2 in blood stream

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26
Q

Cyanosis cause

A

develops when 5grams of hemoglobin is desaturated

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26
Q

Cyanosis

A

Bluish discoloration of skin

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27
Q

Cyanosis won’t be noticed

A

until it is severe
-insensitive indicator of respiratory failure

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28
Q

2 Types of cyanosis

A
  1. Peripheral cyanosis
  2. Central cyanosis
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29
Q

Peripheral cyanosis

A

-cause: poor circulation in fingers/toes due to peripheral vasoconstriction
-best seen in nail beds

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30
Q

Central cyanosis

A

-Cause: decreased arterial oxidation (Low PaO2) from pulmonary disease
-best detected in buccal mucosa membranes and lips

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31
Q

Clubbing

A

-bulbus formations at ends of fingertips and toes

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32
Q

Clubbing cause

A

disease that disrupt pulmonary circulation causing hypoxemia
-rarely visible

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33
Q

Pain from pulmonary disorders

A

-almost always localized in chest wall
-can be pinpointed by unique sound called the pleural friction rub
-reproduced by pressing on sternum or ribs

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34
Q

Pleural friction rub

A

Pleural walls rub together to reduced fluid in pleural cavity

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35
Q

HypERcapnia causes

A

-Decreased drive to breath
-Depression of respiratory center
-Disease to medulla oblongata

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36
Q

HypERcapnia result

A

Increased work of breathing

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37
Q

HypERcapnia effect

A

-Electrolyte (ionic) imbalances
= Dysrhythmia
-Severe = Coma

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38
Q

Dysrhythmia

A

irregular heart rate

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39
Q

What is overlooked and appears normal

A

-HypOventilation
-It is important to obtain blood gases to confirm

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40
Q

Hypoxemia causes

A
  1. related to issues with delivery of O2 to alveoli (ventilation) and delivery of blood to lung (Perfusion)
  2. Thickening of alveolar membrane or destruction of alveoli
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41
Q

Hypoxemia related to O2 delivery

A

-Amount of air entering to blood, depends on 2 factors
1. Amount of air entering alveoli (V)
2. Amount of blood perfusing capillaries around alveoli (Q)
-An abnormal ventilation/perfusion ratio (V/Q) most common cause of hypoxemia

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42
Q

Shunt

A

-Normal perfusion
-inadequate ventilation

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43
Q

Normal alveolar Dead space

A

-Normal ventilation
-Inadequate perfusion

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44
Q

Acute respiratory failure Definition

A

Inadequate gas exchange

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45
Q

Acute respiratory failure gas levels

A

-PaO2 <60mmHg (TX: supplemental oxygen)
-PaCO2>50mmHg (TX: ventilatory support)
-pH < or = to 7.25 (normal 7.4)

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46
Q

Acute respiratory failure is a potential

A

complication of major surgical procedures

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47
Q

Prevention of acute respiratory failure

A

-frequent turning and position changes
-deep breathing exercises
-early ambulation

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48
Q

Causes of acute respiratory failure

A

-Pneumonia
-edema
-embolism

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49
Q

Chest wall restrictions (CWR): Cause

A

-deformity
-obesity
-neuromuscular disease

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50
Q

CWR Result

A

-increased work of breathing
-usually decrease in tidal volume

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51
Q

CWR pain from

A

-injury
-disease can can cause hypOventilation

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52
Q

CWR

A

-Decreased tidal volume/increased breathing rate
-can lead to respiratory failure

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53
Q

CWR Flail Chest

A

-Fracture of consecutive ribs w or w/o sternum damage

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54
Q

Flail Chest result

A

chest wall instability = paradoxical movement of chest when breathing

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55
Q

Paradoxical Breathing: Inspiration

A

-unstable portion of chest wall moves inward
(normal movement would be outward)

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56
Q

Paradoxical Breathing: Expiration

A

-portion moves outward
(normal movement would be inward)

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57
Q

Paradoxical breathing result

A

impaired ventilation of alveoli

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58
Q

Pleural abnormalities

A

-Pneumothorax
-Pleural Effusion

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59
Q

Pneumothorax

A

-Air or gas in pleural space

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60
Q

Pneumothorax cause

A

rupture to visceral pleural (closest layer to lungs)

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61
Q

Pneumothorax result

A

collapsed lungs

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62
Q

Pleural Effusion

A

-Fluid in pleural space from blood or lymph

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63
Q

Pleural Effusion diagnosis

A

-Chest x-ray
-Thoracentesis: Needle aspiration

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64
Q

Empyema

A

-infected pleural effusion by microorganism

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65
Q

Empyema indicatio

A

pus in pleural space

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66
Q

Empyema cause

A

pulmonary lymphatic tissue becomes blocked = contaminated lymphatic fluid moves into pleural space

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67
Q

Empyema result from

A

surgery or bronchial obstruction

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68
Q

Empyema TX

A

antibiotics and drainage of pleural space with chest tube

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69
Q

Restrictive lung disease

A

difficulty with inspiration
(Expanding their lungs)

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70
Q

Obstructive lung disease

A

difficulty with expiration

71
Q

Restrictive lung disease characterized

A

by decreased lung compliance = increased work of breathing at tidal volume

72
Q

Aspiration

A

passage of fluids/solids into lungs

73
Q

Aspiration cause

A

-abnormal swallowing mechanism
-cough reflex impaired
-can lead to pneumonia
-CNS or PNS abnormalities

74
Q

Aspiration TX

A

-Bronchoscopy
-Failure to remove results in infalmmation

75
Q

Atelectasis

A

collapse of lung

76
Q

Atelectasis: 2 types of alveoli collapse

A
  1. Compression atelectasis
  2. Surfactant impairment
77
Q

Compression Atelectasis

A

Caused by external pressure (tumor or fluid)

78
Q

Surfactant impairment

A

decreased production of surfactant

79
Q

When does Atelectasis tend to occur?

A

after surgery when using general anesthetic

80
Q

Atelectasis TX

A

Deep breathing exercises promotes ciliary removal of secretions

81
Q

Bronchiectasis

A

persistent abnormal dilation of bronchi (large airways)

82
Q

Obstructive bronchitis cause

A

-Inflammation due to mucus plugs
-Chronic inflammation

83
Q

Chronic inflammation

A

destruction of elastic/muscular bronchi wall = permanent dilation

84
Q

Bronchitis symptoms

A

-Chronic productive cough
-large amount of foul-smelling sputum

85
Q

itis

A

inflammation

86
Q

Bronchiolitis

A

inflammatory obstruction of small airways

87
Q

Bronchiolitis obliterans

A

fibrosis of airways = scarring

88
Q

BOOP

A

alveoli become filled with connective tissue

89
Q

Manifestations of Bronchiolitis

A

-rapid ventilatory rate
-dry non-productive cough

90
Q

Pulmonary fibrosis

A

-Excessive amount of fibrous/connective tissue at alveoli

91
Q

Pulmonary fibrosis cause

A

-scar tissue left from previous disease (eg. tuberculosis)
-multiple injuries at different lung sites associated with abnormal healing

92
Q

Pulmonary fibrosis result

A

decreased lung compliance and external respiration (O2/CO2 exchange)

93
Q

Pulmonary fibrosis symptoms

A

dyspnea on exertion

94
Q

Pulmonary edema

A

excessive water on lungs
(normal lung is dry)

95
Q

Pulmonary edema cause

A

-left side heard disease

96
Q

Steps of pulmonary edema

A

-reduced left side CO
-blood cacked up from heart into lungs
-increased blood pressure in pulmonary capillaries
-fluid forced into interstitial space between capillary and alveoli
-when fluid flow exceeds lymph system capability to remove

causes pulmonary edema

97
Q

Severe COVID-19

A

manifested as viral pneumonia-induced Acute Respiratory Distress Syndrome (ARDS)

98
Q

ARDS

A

Acute Respiratory Distress Syndrome

99
Q

Post-mortem studies

A

mortality patients had undetectable viral loads
-cytotoxic effects of virus not main cause of death
-Death caused by hosts runaway immune system

100
Q

Management of sever lung issues

A

intubation

101
Q

Asthma signs and symptoms

A

-dyspnea
-wheezing

102
Q

Restrictive lung disease examples

A

-Aspiration
-Atelectasis
-Bronchiectasis
-Bronchiolitis
-Pulmonary fibrosis
-Pulmonary edema
-COVID-19

103
Q

Obstructive lung disease examples

A

-Asthma
-COPD

104
Q

COPD

A

Chronic Obstructive Pulmonary Disease

105
Q

Types of COPD

A

-Emphysema
-Chronic bronchitis

106
Q

Aspirin

A

Commonly used for relieving pain, lowering fever, and reducing inflammation

107
Q

Asthma

A

-Chronic inflammatory disorder of bronchial mucosa

108
Q

Inflammation in asthma

A

-restricts airways
-hyper-immune response to irritants

109
Q

Early asthma attack

A

-Classic immune response: dendritic cells/helper T cells/T +B cells

110
Q

Early asthma attack result

A

-inflammation
-increased capillary permeability
-Increased fluid

111
Q

Late asthma attack

A

-4-8h after early attack
-Latent release of inflammatory mediators from original site

112
Q

Late asthma attack result

A

Increased damage of epithelial cells
= scarring
-increased mucus forming plugs
-increased airway resistance

113
Q

Asthma manifestation

A

-Individuals normal between attacks and pulmonary tests are normal
-Bronchospasms not reversed by usual treatment

114
Q

What are asthma attack manifestations considered

A

status asthmaticus

115
Q

in asthma if PaCO2 is > 70mmHg

A

sign of impending death

116
Q

Asthma TX

A

-Mild short acting inhalers
-Persistent: inhaled corticosteroids

117
Q

Pathophysiology of asthma

A

-inhaled antigen passes epithelial layer
-antigen binds to mast cells = release of mediators
-Mediators = mucus production in airway
-dendritic cells present antigen to helper T cells
-Helper T cells also activate eosinophil/neutrophil

118
Q

Mediators in asthma pathophysiology

A

-increase mucus production in airway
-broncho spasm
-edema from increased capillary permeability

119
Q

Dendritic cells in asthma pathophysiology

A

-present antigen to helper T cells
= B cell activation/activated B cells release antibodies

120
Q

Helper T cells in asthma pathophysiology

A

-Activate eosinophil/neutrophils
-inflammation from both result in airway obstruction

121
Q

Most common lung disease

A

COPD

122
Q

4th leading cause of death in the world

A

COPD

123
Q

COPD characteristics

A

-Persistent airflow limitation
-Chronic inflammatory response to noxious particle gas
-progressive

124
Q

COPD Chronic bronchitis

A

hypersecretion of mucus/chronic productive cough for at least 3 months of the year for 2 consecutive years

125
Q

COPD Chronic bronchitis cause

A

-inspiration irritants = inflammation/thickening of mucous membrane
=reduced radius of airways
=obstruction

126
Q

COPD Chronic bronchitis affects

A

initial large airways eventually all airways

127
Q

COPD airways collapse

A

in early exhaustion
= all air gets trapped in distal portion of the lungs
=hyperinflation
=hypoventilation

128
Q

COPD emphysema

A

permanent enlargement of gas-exchange airways/destruction of alveolar walls

129
Q

COPD emphysema obstruction

A

due to destroyed walls of alveoli NOT mucus production or inflammation

130
Q

COPD emphysema destruction

A
  • of alveolar spaces
    -greatly increases diffusion distance between alveoli and capillary
131
Q

Result of COPD emphysema

A

-Reduced O2 and CO2 diffusion
-Expiration becomes difficult because of loss of recoil of normal alveoli

132
Q

Difference between Chronic Bronchitis and Emohysema

A

CB- Frequent cough with mucus
E- Shortness of breath

133
Q

Acute Bronchitis

A

-Acute infection/inflammation of airways
-Self-limiting
-usually due to viral infection

134
Q

Acute Bronchitis symptoms

A

-similar to pneumonia
-non-productive cough aggravated by cold dry air, dusty air

135
Q

Acute Bronchitis TX

A

-rest
-Aspirin
-cough suppressant
-antibiotics

136
Q

Pneumonia

A

infection of lower respiratory tract

137
Q

Pneumonia cause

A

Microorganisms
-Bacteria
-Viruses
-Fungi
-Protozoa
-Parasites

138
Q

Categories of Pneumonia

A

-Hospital acquires pneumonia (HAP)
-Community acquired pneumonia (CAP)

139
Q

HAP

A

second most common healthcare associated infection
(Most common UTI)

140
Q

Common pathogen causing pneumonia

A

Streptococcus pneumoniae

141
Q

Common infectious route of S. pneumoniae

A

inhalation of infected individuals cough

142
Q

Pneumonia pathophysiology

A

-Bacteria biofilms seed lungs with bacteria from suction tubes
-Guardian cells
-Macrophages
result: immune response fills alveoli with debris
-Microorganisms release toxins causing further damage

143
Q

Guardian Cells

A

lower respiratory tract are cellular alveolar macrophages

144
Q

Macrophages

A

present antigens to adaptive immune system = activation of T + B cells

145
Q

Pneumonia production in hospitals

A

-suction tubes in hospitals become colonized with bacteria biofilms = suction results in seeding lungs with bacteria

146
Q

Tuberculosis cause

A

Mycobacterium tuberculosis

147
Q

Tuberculosis

A

leading cause of death from a CURABLE infectious disease in the world

148
Q

Tuberculosis transmission

A

Person to person via airborne droplets

149
Q

Tuberculosis pathophysiology step 1

A
  1. Pathogen reaches lung/engulfed by macrophages
    -survives and multiplies in macrophages
150
Q

Tuberculosis pathophysiology step 2

A
  1. Reproduction in macrophage causes a chemotactic response = more macrophages respond
    -tubercle forms
151
Q

Tuberculosis pathophysiology step 3

A
  1. macrophage start to die, releasing pathogen/this forms a center tubercle/dormant stage
152
Q

Tuberculosis pathophysiology stage 4

A
  1. tubercule center enlarges (liquification)/enlargement fills with air/aerobic pathogen start to multiply outside macrophage
153
Q

Tuberculosis pathophysiology stage 5

A
  1. Liquification continues/tubercle ruptures/pathogens disseminate throughout lung
154
Q

Pulmonary Vascular Diseases

A

-Pulmonary blood flow disrupted causing occlusions = destruction of vascular bed
-Causes dramatic alterations in perfusion/ventilation ratios

155
Q

Occlusions

A

blocking or closing of blood vessels

156
Q

Pulmonary Embolism

A

Occlusion of portion of pulmonary vascular bed by embolus

157
Q

Pathophysiology of pulmonary embolus

A

Effect depends on
-Extent of pulmonary blood flow obstruction
-size of affect vessel
-nature of embolus
-resulting secondary effects

158
Q

Pulmonary artery hypertension

A

mean pulmonary artery pressure greater than 25 mmHg

159
Q

Pulmonary artery hypertension pathophysiology

A

-endothelial dysfunction/over production of vasoconstrictors
-Increased growth factors = fibrosis = thickening of vessel walls
-narrowing of vessels/gas exchange reduced

160
Q

increase in pulmonary artery pressure =

A

increase pressure in right ventricle = right ventricle hypertrophy

161
Q

right ventricle hypertrophy =

A

failure (Cor Pulmonale)

162
Q

Cor Pulmonale

A

right ventricle enlargement due to hypertrophy or dilation or both

163
Q

The result of pulmonary artery hypertension (PAH)

A

Cor Pulmonale

164
Q

Increased work of right ventricle =

A

increased hypertrophy of normally thin-walled heart muscle

165
Q

Pressure overload

A

dilation/hypertrophy

166
Q

Dilation/hypertrophy =

A

failure of right ventricle

167
Q

Laryngeal cancer

A

-Primary risk factor: smoking/ risk increases when smoking is combined with alcohol consumption

168
Q

Laryngeal cancer sis linked to what virus

A

Human Papillomavirus (HPV)

169
Q

Pathophysiology of Laryngeal cancer

A

-Carcinoma of vocal cords
-Metastasis occurs in lymph nodes but distant metastasis is rare

170
Q

Laryngeal cancer manifestations

A

-Hoarseness
-dyspnea
-cough
-cough following swallowing

171
Q

Laryngeal cancer diagnosis/ TX

A

-Biopsy
-radiation
-chemotherapy

172
Q

Lung Cancer

A

-tumors on respiratory tract epithelium
-leading cause of death in Canadians

173
Q

Leading causes of lung cancer

A

-Smoking
-gas exposure
-second hand smoke

174
Q

lung cancer pathophysiology

A

-tobacco smoke: contains 30 carcinogens/responsible for 90% of lung cancers
-tumor: result of GF and production of free radicals
-bronchial mucosa: suffers “hits” from tobacco smoke = epithelial damage
-progression: metastasis to brain bone marrow and liver

hlsc 222 (9 decks)

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