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Adv Patho > Exam 2_Respiratory > Flashcards

Exam 2_Respiratory Flashcards

1
Q

What is ventilation?

A

movement of air in and out of lungs

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2
Q

What is gas exchange?

A

Diffusion of O2 and CO2 between alveoli in lung and the blood

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3
Q

What is perfusion?

A

movement of blood into and out of the capillary beds.

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4
Q

What is transport?

A

movement of O2 and CO2 via blood and circulatory system

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5
Q

What structures make up the extra-thoracic cavity?

A

nose
pharynx
larynx
trachea

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6
Q

What structures make up the intra thoracic cavity?

A

trachea
bronchi
bronchioles

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7
Q

What lines the respiratory passage?

A
  1. goblet cell-secrete mucous

2. cilia-clear debris from airways and keep airways moist

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8
Q

Vocal cords are ______ during breathing

A

open

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9
Q

Vocal cords are _______ during phonation

A

closed

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10
Q

What does the epiglottis due in adults that it does not in infants?

A

flaps during eating to block airways

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11
Q

Bronchioles do not have _______ but the trachea and bronchi do.

A

Bronchioles do not have cartilage and depend on transpulmonary pressure to remain open. It has smooth muscle instead of cartilage.

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12
Q

Respiratory smooth muscle is innervated by what nerve fibers?

A
  1. sympathetic nerve fibers that act on beta 2 receptors to relax smooth muscle
  2. parasympathetic nerve fibers that come from the vagus nerve
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13
Q

What does epinepherine do?

A

causes relaxation of smooth muscle and bronchodilation

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14
Q

What do parasympathetic nerve fibers secrete?

A

acetylcholine which causes contraction of bronchiolar smooth muscle and bronchoconstriction.

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15
Q

What do Leukotrienes do?

A

constrict

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16
Q

What do histamine and substance from mast cells (anaphylaxis) do?

A

constrict

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17
Q

How many lobes make the right lung and left?

A

Right-3

Left-2

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18
Q

What makes up the respiratory zone?

A

terminal bronchioles
alveoli
alveolar capillaries

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19
Q

Pores of Kohn and Canal of Lambert

A
  • channels between alveoli to allow communication

- implicated in alveolar disease and ease of spread of pulmonary infections

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20
Q

What is surfactant?

A

Coats inner alveoli and allows expansion during inhalation and prevents alveolar collapse on exhalation

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21
Q

What happens with the diameter of the conducting zone decreases?

A
  • there is an increase in resistance

* a 1mm change in airway diameter due to edema results in 81% of adult airway remaining patent vs 44% in a neonate

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22
Q

What does the diaphragm do?

A
  • adjust the size of the chest cavity
  • contraction pulls lungs down during inhalation
  • relaxation/elastic recoil moves lungs up during exhalation, forced exhalation uses abdominal muscles to push lungs up
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23
Q

What do intercostal muscles do?

A
  • External intercostals: raise and expand rib cage with help of sternocleidomastoid muscles on inhalation
  • Internal intercostals and abd recti: pull rib cage down and in during exhalation
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24
Q

What is the pleura and what is it made of?

A

-tissue lining of the lungs and rib cage

  1. visceral pleura-connected to lungs
  2. parietal pleura- connected to rib cage
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25
Q

What is between the pleural spaces?

A

pleural fluid

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26
Q

What kind of pressure causes the lung to move with the rib cage?

A

Negative pressure

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27
Q

What pressures changes move air?

A
  1. Pleural pressure
  2. Alveolar presssure
  3. Transpulmonary pressure
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28
Q

Pleural Pressure

A

Normall -5cm H2O, when chest expands decreases to -7.5 cm H2O which increases suction forces pulling lungs with rib cage

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29
Q

Alveolar Pressure

A

pressure in alveoli = pressure in respiratory tree when glottis is open = atmospheric pressure = 0 cm H2O

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30
Q

What happens when the chest wall expands?

A

Alveoloar pressure decrease to -1cm H2O and air moves in

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31
Q

What happens when the chest recoils?

A

Alveolar pressure increase to +1 cm H2O and air moves out

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32
Q

Transpulmonary Pressure

A

Pressure difference between pleural and alveolar pressure

*elastic forces that cause lung collapse at the end of exhalation are counteracted by PEEP, surfactant, and close glottis

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33
Q

What happens if the pressure inside and outside of the lungs is the same?

A

It will collapse

-can be caused by asthma or trauma

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34
Q

What is compliance?

A

degree lungs expand per unit of change in transpulmonary pressure

**how much air can you get in vs how much pressure you can give

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35
Q

Compliance is determined by:

A

elastic forces in lung tissue and elastic forces of pleural tension in alveoli and lung interstitum

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36
Q

What is surface tension elastic force?

A

air fluid interface creates a force that cause alveoli to collapse inward

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37
Q

What does surfactant do to the surface tension?

A

Reduces it and it disrupts the water molecules

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38
Q

What could cause decreased compliance?

A

Bronchitits, PNA, COPD

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39
Q

Difference between adult and children rib cages?

A

Adult is rigid and needs more effort to expand and chest wall has limited recoil.

Children have cartilaginous ribs which makes it easier to expand and has a strong recoil but more potential for collapse during exhalation

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40
Q

When is more muscular effect need for breathing?

A
  • lung compliance is decreased (pulmonary edema or infection)
  • chest wall compliance (scoliosis or obesity)
  • airways are obstructed (bronchospasm or mucous plugging)
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41
Q

What is tidal volume?

A

volume of inspired and expired air with each normal breath

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42
Q

What is inspiratory reserve volume?

A

maximum extra volume of air that can be inspired at the end of a normal tidal volume

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43
Q

What is expiratory reserve volume?

A

max extra volume of air that can be expired at the end of normal tidal volume

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44
Q

What is residual volume?

A

the volume of air that remains in the lungs at then end of a forceful exhalation

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45
Q

What is inspiratory capacity?

A

tidal volume + inspiratory reserve volume

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46
Q

What is functional residual capacity?

A

expiratory reserve volume + residual volume (the amount of air that remains at the end of normal exhalation)

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47
Q

What is vital capacity?

A

inspiratory reserve volume + tidal volume + expiratory reserve volume (max volume that can be exhaled after max inhale)

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48
Q

What is total lung capacity?

A

vital capacity + residual volume (max volume lung can be expanded)

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49
Q

Minute ventilation

A

total amount of new air moved into the respiratory system each minute

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50
Q

What is alveolar ventilation?

A
  • Rate new air reaches the gas exchange areas of the lungs

- Where gas exchange happens

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51
Q

What is dead space?

A

space in respiratory system where there is no gas exchange

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52
Q

Where can you find a dead space?

A

places where alveoli do not have any blood flow

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53
Q

Route of pulmonary circulation

A

RV&raquo_space; Pulmonary Artery&raquo_space; Pulmonary capillary bed (where gas is exchanged)&raquo_space; pulmonary vein&raquo_space; LA

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54
Q

What do bronchial vessels do?

A

provide oxygenated blood to trachea, bronchi, lungs, espophagus, visceral pleural and pulmonary arteries

** does not contribute to gas exchange

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55
Q

What happens during the hypoxic pulmonary vasoconstriction response?

A

Results in increased pulmonary vascular resistance in the lung unit that is not well ventilated which leads to shunting of pulmonary blood flow to areas of the lung that are adequately ventilated

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56
Q

What is V/Q mismatch?

A

Ventilation perfusion mismatch or V/Q defects are defects in the total lung ventilation/perfusion ratio. It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen.

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57
Q

Cause of V/Q mismatching

A 
Asthma
Chronic bronchitis
Pneumonia
Atelectasis
Pulmonary Embolism
58
Q

What is V/Q matching?

A

balance between alveolar ventilation and alveolar blood flow

59
Q

What happens in physiologic shunting?

A

V/Q is below normal = inadequate ventilation to oxygenate blood flowing through alveolar capillaries

60
Q

What happens in physiologic dead space?

A

V/Q is above normal = alveoli are well ventilated but there is alveoli that are not well perfused

61
Q

True or False

Dependent regions of the lung get more blood flow due to compression of capillaries in low pressure areas

A

True

62
Q

True or Flase

Lying supine, posterior aspects get more blood flow than anterior aspects

A

True

**why we lay covid patients prone

63
Q

How many pulmonary blood flow zones are there and what happens in each one?

A

Zone 1: no blood flow

Zone 2: intermittent blood flow

Zone 3: continuous blood flow

64
Q

How do blood flow zones work?

A

Normal and upright, you get blood flow in zones 2 and 3.

65
Q

What happens if you get blood flow in Zone 1?

A

PA (pulmonary artery) pressure is too high like in right sided heart failure or alveolar pressure is too high (hyperinflation)

66
Q

What is mean filtration pressure?

A

net fluid movement from alveoli to interstitial space and then drains to lymphatics

67
Q

What is pulmonary edema?

A

-excessive fluid in the alveoli which impairs gas exchange and decreases lung compliance

68
Q

Causes of pulmonary edema?

A
  • increased left side heart pressures
  • pulmonary over circulation
  • increased pulmonary capillary permeability (inflammation)
69
Q

What is pleural fluid

A

pleural fluid keeps the pleura moist and reduces friction between the membranes when you breathe. The area that contains pleural fluid is known as the pleural space. Normally, there is a small amount of pleural fluid in the pleural space

70
Q

What system pumps aways excess fluid in lungs?

A

lymphatic vessels

71
Q

Pleural effusion

A

excess fluid in pleural space

72
Q

Causes of pleural effusion

A
  • blocked lymph drainage
  • left sided heart failure
  • reduced plasma oncotic pressure
  • increased permeability of pleural membrane
73
Q

What happens in the concentration gradient?

A

gases move from areas of high concentration to low concentration

74
Q

What does gas exchange in the respiratory system rely on?

A

Net diffusion (movement of gases between air and blood)

75
Q

SpO2 in arterial blood is normally

A

97-100%

76
Q

SpO2 in venous blood is normally

A

75%

77
Q

On the oxy-hemoglobin dissociation curve a shift to the left means:

A
  • increased affinity of hemoglobin
  • acute alkalosis
  • decreased PCO2
  • decreased temp
78
Q

On the oxy-hemoglobin dissociation curve a shift to the right means:

A
  • decreased affinity of hemoglobin
  • acute acidosis
  • high PCO2
  • increased temp
79
Q

Bohr effect

A

hgb oxygen binding is inversely related both to acidity and to the concentration of carbon dioxide

80
Q

How is CO2 removed from body?

A
  • CO2 is bound to Hgb and transported as carboxyhemoglobin where it is then transported as bicarbonate where it is combined with blood proteins as carbamino compounds
  • dissolved CO2 is ventilated out of the body through the alveoli (O2 displaces the CO2 on Hgb promoting CO2 removal)
81
Q

What part of medulla is responsible for in breathing?

A

Doral respiratory group - inspiration

Ventral respiratory group - exhalation

82
Q

What do the Pons do with breathing?

A

pneumotaxic center which controls the rate and pattern of breathing

83
Q

Dorsal Respiratory Neurons

A
  • vagal and glossopharyngeal nerves end in the medulla
  • transmit signals from chemoreceptors and baroreceptors
  • den signals to diaphragm and intercostal muscles to control rate of breathing and inspiration time
84
Q

Ventral Respiratory Neurons

A
  • inactive during normal breathing
  • fire during hypoventilations and signal inspiration
  • stimulate abd muscle contraction for forceful exhalation
85
Q

Central Chemoreceptors

A
  • neurons in medulla

- sense changes in pH and CSF

86
Q

Peripheral Chemoreceptors

A
  • located in carotid and aortic bodies

- sense changes in O2 concentration (decreased PO2 will increase respiratory rate)

87
Q

What makes up lung innervation?

A
  1. Irritation receptors
  2. Stretch receptors
  3. Pulmonary C fiber receptors
88
Q

Irritation receptors

A
  • epithelium of conducting airways

- sensitive to aeirosols, gases, particulate matter–induces cough

89
Q

Stretch receptors

A

-when smooth muscle in bronchi, bronchioles or lung parenchyme stretched&raquo_space; signal medulla dorsal respiratory neurons to switch off inspiration

90
Q

Pulmonary C fiber receptors

A

-respond to increased pulmonary capillary pressures (ex left side heart failure)&raquo_space; initiate rapid shallow breathing, causes laryngeal vasoconstriction and mucous secretion

91
Q

What can cause CNS depression?

A

brain injury or anesthesia

92
Q

What is a PE pulmonary embolism?
How is it diagnosed?
Treatment?

A

A PE is an occlusion or partial occlusion of pulmonary artery or branches.

Can be caused by: DVT, fat (lipids), air bubbles or amniotic fluid

DX: elevated d-dimer, CT-A or MRA, EKG with right strain, troponin to help risk stratify

Tx: fibrinolytics to dissolve clot

93
Q

Signs and symptoms of PE

A 
tachypnea
dyspnea
chest pain
increased dead space
V/Q imbalance
decreased PaO2
pulmonary infarction 
pulmonary HTN
decreased cardiac output
systemic hypotension
shock
94
Q

What happens during a a PE?

A

hypoxic vasoconstriction&raquo_space; decreased surfactant&raquo_space; release of neurohumoral and inflammatory substances&raquo_space; pulmonary edema&raquo_space; atelectasis

95
Q

What is Pulmonary Artery Hypertension?

A

PAH is a pulmonary artery pressure >25 mmHg (<20mmHg is normal)

Cause: idiopathic, genetic, connective tissue disease; associated with chronic hypoxia, left ventricular heart failure, valve disease

Patho: vasoconstricition overwhelm pulmonary vasodilators&raquo_space; resistance of blood flow to lungs&raquo_space; remodeling of RV&raquo_space; cor pulmonale (right side heart failure)

Symptoms: dyspnea, chest pain, tachypnea, cough, jugular vein distention (which is sign of right sided HF)

Associated with COPD

96
Q

Hallmark signs of an obstructive process

A
  • worse on expiration&raquo_space; prolonged expiratory phase and decreased FEV (forced expiratory volume)
  • dyspnea
  • wheezing in lower airway and stridor in upper airway
97
Q

Asthma

A
  • a chronic inflammatory disorder of bronchial mucosa which leads to bronchial hyper-responsiveness, bronchoconstriction and obstruction
98
Q

What is an early response in asthma?

A

Antigen exposure&raquo_space; inflammatory cytokine response&raquo_space; increased capillary permeability&raquo_space; mucosal edema&raquo_space; mucous production and bronchospasm

99
Q

What is a late response in asthma?

A
  • Inflammatory mediators&raquo_space; bronchospasm&raquo_space; secretions&raquo_space; obstruction
  • Obstruction&raquo_space; air trapping&raquo_space; hyperinflation&raquo_space; V/Q mismatching&raquo_space; hypoxemia&raquo_space; CO2 retention&raquo_space; acidosis&raquo_space; respiratory failure
100
Q

True or False?

Asthma can be familial or environmental

A

TRUE

101
Q

What is the treatment for asthma?

A
  • Beta 2agonists (albuterol) - relaxes bronchial smooth muscle
  • Anticholinergic stimulators - relaxes bronchial smooth muscle
  • Steroids - act to decrease inflammatory mechanism and mast cell degranulation
  • Antihistamines - if allergen mediated
102
Q

What can happen if you have exacerbation and remission of asthma?

A

it can lead to chronic airway remodeling

103
Q

What is COPD

A

Airflow limitation (obstruction) that is not fully reversible and generally progressive

Usually acquired but some genetic basis (alph1-antitrypsin deficiency)

104
Q

What are the 2 types of COPD

A
  1. chronic bronchitis

2. emphysema

105
Q

What happens in chronic bronchitis?

A
  • hypersecretion of mucous and chronic productive cough (3 month/yr, 2+ years)
  • initially impacts large airways but ultimately affects all bronchial smooth muscle
  • Bronchial inflammation&raquo_space; edema&raquo_space; increased size and number of mucosal glands and goblet cells&raquo_space; air trapping on expiration

V/Q mistmatch&raquo_space; hypoxemia&raquo_space; mild cyanosis
DOE
chronic hypercarbia

106
Q

Emphysema

A
  • englargment of respiratory zone airways and destruction of alveolar walls (when you lose the walls you lose elastic recoil and results in air trapping)
107
Q

Symptoms of Chronic Bronchitis

A 
Productive cough- CLASSIC SIGN
Dyspnea- late in course
Wheezing- intermittent
Barrel chest - occasionally
Prolonged exhalation- always present
Cyanosis- common
Chronic hypoventilation- common
Cor pulmonale-common
108
Q

Symptoms of Emphysema

A 
Productive cough - Late in course
Dyspnea - Common
Wheezing - Minimal
Barrel chest - CLASSIC SIGN
Prolonged exhalation - always present
Cyanosis- Uncommon
Chronic hypoventilation - Late in course
Cor pulmonale - Late in course
109
Q

What is cor pulmonale?

A

condition that causes the right side of the heart to fail. Long-term high blood pressure in the arteries of the lung and right ventricle of the heart can lead to cor pulmonale

110
Q

Upper airway-pediatric

2 examples

A
  1. Croup-acute viral infection
    *subglottic edema causes narrowing of airway and
    respiratory distress
    • BARKY cough, inspiratory stridor
  2. Acute epiglottis - associated with bacterial infections
    (H Flu)
    *rapid edema of epiglottis-severe and life threatenigg
    obstruction
    *inspiratory stridor, tripoding, drooling
    *keep calm and get to safe place to protect airway
111
Q

Cystic fibrosis

A
  • autosomal recessive genetic d/o
  • defective chloride ion transport (thick secretions of respiratory and/or digestive)

*changes in chloride ion transport makes things stickier and less clearable which can cause mucous plugging

112
Q

Respiratory effects of cystic fibrosis

A
  1. mucous plugging with increased submucosal gland and goblet cells
  2. chronic inflammation with excessive cytokine and neutrophil activation
  3. recurrent infections
113
Q

What are structural restrictions and examples?

A

-Increased effort to expand lungs (lead to dyspnea, tachypnea, and difficulty with secretion clearance)
Ex: scoliosis, muscular dystrophy, and morbid obesity

114
Q

What is aspiration?

A
  • Passage of fluids and solids into the lungs
  • Associated with impaired cough and swallowing

Patho:

  • bronchial damage with inflammation&raquo_space; loss of cilia function&raquo_space; bronchospasm
  • alveolocapillary membrane damage&raquo_space; hemorrhagic pneumonitis&raquo_space; stiff non compliant alveoli
115
Q

What is atelectasis?

A

-Blockage of airway from
pressure outside the lung that keeps it from expanding
* not enough surfactant to expand

Causes: Pneumonia, mucous, tumor

Patho: (build up of secretion in lungs that block airways)

  • increase pulmonary shunt&raquo_space; hypoxia
  • decreased compliance
116
Q

Bronchiolitis

A

-Inflammation of the bronchioles: occurs with chronic bronchitis, viral respiratory illness, toxic gas inhalation

  • Atelectasis or emphysematous destruction of alveoli beyond area of inflammation
  • decreases V/Q matching&raquo_space; hypoxemia
  • decreases V/Q matching&raquo_space; decreased minute ventilation&raquo_space; hypercarbia&raquo_space; tachypnea
117
Q

Pulmonary Fibrosis

A
  • Excessive fibrosis and connective tissue in lungs
  • scar tissue after pulmonary disease (ARDS, TB)
  • autoimmune disorders (RA, sarcoidosis)
  • inhalation of harmful substance (coal, dust, asbestos)
  • idiopathic

Chronic inflammation&raquo_space; fibrosis of alveolar epithelium&raquo_space; myofibroblast proliferation&raquo_space; stiff alveoli&raquo_space; decreased compliance&raquo_space; V/Q mismatch&raquo_space; hypoxia

118
Q

What is respiratory failure?

A

-inadequate gas exchange (hypoxia, hypercarbic)

Cause: injury to lungs, airway or chest, but also result of disease/injury to another body system

Test for severity: AA gradient

119
Q

Hypoxemia

A

-reduced oxygenation of arterial blood (PaO2): can occur with or without hypoxia, decreased oxygenation of tissues

Normal value: 80-100 mmHg/
RESPIRATORY FAILURE: ≤ 50 mmHg

Causes; hypoventilation, V/Q mismatch, increased alveolocapillary membrane thickness, heart failure

Manifestations: tachy, cyanosis, confusion

120
Q

Hypercarbia/Hypercapnia

A

-increased CO2 in arterial blood (PaCO2) and decreased serum pH

PaCO2 ≥ 50 and ph ≤ 7.25 (acidosis)

Causes: hypoventilation, decreased respiratory drive, neuromuscular disease, airway obstruction, physiologic dead space, chest wall deformities

Manifestations: +/- confusion, LETHARGY

121
Q

Labs:

Alveolar-arterial oxygen gradient

A

Defines oxygenation disorders

Normal: 5-15 mmHg

*if elevated think pulmonary causes

122
Q

Labs:

P/F Ratio

A

Severity of hypoxemic respiratory failure (IMPORTANT!)

P/F Ratio = PaO2/FiO2

Example to calculate:
PaO2 of 85 mmHg and FiO2 of .4 (40%)
=85/.4
=212.5

**less than 200 is acute respiratory syndrome
200-300 acute inury
more than 300 is normal

123
Q

Acute lung injury can lead to ARDS

A

-Inflammatory process in lungs that lead to alveolar epithelial and vascular endothelial injury in lungs (can be infective or non-infective)

3 criteria:

  • acute onset (<7 days)
  • bilateral infiltrates
  • resp failure not explained by cardiac causes or fluid overload

3 phases:
Excudative
Proliferative
Fibrotic

ALI is P/F ratio ≤ 300
ARDS is P/F ratio ≤200

124
Q

What makes up the conducting airways and respiratory zones?

A

Conducting airways: the trachea, the two stem bronchi, the bronchi, and the bronchioles

Respiratory zones: the respiratory bronchioles, alveolar ducts, and alveoli

125
Q

What factors affect the muscles in the bronchi and bronchioles???

A
  1. cartilage
  2. goblet cells-secrete mucous
  3. bronchial lining
  4. ciliated epithelial cells
126
Q

Describe the the intrathoracic pressure changes that results in air movement into and out of the alveoli

A

a. Inspiration drops intrathoracic pressure, dilates the thoracic vena cava, and acutely decreases atrial filling. Cardiac output falls, and consequently arterial pressure falls. The drop in arterial pressure reduces stretch on the arterial baroreceptors, causing a reflex increase in heart rate.
b. Exhalation reverses the above steps.
c. In the valsalva maneuver: During a maintained increase in intrathoracic pressure, venous return is interrupted, and cardiac output falls. The subsequent fall in arterial pressure reduces cerebral blood flow.

127
Q

What does an increased resistance compliance curve mean and what disease process is associated with it?

A

can indicate a state of disease where there is degeneration of tissue that causes the lungs to have to work harder to expand, such as emphysema. With emphysema, the tissue damage means that it is easier to inhale, as there is less resistance, but it is harder to exhale

128
Q

What does a decreased compliance curve mean and what disease process is associated with it.

A

Associated with bronchitis, COPD, or pneumonia (restrictive lung disease);

Takes a lot more pressure to get air in

129
Q

What are the 2 types of dead space?

A
  1. Anatomic:
    - conducting zone is = 30% of TLC

Anatomic dead space is the total volume of the conducting airways from the nose or mouth down to the level of the terminal bronchioles,

  1. Physiologic
    - alveoli without blood flow

includes all the non-respiratory parts of the bronchial tree included in anatomic dead space, but also factors in alveoli as well
*anatomic dead space + alveoli without blood flow = “physiologic dead space”

130
Q

Pulmonary Edema

A

Etiology: Excess water in lungs.
Clinical Manifestations: dyspnea, hypoxemia, increased work of breathing, inspiratory crackles, dullness to percussion over the lungs bases, and evidence of ventricular dilation. Severe: pink and frothy sputum,
Patho:
1. valvular dysfunction/CAD/LV dysfunction &raquo_space; increased left atrial pressure&raquo_space; increased pulmonary capillary hydrostatic pressure
2. injury to capillary endothelium&raquo_space; increased capillary permeability and disruption of surfactant production by alveoli&raquo_space; movement of fluid and plasma proteins from capillary to interstitial space and alveoli
3. blockage of lymphatic vessels&raquo_space; inability to remove excess fluid from interstitial space&raquo_space; accumulation of fluid in interstitial space

131
Q

Pleural effusion

A

Etiology: presence of fluid in the pleural space

Clinical Manifestations: Dyspnea, compression atelectasis with impaired ventilation, and pleural pain, decreased breath sounds and dullness to percussion on the affetced side; pleural friction rub can be heard over areas of inflamed pleura

Patho: traumatic injuries, pulmonary infections, cardiovascular disease that causes high BP; liver or kidney disease that disrupts plasma protein production, causing hypoproteinemia (decreased oncotic pressure in the blood vessels), infection/inflammation/or malignancy of the pleurae that stimulates mast cells to release biochemical mediators that increase capillary permeability

132
Q

Why does an elevated PCO2 results in acidosis?

A

there will be a shift to carbonic acid, ultimately causing the generation of hydrogen cations and bicarbonate anions. It is with this increased production of hydrogen ions that bodily pH will begin to decrease, causing acidosis from acidemia

133
Q

ARDS

Exudative Phase (1st)

A

within 72 hrs of injury ; lung become less compliant, work of breathing increases, ventilation of alveoli decreases, and hypercapnia develops

Patho:
Pulmonary edema and hemorrhage with severe impairment of alveolar ventilation

134
Q

ARDS

Proliferative phase (2nd)

A

Within 1-3 weeks after initial lung injury. Resolution of pulmonary edema

Patho: Proliferation of tyepe II pneumocytes, fibroblasts, and myofibroblasts. Formation of hyaline membranes

135
Q

Clinical manifestation of ARDS

A

Dyspnea and hypoxemia&raquo_space; hyperventilation and resp alkalosis&raquo_space; decreased tissue perfusion, metabolic acidosis, and organ dysfunction&raquo_space; increased work of breathing, decreased tidal volume, and hypoventilation, hypercapnia, resp acidosis, and worsening hypoxemia, decreased cardiac output, hypotension, and death

136
Q

How do you measure severity of resp failure

A

P/F ratio

Normal >300

137
Q

What is the brain stem’s role in breathing?

A

Respiratory center in brainstem controls respiration by transmitting impulses to the respiratory muscles, causing them to contract and relax.

Made up of: respiratory center, VRG (ventral respiratory group), and DRG (dorsal ventral group)

138
Q

What are chemeoreceptors roles in breathing?

A

monitor pH, PaCO2, and PaO2

Central chemoreceptors monitor arterial blood indirectly by monitoring changes in pH in CSF.

-peripheral chemoreceptors monitor oxygen levels and arterial blood

139
Q

What is the role of lung innervation in breathing?

A

innervated by CNS and ANS to control smooth muscle relaxation and contraction

140
Q

What effects compliance?

A
  1. elasticity of lungs
  2. surface tension
  3. elasticity of chest wall
141
Q

Fibrosis of the lungs does what? (like with pulmonary fibrosis)

A
  1. decrease compliance

2. increases elasticity

Adv Patho (23 decks)

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