Ch. 27 Flashcards
1
Q
Ventilation
A
Movement of air in and out of lungs
2
Q
Oxygenation
A
loading of oxygen molecules onto hemoglobin
3
Q
Respiration
A
O2 and CO2 exchange of alveoli (external) and systemic capillaries (Internal)
4
Q
Perfusion
A
Delivery of blood to a capillary bed in tissue
5
Q
Dyspnea
A
Breathlessness
-Subjective experience of breathing difficulty
-Work of beathing>result
6
Q
Dyspnea signs
A
-Flaring nostrils
-use of accessory muscles
-Head bobbing in children
7
Q
Paroxysmal Nocturnal Dyspnea
A
Pulmonary condition that wakes you up gasping for breath in the middle of the night
8
Q
Sputum
A
-Color provides information of progression of a disease
-Microscopic appearance allows microorganism identity
9
Q
Hemoptysis
A
-Coughing up blood = usually indicates infection or inflammation of bronchiole
-Severe indicates cancer
10
Q
Eupnea
A
Normal Breathing
-Rhythmic + effortless
-Short expiratory pause with each breath
-occasional deeper breath (Sigh)
11
Q
Sigh
A
1.5 - 2x normal tidal volume
12
Q
Abnormal Patterns of breathing
A
patterns of breathing automatically adjust to minimize WOB
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
14
Q
Hyperpnea: Kussmaul Respiration
A
Occurs with Strenuous activity
-Increased ventilation rate/ greatly increases tidal volume
-no pause at the end of expiration
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
16
Q
Cheyne-Stokes Syndrome cause
A
-Reduced blood flow to brain
-reduced brain impulses to respiratory center
17
Q
Hypo/hyperventilation determination
A
Blood gasses
18
Q
HypOventilation
A
Inadequate ventilation
19
Q
Hypoventilation issue
A
CO2removal doesn’t keep up with CO2 production
20
Q
Hypoventilation Result
A
HypERcapnia
21
Q
HypERcapnia
A
Increased CO2 in blood stream
22
Q
HypERventilation
A
Alveolar ventilation exceeds needs
23
Q
Hyperventilation issue
A
Removal of more CO2 then produced
24
Q
Hyperventilation Result
A
HypOcapnia
25
HypOcapnia
reduced CO2 in blood stream
26
Cyanosis cause
develops when 5grams of hemoglobin is desaturated
26
Cyanosis
Bluish discoloration of skin
27
Cyanosis won't be noticed
until it is severe
-insensitive indicator of respiratory failure
28
2 Types of cyanosis
1. Peripheral cyanosis
2. Central cyanosis
29
Peripheral cyanosis
-cause: poor circulation in fingers/toes due to peripheral vasoconstriction
-best seen in nail beds
30
Central cyanosis
-Cause: decreased arterial oxidation (Low PaO2) from pulmonary disease
-best detected in buccal mucosa membranes and lips
31
Clubbing
-bulbus formations at ends of fingertips and toes
32
Clubbing cause
disease that disrupt pulmonary circulation causing hypoxemia
-rarely visible
33
Pain from pulmonary disorders
-almost always localized in chest wall
-can be pinpointed by unique sound called the pleural friction rub
-reproduced by pressing on sternum or ribs
34
Pleural friction rub
Pleural walls rub together to reduced fluid in pleural cavity
35
HypERcapnia causes
-Decreased drive to breath
-Depression of respiratory center
-Disease to medulla oblongata
36
HypERcapnia result
Increased work of breathing
37
HypERcapnia effect
-Electrolyte (ionic) imbalances
= Dysrhythmia
-Severe = Coma
38
Dysrhythmia
irregular heart rate
39
What is overlooked and appears normal
-HypOventilation
-It is important to obtain blood gases to confirm
40
Hypoxemia causes
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
41
Hypoxemia related to O2 delivery
-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
42
Shunt
-Normal perfusion
-inadequate ventilation
43
Normal alveolar Dead space
-Normal ventilation
-Inadequate perfusion
44
Acute respiratory failure Definition
Inadequate gas exchange
45
Acute respiratory failure gas levels
-PaO2 <60mmHg (TX: supplemental oxygen)
-PaCO2>50mmHg (TX: ventilatory support)
-pH < or = to 7.25 (normal 7.4)
46
Acute respiratory failure is a potential
complication of major surgical procedures
47
Prevention of acute respiratory failure
-frequent turning and position changes
-deep breathing exercises
-early ambulation
48
Causes of acute respiratory failure
-Pneumonia
-edema
-embolism
49
Chest wall restrictions (CWR): Cause
-deformity
-obesity
-neuromuscular disease
50
CWR Result
-increased work of breathing
-usually decrease in tidal volume
51
CWR pain from
-injury
-disease can can cause hypOventilation
52
CWR
-Decreased tidal volume/increased breathing rate
-can lead to respiratory failure
53
CWR Flail Chest
-Fracture of consecutive ribs w or w/o sternum damage
54
Flail Chest result
chest wall instability = paradoxical movement of chest when breathing
55
Paradoxical Breathing: Inspiration
-unstable portion of chest wall moves inward
(normal movement would be outward)
56
Paradoxical Breathing: Expiration
-portion moves outward
(normal movement would be inward)
57
Paradoxical breathing result
impaired ventilation of alveoli
58
Pleural abnormalities
-Pneumothorax
-Pleural Effusion
59
Pneumothorax
-Air or gas in pleural space
60
Pneumothorax cause
rupture to visceral pleural (closest layer to lungs)
61
Pneumothorax result
collapsed lungs
62
Pleural Effusion
-Fluid in pleural space from blood or lymph
63
Pleural Effusion diagnosis
-Chest x-ray
-Thoracentesis: Needle aspiration
64
Empyema
-infected pleural effusion by microorganism
65
Empyema indicatio
pus in pleural space
66
Empyema cause
pulmonary lymphatic tissue becomes blocked = contaminated lymphatic fluid moves into pleural space
67
Empyema result from
surgery or bronchial obstruction
68
Empyema TX
antibiotics and drainage of pleural space with chest tube
69
Restrictive lung disease
difficulty with inspiration
(Expanding their lungs)
70
Obstructive lung disease
difficulty with expiration
71
Restrictive lung disease characterized
by decreased lung compliance = increased work of breathing at tidal volume
72
Aspiration
passage of fluids/solids into lungs
73
Aspiration cause
-abnormal swallowing mechanism
-cough reflex impaired
-can lead to pneumonia
-CNS or PNS abnormalities
74
Aspiration TX
-Bronchoscopy
-Failure to remove results in infalmmation
75
Atelectasis
collapse of lung
76
Atelectasis: 2 types of alveoli collapse
1. Compression atelectasis
2. Surfactant impairment
77
Compression Atelectasis
Caused by external pressure (tumor or fluid)
78
Surfactant impairment
decreased production of surfactant
79
When does Atelectasis tend to occur?
after surgery when using general anesthetic
80
Atelectasis TX
Deep breathing exercises promotes ciliary removal of secretions
81
Bronchiectasis
persistent abnormal dilation of bronchi (large airways)
82
Obstructive bronchitis cause
-Inflammation due to mucus plugs
-Chronic inflammation
83
Chronic inflammation
destruction of elastic/muscular bronchi wall = permanent dilation
84
Bronchitis symptoms
-Chronic productive cough
-large amount of foul-smelling sputum
85
itis
inflammation
86
Bronchiolitis
inflammatory obstruction of small airways
87
Bronchiolitis obliterans
fibrosis of airways = scarring
88
BOOP
alveoli become filled with connective tissue
89
Manifestations of Bronchiolitis
-rapid ventilatory rate
-dry non-productive cough
90
Pulmonary fibrosis
-Excessive amount of fibrous/connective tissue at alveoli
91
Pulmonary fibrosis cause
-scar tissue left from previous disease (eg. tuberculosis)
-multiple injuries at different lung sites associated with abnormal healing
92
Pulmonary fibrosis result
decreased lung compliance and external respiration (O2/CO2 exchange)
93
Pulmonary fibrosis symptoms
dyspnea on exertion
94
Pulmonary edema
excessive water on lungs
(normal lung is dry)
95
Pulmonary edema cause
-left side heard disease
96
Steps of pulmonary edema
-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
Severe COVID-19
manifested as viral pneumonia-induced Acute Respiratory Distress Syndrome (ARDS)
98
ARDS
Acute Respiratory Distress Syndrome
99
Post-mortem studies
mortality patients had undetectable viral loads
-cytotoxic effects of virus not main cause of death
-Death caused by hosts runaway immune system
100
Management of sever lung issues
intubation
101
Asthma signs and symptoms
-dyspnea
-wheezing
102
Restrictive lung disease examples
-Aspiration
-Atelectasis
-Bronchiectasis
-Bronchiolitis
-Pulmonary fibrosis
-Pulmonary edema
-COVID-19
103
Obstructive lung disease examples
-Asthma
-COPD
104
COPD
Chronic Obstructive Pulmonary Disease
105
Types of COPD
-Emphysema
-Chronic bronchitis
106
Aspirin
Commonly used for relieving pain, lowering fever, and reducing inflammation
107
Asthma
-Chronic inflammatory disorder of bronchial mucosa
108
Inflammation in asthma
-restricts airways
-hyper-immune response to irritants
109
Early asthma attack
-Classic immune response: dendritic cells/helper T cells/T +B cells
110
Early asthma attack result
-inflammation
-increased capillary permeability
-Increased fluid
111
Late asthma attack
-4-8h after early attack
-Latent release of inflammatory mediators from original site
112
Late asthma attack result
Increased damage of epithelial cells
= scarring
-increased mucus forming plugs
-increased airway resistance
113
Asthma manifestation
-Individuals normal between attacks and pulmonary tests are normal
-Bronchospasms not reversed by usual treatment
114
What are asthma attack manifestations considered
status asthmaticus
115
in asthma if PaCO2 is > 70mmHg
sign of impending death
116
Asthma TX
-Mild short acting inhalers
-Persistent: inhaled corticosteroids
117
Pathophysiology of asthma
-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
Mediators in asthma pathophysiology
-increase mucus production in airway
-broncho spasm
-edema from increased capillary permeability
119
Dendritic cells in asthma pathophysiology
-present antigen to helper T cells
= B cell activation/activated B cells release antibodies
120
Helper T cells in asthma pathophysiology
-Activate eosinophil/neutrophils
-inflammation from both result in airway obstruction
121
Most common lung disease
COPD
122
4th leading cause of death in the world
COPD
123
COPD characteristics
-Persistent airflow limitation
-Chronic inflammatory response to noxious particle gas
-progressive
124
COPD Chronic bronchitis
hypersecretion of mucus/chronic productive cough for at least 3 months of the year for 2 consecutive years
125
COPD Chronic bronchitis cause
-inspiration irritants = inflammation/thickening of mucous membrane
=reduced radius of airways
=obstruction
126
COPD Chronic bronchitis affects
initial large airways eventually all airways
127
COPD airways collapse
in early exhaustion
= all air gets trapped in distal portion of the lungs
=hyperinflation
=hypoventilation
128
COPD emphysema
permanent enlargement of gas-exchange airways/destruction of alveolar walls
129
COPD emphysema obstruction
due to destroyed walls of alveoli NOT mucus production or inflammation
130
COPD emphysema destruction
- of alveolar spaces
-greatly increases diffusion distance between alveoli and capillary
131
Result of COPD emphysema
-Reduced O2 and CO2 diffusion
-Expiration becomes difficult because of loss of recoil of normal alveoli
132
Difference between Chronic Bronchitis and Emohysema
CB- Frequent cough with mucus
E- Shortness of breath
133
Acute Bronchitis
-Acute infection/inflammation of airways
-Self-limiting
-usually due to viral infection
134
Acute Bronchitis symptoms
-similar to pneumonia
-non-productive cough aggravated by cold dry air, dusty air
135
Acute Bronchitis TX
-rest
-Aspirin
-cough suppressant
-antibiotics
136
Pneumonia
infection of lower respiratory tract
137
Pneumonia cause
Microorganisms
-Bacteria
-Viruses
-Fungi
-Protozoa
-Parasites
138
Categories of Pneumonia
-Hospital acquires pneumonia (HAP)
-Community acquired pneumonia (CAP)
139
HAP
second most common healthcare associated infection
(Most common UTI)
140
Common pathogen causing pneumonia
Streptococcus pneumoniae
141
Common infectious route of S. pneumoniae
inhalation of infected individuals cough
142
Pneumonia pathophysiology
-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
Guardian Cells
lower respiratory tract are cellular alveolar macrophages
144
Macrophages
present antigens to adaptive immune system = activation of T + B cells
145
Pneumonia production in hospitals
-suction tubes in hospitals become colonized with bacteria biofilms = suction results in seeding lungs with bacteria
146
Tuberculosis cause
Mycobacterium tuberculosis
147
Tuberculosis
leading cause of death from a CURABLE infectious disease in the world
148
Tuberculosis transmission
Person to person via airborne droplets
149
Tuberculosis pathophysiology step 1
1. Pathogen reaches lung/engulfed by macrophages
-survives and multiplies in macrophages
150
Tuberculosis pathophysiology step 2
2. Reproduction in macrophage causes a chemotactic response = more macrophages respond
-tubercle forms
151
Tuberculosis pathophysiology step 3
3. macrophage start to die, releasing pathogen/this forms a center tubercle/dormant stage
152
Tuberculosis pathophysiology stage 4
4. tubercule center enlarges (liquification)/enlargement fills with air/aerobic pathogen start to multiply outside macrophage
153
Tuberculosis pathophysiology stage 5
5. Liquification continues/tubercle ruptures/pathogens disseminate throughout lung
154
Pulmonary Vascular Diseases
-Pulmonary blood flow disrupted causing occlusions = destruction of vascular bed
-Causes dramatic alterations in perfusion/ventilation ratios
155
Occlusions
blocking or closing of blood vessels
156
Pulmonary Embolism
Occlusion of portion of pulmonary vascular bed by embolus
157
Pathophysiology of pulmonary embolus
Effect depends on
-Extent of pulmonary blood flow obstruction
-size of affect vessel
-nature of embolus
-resulting secondary effects
158
Pulmonary artery hypertension
mean pulmonary artery pressure greater than 25 mmHg
159
Pulmonary artery hypertension pathophysiology
-endothelial dysfunction/over production of vasoconstrictors
-Increased growth factors = fibrosis = thickening of vessel walls
-narrowing of vessels/gas exchange reduced
160
increase in pulmonary artery pressure =
increase pressure in right ventricle = right ventricle hypertrophy
161
right ventricle hypertrophy =
failure (Cor Pulmonale)
162
Cor Pulmonale
right ventricle enlargement due to hypertrophy or dilation or both
163
The result of pulmonary artery hypertension (PAH)
Cor Pulmonale
164
Increased work of right ventricle =
increased hypertrophy of normally thin-walled heart muscle
165
Pressure overload
dilation/hypertrophy
166
Dilation/hypertrophy =
failure of right ventricle
167
Laryngeal cancer
-Primary risk factor: smoking/ risk increases when smoking is combined with alcohol consumption
168
Laryngeal cancer sis linked to what virus
Human Papillomavirus (HPV)
169
Pathophysiology of Laryngeal cancer
-Carcinoma of vocal cords
-Metastasis occurs in lymph nodes but distant metastasis is rare
170
Laryngeal cancer manifestations
-Hoarseness
-dyspnea
-cough
-cough following swallowing
171
Laryngeal cancer diagnosis/ TX
-Biopsy
-radiation
-chemotherapy
172
Lung Cancer
-tumors on respiratory tract epithelium
-leading cause of death in Canadians
173
Leading causes of lung cancer
-Smoking
-gas exposure
-second hand smoke
174
lung cancer pathophysiology
-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
