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Pathophysiology > Week 4 (ch. 13) > Flashcards

Week 4 (ch. 13) Flashcards

1
Q

Respiratory system function

A

transport of o2 from air to blood and removal of co2 from the blood

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2
Q

carbon dioxide

A

a waste product from metabolism and influences acid-base balance

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3
Q

URT

A

passageway of air from atmosphere to lungs

- resident flora

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4
Q

LRT

A

where gas exchange occurs

- sterile

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5
Q

nasal cavity

A

warming and moistening of air, foriegn material trapped by mucous secretions

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6
Q

nasopharynx

A

pharyngeal tonsils in posterior wall

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7
Q

palatine tonsils

A

lymphoid tissue in posterior portion of the oral cavity

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8
Q

oropharynx

A

common passage for air and food

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9
Q

epiglottis

A

protects opening into larynx, closes over glottis at swallowing to prevent aspiration

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10
Q

larynx

A

2 paid of vocal cords

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11
Q

trachea

A

lined by pseudo-stratified ciliated epithelium, C-shaped rings of cartilage

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12
Q

Trachea branches into what

A

Right and left primary bronchus
- right is larger and staighter and more likely a destination for aspiration material

secondary bronchi (from inverter bronchial tree)

bronchioles

alveolar ducts

alveoli

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13
Q

Alveoli

A

lined by simple squamous epithelium and surfactant to reduce surface tension and maintain inflation

  • end point for inspired air
  • site of gas exchage
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14
Q

how many lobes to the left and right lungs have

A 
right = 3
left = 2
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15
Q

what is each lung covered with?

A

pleural membrane

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16
Q

thorax

A

provides a rigid protection wall for the lungs

- external and internal intercostal muscles move thoracic structures during ventilation

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17
Q

ventilation depends on what

A

Pressure gradient (Boyle law) - air always moves from high pressure to low pressure

– atmospheric pressure higher than pressure in alveoli (inspiration)

– pressure in alveoli is higher than in atmosphere (expiration)

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18
Q

pulmonary volumes is what

A

measure of ventilatory capacity

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19
Q

tidal volume

A

amount of air exchanged with quiet inspiration and expiration

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20
Q

residual volume

A

volume of air remaining in lungs after maximum respiration

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21
Q

vital capacity

A

max. amount of air that can be moved in and out of lungs with a single forced inspiration and expiration

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22
Q

where are the primary control centers for breathing location

A

medulla and pons

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23
Q

what detect changes in carbon dioxide level, hydrogen ion, and o2 levels in blood or CSF

A

chemoreceptors

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24
Q

central vs peripheral chemoreceptors

A

central - located in medulla

peripheral - located in carotid bodies

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25
Q

hypercapnia

A

co2 levels in blood increase
co2 can easily diffuse into CSF
– lowers pH and stimulates respiratory center
– increased rate of respirations (hyperventilation)
–causes respiratory acidosis

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26
Q

hypoxemia

A

decrease in o2

  • chemoreceptors respond
  • important control mechanism in individuals with chronic lung disease - move to hypoxic drive
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27
Q

hypocapnia

A

Caused by low co2 concentration (low partial pressure of co2)

  • may be caused by hyperventilation (excessive amounts of co2 expired)
  • causes respiratory alkalosis
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28
Q

external respiration

A

flow of gases between the alveolar air and blood

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29
Q

gas exchage depends on what

A

relative concentrations (partial pressure) of the gases

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30
Q

Po2 =

Pco2 =

A

partial pressure of o2

partial pressure of co2

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31
Q

Dalton law

A

each gas in a mixture moves along its partial pressure gradient, independent of other gases

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32
Q

pulmonary arteries

A

bring venous blood from right ventricles to be oxygenation

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33
Q

pulmonary capillaries

A

where diffusion or gas exhange occurs

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34
Q

pulmonary veins

A

return oxygenated blood to let atrium of heart

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35
Q

where do the left ventricle and left atrium lead to

A

into aorta out to systemic circulation

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36
Q

what factors influence the diffusion of gases?

A
  1. Partial pressure gradient
  2. Thickness of respiratory membrane
    - - fluid accumulation in alveoli or interstitial tissue
  3. Total surface area available for diffusion
    - - if part of alveolar wall is destroyed, surface area is reduced –> less gas exchange
  4. ventilation-perfusion ratio
    - - ventilation (air flow) and perfusion (blood flow) need to match for maximum gas exhange
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37
Q

Describe the transport of o2

A

About 1% is dissolved in plasma

– most is reversibly bound to hemoglobin by iron molecules

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38
Q

binding and release of o2 to hemoglobin is dependent on what?

A

Po2, Pco2, temp, plasma pH

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39
Q

describe the transport of co2

A

about 7% dissolved in plasma
about 20% reversibly bound to hemoglobin
most diffused into RBC - converted into bicarbonate ions

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40
Q

how does co2 play role in control of blood ph

A

through bicarbonate buffer system

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41
Q

Diagnostic test: Spirometry

A

Pulmonary function test (PFT)

- test pulmonary volumes and airflow times

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42
Q

Diagnostic test: arterial blood gas determination

A

checks o2, co2, bicarbonate, serum pH

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43
Q

Diagnostic test: Oximetry

A

measures o2 saturation

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44
Q

Diagnostic test: exercise tolerance testing

A

for patients with chronic pulmonary disease

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45
Q

Diagnostic test: radiography

A

helpful in evaluating tumors and evaluate infections

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46
Q

What are some other diagnostic tests for respiratory function

A 
Bronchoscopy 
Biopsy
check site of lesion or bleeding 
culture and sensitivity tests
sputum testing and presence of pathogens
Determine antimicrobial sensitivity of pathogen
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47
Q

Sneezing

A

Reflex response to irritation in URT

– assists in removing irritants, associated with inflammation or foreign material

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48
Q

coughing

A

irritation caused by nasal drainage, inflammation or foreign material LRT caused by inhaled irritants

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49
Q

Sputum: thin, clear colorless

A

normal

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50
Q

Sputum: yellowish, green, thick, cloudy

A

bacterial

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51
Q

Sputum: rusty or dark

A

pneumococcal pneumonia

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52
Q

Sputum: purulent (pus like), foul odor

A

bronchiectasis

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53
Q

Sputum: Thick, tenacious (sticky) mucus

A

asthma or cystic fibrosis patients

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54
Q

Sputum: hemoptysis; bright red blood tinged frothy sputum

A

= pulmonary edema

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55
Q

Breathing patterns and sounds: Eupnea

A

normal rate

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56
Q

Breathing patterns and sounds: Kussmaul Respirations

A

Deep rapid respirations - typical for acidosis; may follow strenuous exercise

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57
Q

Breathing patterns and sounds: labored respiration or prolonged inspiration or expiration

A

often associated with obstruction of airways

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58
Q

Breathing patterns and sounds: wheezing or whistling sounds

A

indicate obstruction in small airways

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59
Q

Breathing patterns and sounds: Stridor

A

high pitched crowing noise (usually indicate upper airway obstruction)

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60
Q

Breathing patterns and sounds: Rales

A

light, bubbly, or crackling sounds with serous secretion

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61
Q

Breathing patterns and sounds: Rhonchi

A

Deeper or harsher sounds from thicker mucus

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62
Q

Breathing patterns and sounds: Absence

A

non aeration or lung collapse

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63
Q

Dyspnea

A

feel like you cannot inhale enough air

  • subjective feeling
  • may be caused by co2 or hypoxemia, often noted on exertion, such as climbing stairs
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64
Q

How is severe dyspnea indicative of respiratory distress?

A

flaring of nostrils, use of accessory respiration muscles, retraction of muscles between or above ribs

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65
Q

orthopnea

A

trouble breathing when lying down

- usually caused by pulmonary congestion

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66
Q

Paroxysmal nocturnal dyspnea

A

sudden acute type of dyspnea

- common in patients with left-sided congestive heart failure

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67
Q

Cyanosis

A

bluish coloring of skin and mucous membranes

- caused by large amounts of unoxygenated hemoglobin in blood

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68
Q

Pleural pain

A

results from inflammation or infection of parietal pleura

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69
Q

friction rub

A

soft sound produced as rought, inflamed or scarred pleural move against each other

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70
Q

Clubbed digits

A

painless, firm, fibrotic enlargement at the end of the digit

- results from chronic hypoxia associated with respiratory or CV diseases

71
Q

Hypoxemia vs hypercapnea

A

Hypoxemia - inadequate o2 in blood

hypercapnea - increased co2 in blood

72
Q

infectious diseases of the URT

A 
common cold
sinusitis
epiglottitis
influenze
scarlet fever
73
Q

URT: Common cold

A

Viral infection; spread through respiratory droplets

74
Q

common cold symptoms

A

congestion, sore throat, headache, fever, malaise, cough, may see pharyngitits, laryngitis, or acute bronchitis

– symptomatic treatment

75
Q

what secondary bacterial infections may occur from a common cold

A

Usually caused by streptococci

Purulent exudate; systemic signs (fever)

Can lead to rheumatic fever or group A beta hemolytic Streptococcus pneumoniae

76
Q

URT: Sinusitis

A

usually bacterial infectors
analgesics for headache and pain
course of antibiotics often required

77
Q

URT: Laryngotracheobronchitis (croup)

A

common viral infection, particularily in children

    • common causative organism
    • parainfluenza viruses and adenoviruses

infection usually self limited

78
Q

URT: Epiglottitis

A

Caused by Haemophilus influenzae type B
- age 3-7, rapid onset, fever and sore throat, drooling, refuse to swallow, heightened anxiety

  • swelling of larynx, supraglottic area and epiglottis - may obstruct airways
  • treatment: ox2, antimicrobial therapy, intubation
79
Q

URT: Influenza (FLU): what is it?

A

Viral infection - 3 groups of influenza virus

  • type A (common), b and c
  • virus constantly mutate
80
Q

URT: Influenza (FLU): s/s

A

sudden, acute onset with fever, fatigue, aching pain in the body
– May also cause viral pneumonia, Mild case of influenza may be complicated by secondary bacterial pneumonia.
Commonly, deaths in flu epidemics result from pneumonia.

81
Q

URT: Influenza (FLU): treatment

A

Symptomatic and supportive

    • Antiviral drugs – Amantadine, Zanamivir, Oseltamivir
    • Prevention highly recommended, vaccination
82
Q

Scarlet Fever is caused by what

A

group A beta-hemolytic S. pyogenes

83
Q

Scarlet fever symptoms

A

“strawberry tongue”

  • fever, sore throat
  • chills, vomiting, abdominal pain, malaise
84
Q

scarlet fever treatment

A

antibiotics

85
Q

Bronchiolitis: cause

A

caused by respiratory syncytial virus (RSV)

- common in children 2-12 months

86
Q

Bronchiolitis: transmitted

A

oral droplet

87
Q

Bronchiolitis: s/s

A

Wheezing and dyspnea, rapid shallow respirations, cough, rales, chest retractions, fever, malaise, can have severe cases`

88
Q

Bronchiolitis: Treatment

A

Supportive and symptomatic

At risk population could have RSV immunoglobulin serum- palivizumab (synagis)

Expensive, given every 28 days through RSV season

89
Q

Pneumonia: classification

A

Classification is based on:
- causative agent (bacteria, viral, fungal)

Anatomical location of infection
- through out both lungs, or one lobe

Pathophysiologic changes
- changes in interstitial tissue, alveolar septae, alveoli

Epidemiologic data

  • nosocomial
  • community acquired
90
Q

Tuberculosis: causative agent

A

mycobacterium tuberculosis

91
Q

tuberculosis: transmission

A

oral droplets

92
Q

tuberculosis is common where

A

crowded living conditions, immunodeficiency, malnutrition, alcoholism, war, chronic disease, HIV/AIDS

93
Q

Describe TB bacteria

A

acid-fast, slow growing bacillus

  • somewhat resistance to drying and many disinfectants
  • survive in dried sputum for weeks
  • destroyed by UV lights, heat, alcohol, formaldehyde
  • cell wall protects bacillus from body’s normal defenses
  • normal neutrophil response does not occur
94
Q

TB: Primary infection

A

Bacteria first enter the lungs
Local inflammatory reaction
- engulfed by macrophages (local inflammation)

if cell mediated immunity is inadequate, mycobacteria reproduce and begin to destroy lung tissue (contagious). If it is adequate, it remains small and walled off, eventually calcifying lesions called Ghon complexes (chest x-ray)

patient may stay viable in dormant state for years

95
Q

TB: Secondary or reinfection

A

Stage of active infection

  • can be years after primary infection
  • occurs when host resistance is decreased
  • organisms multiple - tissue destruction - large area of necrosis; cavitation occurs
  • spread to other parts of lung and expelled in sputum (contagious)
96
Q

TB: s/s

A

Anorexia, Malaise, Fatigue, Wght loss, afternoon low-grade fever & night sweats, prolonged cough becomes productive (sputum producing), sputum contains blood

97
Q

TB: diagnostics

A

Primary TB or latent- Mantoux skin test- false positive if person received vaccination for TB (BCG)

QuantiFeron-TB Gold test – newer blood test in place of Mantoux skin test
–> Common routine in health care workers, if x-ray needed then typically every 5 years

98
Q

Active TB diagnostics

A

Sputum culture, Acid-fast sputum test, x-ray, & CT scan, Nucleic acid amplification (NAA) test

99
Q

Why is TB becoming and increasinly serious problem

A

homelessness (over crowding in shelters)
HIV infection
lack of health care
multidrug resisant TB

100
Q

Treatment for Latent TB

A

Isoniazid (INH)
Rifapentine
Rifampin

101
Q

Active TB treatment

A 
Isoniazid 
Rifampin
Ethambutol
Pyrazinamide
Streptomycin
102
Q

Cystic Fibrosis

A

inherited disorder – gene located on chromosome 7

  • -> tenacious mucus from enodocrine glands
  • -> effets lung and pancrease
103
Q

Cystic fibrosis: Lungs

A

mucus obstructs airflow and bronchioloes and small bronchi

– permanent damage to bronchial walls

104
Q

Cystic fibrosis in the lungs is commonly caused by what

A

Pseudomonas aeruginosa and Staphylococcus aureus

105
Q

cystic fribrosis: digestive trace

A

Meconium ileus in newborns
Blockage of pancreatic ducts
Obstruction of bile ducts
Salivary glands often mildly affected

106
Q

Cystic Fibrosis: Reproductive tract

A

Obstruction of vas deferens (male)

Obstruction of cervix (female)

107
Q

Cystic Fibrosis: sweat glands

A

sweat has high sodium chloride content

108
Q

Cystic Fibrosis: s/s

A

a. Meconium ileus may occur at birth.
b. Salty skin
c. Signs of malabsorption
d. Chronic cough and frequent respiratory infections
e. Failure to meet normal growth milestones

109
Q

Cystic Fibrosis: Diagnosis

A 
genetic testing
sweat test
testing of stool
radiography, pulmonary function
blood gas analysis
110
Q

Cystic Fibrosis treatment

A

Replacement therapy and well-balanced diet

Chest physiotherapy – postural drainage, percussion, coughing techniques - Daily

111
Q

Aspiration s/s

A 
coughing and choking
loss of voice
stridor and horsness 
wheezing 
tachcardia and tachpnea
nasal flaring, chest retrations, hypoxia 
cardiac or respiratory arrest
112
Q

aspiration treatment

A

swallow study

keep objects away from children

113
Q

Asthma

A

Bronchial obstruction

- occurs in persons with hypersensitive and hyperresponsive airways

114
Q

Asthma pathophysiology

A

changes in bronchi and bronchioles
- inflammation of the mucosa with edema

  • bronchoconstriction caused by contraction of smooth muscle

increased secretion of thick mucus in airways

115
Q

extrinsic asthma

A

acute episodes triggered by type 1 hypersensitivity reactions

116
Q

intrinsic asthma

A

onset during adulthood

hyperresponsive tissue in airway initiates attact

117
Q

asthma stimuli

A

Respiratory infections, Stress, Exposure to cold, Inhalation of irritants, Exercise, Drugs

118
Q

asthma s/s

A 
cough
dyspnea
tight feeling chest 
wheezing
rapid and labored breathing 
expulsion of thick / sticky mucus
tachycardia
hypoxia
119
Q

respiratory alkalosis caused by

A

hyperventilation

120
Q

respiratory acidosis cause

A

air trapping

121
Q

severe respiratory distress leads to

A

hypoventilation leads to hyperoxemia and respiratory acidosis

122
Q

respitatory failure indicated by what

A

decreasing responsiveness, cyanosis

123
Q

chronic asthma attacks can lead to

A

chronic asthma and COPD

- bronchial wall thickening and fibrous tissue

124
Q

Asthma: Acute episode

A

Persistent severe attack of asthma

    • does not respond to usual therapy
  • medical emergency
  • may be fatal because of severe hypoxia and acidosis
125
Q

Asthma treatment: general measures

A 
Skin tests for allergic reactions
Avoidance of triggering factors
Good ventilation of environment
Swimming and walking
Use of maintenance inhalers or drugs
126
Q

Asthma treatment: measure for acute attacks

A

controlled breathing tech.
inhalers
glucocorticoids

127
Q

Asthma treatment: measures for status Asthma asthmaticus

A

hospital care if no response to bronchodilator

128
Q

Asthma treatment: prophylaxis and treatment for chronic asthma

A

Leukotriene receptor antagonist

  • block inflammation response in presence of stimulus
  • not effective for treatment f acute attacks
129
Q

Asthma treatment: Cromolyn sodium

A

Prophylactic medication
Inhalation on a daily basis
Useful for athletes and sports enthusiasts
No value during an acute attack

130
Q

COPD may lead to the development of what

A

corpulmonale (right sided heart failure)

131
Q

What is COPD Emphysema

A

Destruction of alveolar walls and septae

–> leads to large, permanent inflated alveolar air spaces

132
Q

COPD Emphysema is classified by what

A

specific location of changes

133
Q

COPD Emphysema contributing factors

A

genetic, gender, smoking, bacteria

134
Q

COPD Emphysema: breakdown of alveolar wall results in what

A

loss of surface area for gas exchange.- loss of pulmonary capillaries.- loss of elastic fibers.- altered ventilation-perfusion ratio.- decreased support for other structures.

135
Q

COPD emphysema: fibrosis

A

Narrowed airways, Weakened walls, Interference with passive expiratory airflow

136
Q

COPD Emphysema: describe the progressive difficulty with expiration

A

a. Air trapping and increased residual volume
b. Overinflation of the lungs
c. Fixation of ribs in an respiratory position, increased anterior-posterior diameter of thorax (barrel chest)
d. Flattened diaphragm (on radiograph

137
Q

COPD Emphysema: describe how advanced emphysema leads to loss of tissue

A

Adjacent damaged alveoli coalesce, forming large air spaces.

Pneumothorax
–> Occurs when pleural membrane surrounding large blebs ruptures

Hypercapnia becomes marked.

Hypoxia becomes driving force of respiration.

Frequent infections

Pulmonary hypertension and cor pulmonale
may develop in late stage

138
Q

Emphysema s/s

A

Dyspnea (first on exertion and worsens with disease progression)

hyperventilation w prolonged expiratory phase (barrel chest)

Anorexia / fatigue

Clubbed fingers

139
Q

Emphysema diagnosis

A

Chest radiography

pulmonary function tests (PFT)

140
Q

Emphysema treatment

A
  • Avoid respiratory irritants
  • Immunization
  • Pulmonary rehabilitation
  • Breathing techniques
  • nutrition and hydration
  • Bronchodilators, antibiotics, oxygen therapy as condition advances
  • Lung reduction surgery
141
Q

COPD chronic bronchitis

A

inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years

142
Q

Patho of chronic bronchitis

A

Mucosa inflammed and swollen
hypertrophy and hyperplasia of mucous glands

fibrosis and thickening of bronchial walls

143
Q

chronic bronchitis s/s

A

a. Constant productive cough
b. Tachypnea and shortness of breath
c. Frequent thick and purulent secretions
d. Cough and rhonchi more severe in the morning
e. Hypoxia, cyanosis, hypercapnia
f. Polycythemia, weight loss, signs of cor pulmonale possible
g. As vascular damage and pulmonary hypertension progress

144
Q

Chronic bronchitis treatment

A 
Stop smoking / irritant exposure
treat infection
vaccination
expectorants
bronchodilator
chest therapy
low-flow o2
nutritional supplements
145
Q

Vascular disorders: pulmonary edema what is it

A

fluid collecting in alveoli and interstitial area

  • results from primary conditions
  • reduced amount of o2 diffusing into blood
  • interferes with lung expansion
146
Q

Vascular disorders: pulmonary edema may develop when

A

a. Inflammation in lungs is present.
- Increases permeability of capillaries
b. Plasma protein levels are low.
- Decreases osmotic pressure of plasma
c. Pulmonary hypertension develops.

147
Q

Vascular disorders: pulmonary edema s/s for mild and chronic

A

Mild: cough, orthopnea, rales

chronic:
- hemoptysis often occurs
- frothy sputum
- labored breathing
- hypoxemia increased
- cyanosis

148
Q

Vascular disorders: pulmonary edema treatment

A

treat causative factors
supprtive care
possibly positive pressure mechanical care
keep upper body elevated

149
Q

Pulmonary embolus treatment

A 
Stockings
surgery
heparin or stretokinase
mechanical ventilation
embolectomy
150
Q

pulmonary embolism diagnosis

A

Radiography
Lung scan
MRI
Pulmonary angiography

151
Q

Pleural Effusion: what

A

Prescence of excessive fluid in pleural cavity

– causes increase pressure in pleural cavity and separation of pleural membrances

152
Q

Pleural effusion: Exudate effusion

A

response to inflammation

153
Q

Pleural effusion: transudate effusions

A 
Watery effusions (hydrothorax)
- result of increased hydrostatic pressure or decreased osmotic pressure in blood vessles
154
Q

Pleural effusion: s/s

A

Dyspnea
chest pain
increase RR and HR
usually dullness to percussion and absense of breath sounds over the affected area

tracheal deviation
hypotension

155
Q

Pleural effusion: treatment

A

Remove underlying cause to treat respiratory impairment.

Analyze fluid to confirm cause

Chest drainage, thoracocentesis to remove fluid and relieve pressure

156
Q

pneumothorax is what

A

air in pleural cavity

157
Q

Describe a closed pneumothorax

A

air can enter pleural cavity from internal airways - no opening in chest well

158
Q

closed pneumothorax: simple of spontaneous pneumothorax

A

tear on the surface of the lung

159
Q

closed pneumothorax: secondary pneumothorax

A

associated with underlying respiratory disease

Rupture of an emphysematous bleb on lung surface or erosion by a tumor or tubercular cavitation

160
Q

Open pneumothorax: what is it

A

Atmospheric air enters the pleural cavity through an opening in the chest wall
“sucking” wound – large opening in chest wall

161
Q

Open pneumothorax: tension pneumothorax

A

results of an opening through chest wall and parietal pleura or from a tear in the lung tissue and visceral pleura

  • air enters pleural cavity on inspiration but hole closes on expiration
  • trapping air leads to increase pleural pressure and atelectasis
  • most serious
162
Q

Pneumothorax s/s

A 
Atelectasis
dyspnea
cough
chest pain
reduced breath sounds
unequal check expansion
hypoxia 
interference with venous returne
163
Q

pneumothorax treatment

A

Hospital ASAP

MORE IN PPT

164
Q

Infant respiratory syndrome usually results from what

A

premature birth

165
Q

Infant respiratory syndrome what is it

A

lack of surfactant in alveoli

166
Q

Infant respiratory syndrome pathophysiology for Poorly developed alveoli that are diff. to inflate

A
    • diffuse atelectasis results

- - decrease pulm. blood flow, pulmonary vasoconstriction –> hypoxia

167
Q

Infant respiratory syndrome pathophysiology for poor lung perfusion and lack of surfactant

A

Increased alveolar capillary permeability

– fluid and protein are leaking into the interstitial area and alveoli, hyaline membrane formation

168
Q

Infant respiratory distress syndrom s/s

A

Respiratory difficulties at birth

Resp. = rapid and shallow

Frothy sputum

expiratory grunt

BP falls

cyanosis

peripheral edema

servere hypoxemia and decreased responsiveness

irregular respirations with periods of apnea

169
Q

Infant respiratory distress syndrom diagnostic tests

A

arterial blood gas analysis

170
Q

Infant respiratory distress syndrome treatment

A

Glucocorticoids for women in premature labor

Synthetic surfactant for high-risk neonate

CPAP

o2 therapy

171
Q

Adult respiratory distress syndrome

A

results from injury to the alveolar wall and capillary membrane

172
Q

what does Adult respiratory distress syndrome lead to

A

Release of chemical mediators
– increased permability of alveolar capillary membranes

  • increase fluid and protein in interstitial area and alveoli
  • damage to surfactant producing cells
  • diffuse necrosis and fibrosis if patient survives
173
Q

Adult respiratory distress syndrome s/s

A 
dyspnea
restlessness
rapid, shallow respirations
increase HR 
combination of metabolic and resp. acidosis
174
Q

Adult respiratory distress syndrome treatment

A

treat underlying cause

supportive respiratory therapy

Pathophysiology (11 decks)

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