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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
Q

Leukotrienes

A

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

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26
Q

Bradykinin

A

proinflammatory mediator

can cause bronchospasms

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27
Q

First-line treatments for asthma (2)

A

Bronchodilators: Short-Acting Beta2 Agonists (SABA) = albuterol
Inhaled glucocorticoids

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28
Q

Other Pharmacological Treatments for Asthma

A

Mast cell stabilizer = cromolyn
Leukotriene inhibitors = montelukast
Antihistamines

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29
Q

Concern for Propanalol and Asthma

A

Propanalol = nonselective beta blocker = can bind to either beta 1 or beta 2 receptors
It can block albuterol’s action

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30
Q

Chronic Obstructive Pulmonary Disease

A

airflow limitation that is not fully reversible, caused by exposure of the lungs to noxious particles or gases
includes chronic bronchitis, emphysema, and bronchiectasis

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31
Q

COPD = air can get it but can’t get out

This causes:

A

1) air trapping in the alveoli

2) Retention of CO2

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32
Q

Chronic Bronchitis + Main Cause

A

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

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33
Q

Pathophysiology of Chronic Bronchitis

A

smoking causes chronic irritation of the mucosal lining
goblet cell hyperplasia = secretes excessive mucus
airways accumulate debris

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34
Q

Hypoxia in COPD stimulates pulmonary artery vasoconstriction. This leads to:

A

increased resistance in the main pulmonary artery
pulmonary HTN
and eventual R-sided HF (cor pulmonale)

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35
Q

Early Signs of Chronic Bronchitis

A

productive cough with copious amounts of sputum
DOE, normal to low paO2, increased PaCO2
disease progression can be stopped if pt stops smoking

36
Q

Later Signs of Chronic Bronchitis

A 
Blue Bloater
SOB, decreased PaO2
cyanosis
air trapping
cor pulmonale (R-sided HF)
37
Q

Emphysema

A

hyperinflation and decreased elastic recoil cause air trapping in the alveoli = permanent destruction of the alveoli

38
Q

Centriacinar Emphysema

A

most common type
related to smoking
localized only to the respiratory bronchioles

39
Q

Panacinar Emphysema

A

genetic form
related to alpha-1 antitrypsin deficiency
integrity of alveoli, alveoli sacs, and alveolar ducts is destroyed

40
Q

Chronic smoking impairs alveolar function through:

A

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
Q

Deficiency in Alpha-1 Antitrypsin causes:

A

1) inability to control the amount of elastase produced

2) more elastase = more elastin broken down = destroy lung matrix = reduces elasticity

42
Q

Early Signs of Emphysema

A

Dyspnea that progrressively worsens is the first sign
Normal (or slightly dec) PaO2
Normal PaCO2

43
Q

Late Signs of Emphysema

A 
Pink Puffer
tachypnea
pursed-lip breathing
tripod posture 
barrel chest 
low PaO2 and increased PaCO2
44
Q

Bronchiectasis

A

uncommon type of COPD

permanent dilation of the bronchi and bronchioles that occurs due to destruction of muscle and elastic supporting tissue

45
Q

2 Main Etiologies of Bronchiectasis

A

Mucus obstruction

Persistent infection

46
Q

Clinical Manifestation of Bronchiectasis

A

cough with expectoration of copious amounts of foul-smelling, purulent sputum
hemoptysis
weight loss and anemia

47
Q

Cystic Fibrosis

A

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
Q

Mutation to the CF gene on chromosom 7 leads to:

A 
impaired electrolyte (chloride) transportation across mucosal surfaces 
= production of excessive and thick exocrine secretions 
= leading to obstruction, inflammation, and infection
49
Q

Mucus Plugging

A

the formation of tenacious secretions and a reduced ability to clear the secretions
seen in CF

50
Q

Mucus plugging is the result of:

A

airway dehydration and thickened mucus caused by:

1) impaired chloride secretion
2) excessive sodium absorption
3) decreased water content in the airway tissues

51
Q

Airways and lung tissue in CF are characterized by:

A 
air trapping
hyperinflation
abscess formation
lung tissue consolidation
lung tissue fibrosis
cyst formation
52
Q

____ and _____ are the two main organs also affected by cystic fibrosis

A

Liver and Pancreas

53
Q

Consequences of Liver and Pancreas involvement in CF

A 
bile duct plugged with mucus = biliary cirrhosis
lack of pancreatic enzymes
decrease in digestion/absorption
weight loss
fatty stools (steatorrhea)
54
Q

Standard Diagnostic Test for CF

A

Sweat Test

a sodium and chloride content twice as high as normal is consistent with CF

55
Q

Secondary Atelectasis

A

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
Q

Types of Secondary Atelectasis

A

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
Q

Absorptive Atelectasis

A

surfactant inactivation = surface tension is reduced

less than normal levels of nitrogen being inhaled (can be associated with surgery with general anesthesia)

58
Q

______ acts as a stent to keep alveoli open

A

Nitrogen

59
Q

Obstructive Atelectasis

A

mechanical obstruction of the airways

secretions, mucus plugs foreign bodies

60
Q

Compressive Atelectasis

A

external forces that compress the pleura or lung tissue

pleural effusion, tumors, pneumothorax, or significant abdominal distention

61
Q

Pleural Effusion

A

excessive amount of fluid located in the pleural space between the visceral and parietal layers

62
Q

Pleural effusion results from increased _____________ and decreased __________

A

increased hydrostatic pressure in the pleural capillaries

decreased colloidal osmotic pressure in the circulatory system

63
Q

Types of Fluid that can accumulate to cause pleural effusion

A

transudative
exudative
empyema
chylothorax

64
Q

Transudative Fluid (Pl. Eff.)

A

clear fluid with low protein content

most commonly results from heart failure

65
Q

Exudative Fluid (Pl. Eff.)

A

cloudy fluid, high in protein

has inflammatory or malignant cells within it

66
Q

Empyema Fluid (Pl. Eff.)

A

purulent fluid - contains proteins, leukocytes, glucose, & cellular debris
commonly results from bacterial PNA or a ruptured lung abscess

67
Q

Chylothorax Fluid (Pl. Eff.)

A

effusion of lymph fluid in the pleural cavity

milky fluid due to fat-carrying lipoproteins from the GI tract

68
Q

Clinical Manifestations of Pleural Effusion

A

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
Q

Pneumothorax

A

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
Q

Spontaneous Pneumothorax

A

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
Q

Simple (Primary) Spontaneous Pneumothorax

A

Affects previously health individuals = tall, thin, Caucasian young males
Smoking

72
Q

Secondary Spontaneous Pneumothorax

A

Affects those with preexisting lung diseases that cause air trapping and destruction of lung tissue
Asthma, CF, emphysema, tuberculosis

73
Q

Traumatic Pneumothorax

A

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
Q

Hemothorax

A

presence of blood in the pleural cavity usually the result of trauma

75
Q

Tension Pneumothorax

A

Intrapleural pressure > Atmospheric pressure
air is unable to escape
compression of the opposite lung, trachea, aorta, and vena cava
EMERGENCY

76
Q

Clinical Manifestations of Spontaneous Pneumothorax

A 
ipsilateral CP
increase in RR
asymmetry of chest
hyperresonance during percussion
decreased/absent breath sounds on affected side
77
Q

Clinical Manifestations of Tension Pneumothorax

A

mediastinal shift towards opposite side (trachea)

SV is impaired and CO is decreased

78
Q

Pulmonary Emboli (PE)

A

a blood-borne substance that lodges in a branch of the pulmonary artery (emboli) so that flow becomes obstructed

79
Q

Types of Pulmonary Emboli (4)

A

1) Thrombus
2) Air
3) Fat
4) Amniotic Fluid

80
Q

Respiratory Clinical Manifestations of PE

A

Tachypnea, dyspnea
Cough, hemoptysis
Wheezing, crackles
Central cyanosis

81
Q

Cardiovascular Clinical Manifestations of PE

A

Tachycardia

Pleuritic CP - exacerbated by breathing

82
Q

Neurological Clinical Manifestations of PE

A

Anxiety
Confusion
Syncope

83
Q

Clinical Manifestation of Fat Emboli

A

Petechiae over chest

84
Q

Pulmonary Hypertension

A

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
Q

Primary Pulmonary HTN

A

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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