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Marie- NUR 280 > Gas Exchange > Flashcards

Gas Exchange Flashcards

1
Q

obstructive

A

increased resistance to airflow- bronchi, bronchioles, alveoli

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2
Q

restrictive

A

reduced expansion of lung tissue, decrease in total lung capacity- mechanical

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3
Q

compliance

A

flexibility of lung tissue to expand/contrast

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4
Q

pleural membrane

A

area between membrane lining- should only have surfactant in it to prevent friction, no other air or fluid

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5
Q

hypoxemia

A

lack of oxygen in the bloodstream

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6
Q

hypoxia

A

low O2 available to body tissues

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7
Q

hypercapnia

A

high CO2

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8
Q

major risk factors for pulmonary problems

A
  • SMOKING
  • genetics
  • disease processes
  • environmental/occupational exposure
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9
Q

How do we assess pulmonary function?

A
  • auscultation
  • rate and rhythm
  • depth of breathing
  • accessory muscle use
  • cyanosis
  • thoracic cage (barrel chest)
  • adventitious breath sounds
  • percussion
  • clubbing of fingers
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10
Q

How do we diagnose pulmonary problems?

A
  • PFT
  • chest xray
  • ABGs
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11
Q

How do we treat pulmonary problems in general?

A
  • LABA
  • SABA
  • nebulizers
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12
Q

what makes nebulizers so special

A

they go deeper and will rescue pt faster than inhaler

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13
Q

Asthma

A

hyperreactive disease of the bronchioles

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14
Q

is asthma reversible

A

yes

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15
Q

why is asthma so concerning

A

everytime a pt has an attack, damage is left and it gets worse each time

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16
Q

symptoms of asthma

A
  • T cells, IGEs, leukotrienes combine to make the bronchioles constrict
  • histamines (inflammation)
  • prolonged expiration
  • wheezing
  • cough
  • dyspnea
  • tachypnea
  • use of tripoding
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17
Q

what is asthma diagnosed with? When?

A

PFT during an acute asthma attack (to measure forced expiratory volume)
- low pulmonary function result = worse asthma attack

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18
Q

asthma treatment

A

meds:
SABA: rescue
LABA: maintenance

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19
Q

teaching for asthma

A
  • know your triggers and avoid them
  • use your medication as prescribed
  • no excessive use of SABAs
  • call your provider if your maintenance meds aren’t working bc you may need a new regimen
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20
Q

status asthmaticus

A
  • persistent bronchoconstriction despite attempts to reverse
  • client will be hypercapnic and hypoxic/hypoxemic
  • CAN BE FATAL
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21
Q

What is COPD

A

combination of chronic bronchitis, emphysema, and hyperreactive airways (in exacerbation)

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22
Q

major cause of COPD

A

SMOKING

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23
Q

chronic bronchitis

A
  • hypersecretion of mucus
  • mucus and edema
  • cyanosis
    -cannot get air IN
  • cough- 3 months of year for at least 2 years
  • chronic hypoxia
  • clubbing of fingers
  • pulmonary arterial vasoconstriction
  • nickname: BLUE BLOATER
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24
Q

emphysema

A
  • over distension of alveoli
  • air trapping
  • cannot get air OUT
  • chronic hypercapnia
  • prolonged exhalation
  • barrel shaped chest
  • diaphragm pushed downward
  • nickname: PINK PUFFER
25
Q

how is COPD treated

A

similar to asthma, stepwise approach

26
Q

education for COPD

A
  • STOP SMOKING
  • stay up to date on flu and pneumonia vaccines
  • pursed lip breathing
27
Q

why do you need to be careful with oxygen therapy (COPD)

A

easy to over over oxygenate and knocked out the pts drive to breathe

28
Q

obstructive sleep apnea

A
  • intermittent cessation of airflow from the nose and mouth during sleep
29
Q

what does obstructive sleep apnea sound/look like

A
  • sounds like choking,
  • gasping
  • looks like unrestful sleep
  • daytime sleepiness
30
Q

what worsens sleep apnea

A
  • alcohol
  • sedative- hypnotic medications
  • educate to avoid these things
31
Q

how is obstructive sleep apnea diagnosed

A

through a sleep study

32
Q

treatment for obstructive sleep apnea

A
  • WEAR CPAP
    Why? prevents airway from closing
33
Q

Pneumothorax

A
  • collapsed lung
  • air or fluid gets into the pleural space and puts pressure on the lung and then the lung collapses
34
Q

symptoms of pneumothorax

A
  • chest pain
  • dyspnea
  • increased RR
  • chest may look asymmetrical upon observation
35
Q

will lung sounds be heard on affected side of pneumothorax

A

no

36
Q

primary spontaneous pneumothorax

A

lung just collapses, no disease process has anything to do with it

37
Q

secondary spontaneous pneumothorax

A

lung collapses due to a disease process

38
Q

traumatic pneumothorax

A

penetrating wound to thoracic cage and pleural membrane

39
Q

tension pneumothorax

A

closed wound that allows air into the pleural cavity but not out, can be caused by trauma

40
Q

iatrogenic pneumothorax

A
  • caused by medical procedure complications
  • can often be a “parting gift” from a central line insertion
41
Q

Which types of pneumothorax are treated with chest tube with suction

A
  • primary
  • secondary
  • open traumatic
  • iatrogenic
42
Q

what is a tension pneumothorax treated with

A

needle insertion to remove air

43
Q

pleural effusion

A
  • abnormal collection of fluid in pleural space
  • fluid can be exudate, transudate, purulent, lymph, blood
44
Q

what does pleural effusion result from

A
  • heart failure
  • severe pulmonary infections
45
Q

s/s pleural effusion

A
  • dyspnea
  • tachypnea
  • sharp pleuritic CP
  • dullness to percussion
46
Q

will breath sounds be present with pleural effusion

A

diminished breath sounds on affected side, maybe even absent breath sounds over area of effusion

47
Q

treatment for pleural effusion

A

thoracentesis

48
Q

thoracic cage deformity

A
  • anything that structurally makes it hard for lungs to fully inflate
  • kyphosis
  • scoliosis
49
Q

treatment for thoracic cage deformity

A

orthopedic brace

50
Q

pulmonary fibrosis

A
  • may be idiopathic
  • repeated injury to alveoli, but the cause is unknown
  • may be related to environmental particles
  • coal dust, asbestos, silica, anthrax
  • fibrotic changes decrease lung compliance; lungs become stiff because of repeated inflammation to the alveoli
51
Q

s/s pulmonary fibrosis

A
  • dyspnea
  • tachypnea
  • crackles
  • eventual cyanosis
52
Q

what will a chest xray of a patient with pulmonary fibrosis look like

A

“ground glass” appearance

53
Q

treatment for pulmonary fibrosis

A
  • try to decrease inflammation/inflammatory response and fibrotic changes
  • may treat with O2
  • bronchodilators, corticosteroids
54
Q

pulmonary edema

A
  • edema in the pulmonary veins
  • often caused by heart failure
  • blood backs up into the veins of the lungs, increases pressure
  • when the pressure is too great, fluid is pushed into the alveoli of the lungs
55
Q

pulmonary embolism

A

happens when a DVT dislodges and travels to lungs

56
Q

pulmonary hypertension

A
  • high blood pressure that affects arteries in the lungs, right side of heart
  • walls of pulmonary arteries become thick and stiff and cannot expand very well to allow proper blood flow
57
Q

adult respiratory distress syndrome

A
  • injury to alveoli, pulmonary capillaries that causes sudden, progressive pulmonary edema called flash pulmonary edema
  • arterial hypoxemia does not improve with administration of O2
  • seen in critically ill patients
58
Q

risk factors of ARDS

A
  • SEPSIS
  • trauma
  • massive transfusion
  • acute pancreatitis
  • aspiration
59
Q

treatment for ARDS

A
  • intubation, sedation, and mechanical ventilation
  • death common

Marie- NUR 280 (12 decks)

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