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Adv Pathophysiology > Chapter 30: Ventilation and Gas Exchange > Flashcards

Chapter 30: Ventilation and Gas Exchange Flashcards

1
Q

Hypoxemia

A

reduction in arterial blood oxygen levels

PaO2 < 80 mmHg

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2
Q

3 ways body compensates for chronic hypoxemia

A

1) increasing ventilation
2) pulmonary vasoconstriction (improves V/Q ratio)
3) increased production of RBCs (O2 carrying capacity)

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3
Q

______ is a late sign of hypoxemia and can be central or peripheral

A

CYANOSIS
Central: oral mucosa and lips
Peripheral: nailbeds, nose, or ears

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4
Q

________ provides a direct measure of O2 content in blood and is the best indicator of lung’s ability to oxygenate blood

A

ABGs

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5
Q

Pulse oximeter is unable to distinguish between ___________

A

oxygen-carrying Hgb and carbon-monoxide-carrying Hgb

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6
Q

Hypercapnia

A

increase in CO2 content of arterial blood

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7
Q

3 causes of hypercapnia

A

1) hypoventilation
2) increase in metabolic rate (fever, exercise)
3) high-carb diet

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8
Q

Obstructive Lung Disorders

A

increase in resistance to airflow - harder to get air out (increased compliance)
asthma, emphysema, COPD

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9
Q

Restrictive Lung Disorders

A

reduced expansion of lung tissue with decreased total lung capacity
harder to get air in (decreased compliance)
sarcoidosis, pulmonary fibrosis

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10
Q

Obstructive lung disorders attempt to maintain minute volume by ________ _______ breathing

A

slow, deep breathing

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11
Q

Restrictive lung disorders attempt to maintain minute volume by ________ _______ breathing

A

rapid, shallow breathing

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12
Q

Sarcoidosis

A

restrictive lung disorder in which granulomas are in found in affected tissue and and organ systems

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13
Q

Most common locations for clinical manifestations in sarcoidosis (4)

A

lungs
skin
eyes
neurological system

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14
Q

Clinical Manifestations of Sarcoidosis

A

dry, nonproductive cough and SOB
papules and plaques on skin
uveitis
weakness of CN VII = Bells Palsy

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15
Q

Asthma

A

hyper-reactive (obstructive) airway disease

chronic inflammatory disease that causes episodes of spastic reactivity in the bronchioles

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16
Q

Asthma is characterized by __________ (3)

A 
reversible airway bronchospasm (early)
mucus hypersecretion (late)
bronchial edema (late)
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17
Q

Immune Cells Involved in ASTHMA (3)

A

T-helper cells = Th1 and Th2

IgE

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18
Q

Th1

A

stimulated by microbes or allergens

assists B-lymphocytes to transform into plasma cells (IgE)

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19
Q

Th2

A

attract mast cells, eosinophils, and basophils = promote inflammation

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20
Q

IgE in Asthma

A

Allergen binds to IgE

IgE binds to mast cells and provokes degranulation = chemical mediators

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21
Q

Chemical Mediators Released by Mast Cells in Asthma (4)

A

1) histamine
2) prostaglandins
3) leukotrienes
4) bradykinin

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22
Q

Histamine

A

attaches to receptor sites in larger cronhi causing swelling and contraction of the smooth muscles
stimulates the mucous membranes to secrete excessive mucus (further narrows the bronchial lumen)

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23
Q

Air trapping is a result of ________ on exhalation (in asthma)

A

increased intrathoracic pressure that closes the narrowed bronchial lumen completely

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24
Q

Prostaglandins

A

derived from arachidonic acid - uses the cyclooxygenase pathway
enhances the action of histamine

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25
Leukotrienes
derived from arachidonic acid - uses the lipoxygenase pathway attach to the receptor sites in the smaller bronchi and cause swelling bring WBCs to the inflamed area = WBCs form mucus plugs
26
Bradykinin
proinflammatory mediator | can cause bronchospasms
27
First-line treatments for asthma (2)
Bronchodilators: Short-Acting Beta2 Agonists (SABA) = albuterol Inhaled glucocorticoids
28
Other Pharmacological Treatments for Asthma
Mast cell stabilizer = cromolyn Leukotriene inhibitors = montelukast Antihistamines
29
Concern for Propanalol and Asthma
Propanalol = nonselective beta blocker = can bind to either beta 1 or beta 2 receptors It can block albuterol's action
30
Chronic Obstructive Pulmonary Disease
airflow limitation that is not fully reversible, caused by exposure of the lungs to noxious particles or gases includes chronic bronchitis, emphysema, and bronchiectasis
31
COPD = air can get it but can't get out | This causes:
1) air trapping in the alveoli | 2) Retention of CO2
32
Chronic Bronchitis + Main Cause
increased mucus secretion by the goblet cells of the bronchial tubes, obstruction of the small airways, and presence of persistent, productive cough (>3 mo for 2+ years) main cause is smoking
33
Pathophysiology of Chronic Bronchitis
smoking causes chronic irritation of the mucosal lining goblet cell hyperplasia = secretes excessive mucus airways accumulate debris
34
Hypoxia in COPD stimulates pulmonary artery vasoconstriction. This leads to:
increased resistance in the main pulmonary artery pulmonary HTN and eventual R-sided HF (cor pulmonale)
35
Early Signs of Chronic Bronchitis
productive cough with copious amounts of sputum DOE, normal to low paO2, increased PaCO2 disease progression can be stopped if pt stops smoking
36
Later Signs of Chronic Bronchitis
``` Blue Bloater SOB, decreased PaO2 cyanosis air trapping cor pulmonale (R-sided HF) ```
37
Emphysema
hyperinflation and decreased elastic recoil cause air trapping in the alveoli = permanent destruction of the alveoli
38
Centriacinar Emphysema
most common type related to smoking localized only to the respiratory bronchioles
39
Panacinar Emphysema
genetic form related to alpha-1 antitrypsin deficiency integrity of alveoli, alveoli sacs, and alveolar ducts is destroyed
40
Chronic smoking impairs alveolar function through:
1) triggered inflammatory response 2) neutrophils and macrophages release excess proteolytic enzymes = destroy ECM (elastin ) in the lungs = bulla 3) inability of alveoli to recoil and release CO2 = CO2 retention
41
Deficiency in Alpha-1 Antitrypsin causes:
1) inability to control the amount of elastase produced | 2) more elastase = more elastin broken down = destroy lung matrix = reduces elasticity
42
Early Signs of Emphysema
Dyspnea that progrressively worsens is the first sign Normal (or slightly dec) PaO2 Normal PaCO2
43
Late Signs of Emphysema
``` Pink Puffer tachypnea pursed-lip breathing tripod posture barrel chest low PaO2 and increased PaCO2 ```
44
Bronchiectasis
uncommon type of COPD | permanent dilation of the bronchi and bronchioles that occurs due to destruction of muscle and elastic supporting tissue
45
2 Main Etiologies of Bronchiectasis
Mucus obstruction | Persistent infection
46
Clinical Manifestation of Bronchiectasis
cough with expectoration of copious amounts of foul-smelling, purulent sputum hemoptysis weight loss and anemia
47
Cystic Fibrosis
autosomal-recessive disorder of electrolytes and water ransport that affects certain epithelial cells caused by a mutation of the CF gene located on chromosome 7
48
Mutation to the CF gene on chromosom 7 leads to:
``` impaired electrolyte (chloride) transportation across mucosal surfaces = production of excessive and thick exocrine secretions = leading to obstruction, inflammation, and infection ```
49
Mucus Plugging
the formation of tenacious secretions and a reduced ability to clear the secretions seen in CF
50
Mucus plugging is the result of:
airway dehydration and thickened mucus caused by: 1) impaired chloride secretion 2) excessive sodium absorption 3) decreased water content in the airway tissues
51
Airways and lung tissue in CF are characterized by:
``` air trapping hyperinflation abscess formation lung tissue consolidation lung tissue fibrosis cyst formation ```
52
____ and _____ are the two main organs also affected by cystic fibrosis
Liver and Pancreas
53
Consequences of Liver and Pancreas involvement in CF
``` bile duct plugged with mucus = biliary cirrhosis lack of pancreatic enzymes decrease in digestion/absorption weight loss fatty stools (steatorrhea) ```
54
Standard Diagnostic Test for CF
Sweat Test | a sodium and chloride content twice as high as normal is consistent with CF
55
Secondary Atelectasis
incomplete expansion of a lung or portion of the lung collapse of previously expanded alveoli perfusion occurs w/o ventilation because the collapsed alveoli do not participate in gas exchange
56
Types of Secondary Atelectasis
Absorptive Obstructive Compressive All three types can cause deoxygenated blood to reach the systemic circulation = hypoxia Without adequate oxygen = decrease in production of surfactant
57
Absorptive Atelectasis
surfactant inactivation = surface tension is reduced | less than normal levels of nitrogen being inhaled (can be associated with surgery with general anesthesia)
58
______ acts as a stent to keep alveoli open
Nitrogen
59
Obstructive Atelectasis
mechanical obstruction of the airways | secretions, mucus plugs foreign bodies
60
Compressive Atelectasis
external forces that compress the pleura or lung tissue | pleural effusion, tumors, pneumothorax, or significant abdominal distention
61
Pleural Effusion
excessive amount of fluid located in the pleural space between the visceral and parietal layers
62
Pleural effusion results from increased _____________ and decreased __________
increased hydrostatic pressure in the pleural capillaries | decreased colloidal osmotic pressure in the circulatory system
63
Types of Fluid that can accumulate to cause pleural effusion
transudative exudative empyema chylothorax
64
Transudative Fluid (Pl. Eff.)
clear fluid with low protein content | most commonly results from heart failure
65
Exudative Fluid (Pl. Eff.)
cloudy fluid, high in protein | has inflammatory or malignant cells within it
66
Empyema Fluid (Pl. Eff.)
purulent fluid - contains proteins, leukocytes, glucose, & cellular debris commonly results from bacterial PNA or a ruptured lung abscess
67
Chylothorax Fluid (Pl. Eff.)
effusion of lymph fluid in the pleural cavity | milky fluid due to fat-carrying lipoproteins from the GI tract
68
Clinical Manifestations of Pleural Effusion
Diminished or absent lung sounds * Tracheal deviation away from the affected side Dullness on percussion Decreased diaphragmatic excursion on the affected side and unequal respiratory expansion
69
Pneumothorax
defined as the entrance of air into the pleural cavity, restricting lung expansion and resulting in a complete or partial collapse of the affected lung
70
Spontaneous Pneumothorax
occurs when an air-filled bleb on the lung surface ruptures = atmospheric air entering the pleural cavity alveolar pressure > atmospheric pressure = air flows continues until there is no longer a pressure gradient
71
Simple (Primary) Spontaneous Pneumothorax
Affects previously health individuals = tall, thin, Caucasian young males Smoking
72
Secondary Spontaneous Pneumothorax
Affects those with preexisting lung diseases that cause air trapping and destruction of lung tissue Asthma, CF, emphysema, tuberculosis
73
Traumatic Pneumothorax
due to blunt or penetrating trauma to the chest wall Open = sucking wound; stabbing, GSW Closed = falls or CPR that results in broken ribs that penetrate the lung
74
Hemothorax
presence of blood in the pleural cavity usually the result of trauma
75
Tension Pneumothorax
Intrapleural pressure > Atmospheric pressure air is unable to escape compression of the opposite lung, trachea, aorta, and vena cava EMERGENCY
76
Clinical Manifestations of Spontaneous Pneumothorax
``` ipsilateral CP increase in RR asymmetry of chest hyperresonance during percussion decreased/absent breath sounds on affected side ```
77
Clinical Manifestations of Tension Pneumothorax
mediastinal shift towards opposite side (trachea) | SV is impaired and CO is decreased
78
Pulmonary Emboli (PE)
a blood-borne substance that lodges in a branch of the pulmonary artery (emboli) so that flow becomes obstructed
79
Types of Pulmonary Emboli (4)
1) Thrombus 2) Air 3) Fat 4) Amniotic Fluid
80
Respiratory Clinical Manifestations of PE
Tachypnea, dyspnea Cough, hemoptysis Wheezing, crackles Central cyanosis
81
Cardiovascular Clinical Manifestations of PE
Tachycardia | Pleuritic CP - exacerbated by breathing
82
Neurological Clinical Manifestations of PE
Anxiety Confusion Syncope
83
Clinical Manifestation of Fat Emboli
Petechiae over chest
84
Pulmonary Hypertension
elevated pressures in the pulmonary artery (>25 mmHg at rest and > 30 mmHg on exertion) expected MPAP = 15 mmHg can result in cor pulmonale (RV failure)
85
Primary Pulmonary HTN
The smooth muscle in the pulmonary artery wall hypertrophies for no reason Increases vascular resistance Left ventricular pressure remains normal Leads to RV failure = cor pulmonale

Adv Pathophysiology (22 decks)

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