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NURS 470 > Oxygenation > Flashcards

Oxygenation Flashcards

1
Q

physiology of pulmonary gas exchange

A

inspiration & delivery of O2 from environment -> alveoli, diffusion across alveolar-capillary membrane -> attaches to Hgb, dissolves in blood -> left heart

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2
Q

ventilation

A

movement of gases from atmosphere to alveoli (and vice versa)

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3
Q

diffusion

A

mechanism by which O2 moves across the alveoli and into pulmonary capillary

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4
Q

perfusion

A

O2 leaves alveoli to combine with Hgb (HbO2) or dissolve in blood (PaO2) to be carried to left side of heart

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5
Q

ventilation is dependent ong

A

conducting airways/airway diameter
ventilatory muscles (diaphragm, intercostals)
thorax/flexibility of rib cage
elasticity of the lungs (compliance)
nervous system/regulators

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6
Q

conducting airways

A

trachea
segmental bronchi
bronchioles
alveolar ducts

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7
Q

regulation of ventilation is done by …

A

Controller: CNS (brainstem, cerebral cortex, neurons in spinal cord)
group of effectors (muscles that work in coordinated fashion)

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8
Q

what chemoreceptors are used as sensors in regulation of ventilation

A

central chemoreceptors in the medulla
peripheral chemoreceptors in the aortic arch, carotids

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9
Q

how does the body respond to increase in hydrogen ions (acid)

A

increase ventilation

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10
Q

how does the body respond to decrease in PaO2

A

increase ventilation

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11
Q

how does the body respond to increase in PaCO2

A

increase ventilation

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12
Q

characteristics of inadequate ventilation

A

minimal/absent chest wall motion
use of accessory muscles (WOB)
wheezes
decreased/absent breath sounds
paradoxical chest wall motion
respiratory distress: PaCO2 >= 50, PaO2 <= 60, Ph <= 7.3

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13
Q

diffusion

A

movement of molecules from HIGH concentration to LOW concentration
mechanism by which O2 moves across alveoli and into bloodstream

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14
Q

type 1 alveolar epithelial cells

A

90% of total alveolar surface within lungs
highly susceptible to injury and inflammation

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15
Q

type 2 alveolar epithelial cells

A

produce, store, secrete pulmonary surfactant

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16
Q

surfactant in alveoli

A

phospholipid that lowers surface tension of the lungs
stabilizes alveoli, increases pulmonary compliance, eases WOB
in disease, disruption of synthesis/storage of surfactant = collapse of alveoli, impairment of pulmonary gas exchange

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17
Q

macrophages in alveoli

A

monocytes -> macrophages in alveoli -> phagocytic role
move from alveoli -> alveoli keeping them clean and sterile
release enzymes (H2Ow) when killing microorganisms

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18
Q

what are the 3 factors that affect diffusion of gas across alveolar-capillary membrane

A

pressure gradient (driving pressure)
surface area
thickness

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19
Q

PaO2 gradient

A

driving pressure- difference in pressure concentration concentrations (gradient)

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20
Q

an increase in surface area causes

A

increases amount of gas that can diffuse

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21
Q

interventions to increase surface area

A

incentive spirometer
turn cough, cough breath
sighs/yawn
positive end expiratory pressure (PEEP)

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22
Q

increased thickness of alveolar capillary membrane results in

A

slower rate of diffusion

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23
Q

conditions that increase alveolar capillary membrane thickness

A

ARDS
pulmonary edema
pulmonary fibrosis

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24
Q

what are the 2 ways O2 is transported in the blood

A

oxyhemoglobin (HbO2)
dissolved in blood (PaO2)

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25
Q

respiratory acidosis

A

excessive retention of CO2 due to hypoventilation leading to a decrease in pH below 7.35

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26
Q

respiratory acidosis causes

A

COPD
pneumonia
atelectasis
neuromuscular disease
post-op recovery
narcotics

27
Q

metabolic acidosis

A

decreased HCO3 and decrease in pH below 7.35

28
Q

metabolic acidosis causes

A

diabetic acidosis
starvation
impending shock
ASA OD
diarrhea

29
Q

respiratory alkalosis

A

low PCO2 due to hyperventilation (excess amount of CO2 exhaled)
resulting in pH above 7.45

30
Q

respiratory alkalosis causes

A

hysteria
fear
anxiety
head injury
pain
fever
ventilator

31
Q

metabolic alkalosis

A

increased HCO3 and an increase in pH above 7.45

32
Q

metabolic alkalosis causes

A

diuretics
prolonged NG suction without electrolyte replacement
excessive vomiting
overuse of antacids

33
Q

shift to the left

A

Hgb increases its affinity
easier for the Hgb to pick up O2, but harder to release O2 into the tissues
more O2 stays on Hgb and returns to lungs
result in tissue hypoxia even though there is sufficient O2 in blood

34
Q

effects of shift to the left

A

low CO2
low body temp
high CO
high pH
decreased 2,3-DPG

35
Q

shift to the right

A

Hgb loses its affinity
harder to bind, easier to release

36
Q

shift to the right effects

A

high CO2
high temp
low CO
low pH
increased 2,3-DPG

37
Q

normal V/Q

A

4:5

38
Q

V/Q > 0.8

A

ventilation exceeds perfusion

39
Q

V/Q < 0.8

A

poor ventilation

40
Q

pulmonary perfusion

A

distribution of perfusion is gravity dependent
preferential blood flow to gravity dependent areas

41
Q

causes of impaired perfusion

A

decreased Hgb: anemia, CO poisoning
decreased flow: hemorrhage, PE, pulmonary vasoconstriction
physiologic shunt: anatomic left to right cardiac shunt

42
Q

alveolar dead space

A

occurs in diseased states when alveoli are ventilated but not perfused
only occurs with PE
ventilation with no perfusion

43
Q

pulmonary absolute shunt

A

anatomic shunt + intrapulmonary shunt

44
Q

pulmonary anatomic shunt

A

blood vessel skips alveoli, doesn’t get diffusion
blood that moves from the right heart into the left heart without coming into contact with alveoli

45
Q

intrapulmonary shunt

A

perfusion but no ventilation
no diffusion
no surface area
aka right to left shunt

46
Q

shunt-like effect

A

not a true shunt
excess of perfusion in relation to alveolar ventilation
alveolar ventilation is reduced

47
Q

obstructive lung disease

A

difficulty exhaling all the air from the lungs
abnormally high amount of air still lingers in lungs (air trapping)

48
Q

types of obstructive lung disease

A

COPD
asthma
bronchiectasis
cystic fibrosis

49
Q

restrictive lung disease

A

cannot fully fill their lungs with air
lungs are restricted from fully expanding
from conditions causing stiffness in lungs

50
Q

types of restrictive lung disease

A

interstitial lung disease (idiopathic pulmonary fibrosis)
sarcoidosis
obesity
scoliosis neuromuscular disease (Muscular dystrophy, ALS0

51
Q

signs of impaired gas exchange

A

tachypnea
restlessness
anxiety
confusion
crackles
decreased PaO2, SaO2
increased PaCO2, pH
intrapulmonary shunt
infiltrates by CXR

52
Q

acute respiratory distress syndrom

A

pathologic injury to the lung occurring from a wide diversity of causes and associated conditions
inflammatory syndrome marked by disruption of alveolar-capillary membrane

53
Q

clinical definition of ARDS

A

acute onset
bilateral infiltrates on CXR
PAWP < 18 mmHg or no clinical evidence of left ventricular failure
hypoxemia refractory to O2 tx

54
Q

direct causes of ARDS

A

aspiration of gastric contents or other substances
viral or bacterial pneumonia
chest trauma embolism: fat, air, amniotic fluid, thrombus
inhalation of toxic substance
near-drowning
O2 toxicity
radiation pneumonitis

55
Q

indirect causes of ARDS

A

sepsis
severe massive trauma
acute pancreatitis
anaphylaxis
cardiopulmonary bypass
DIC
opioid drug overdose
severe head injury
shock states
transfusion-related

56
Q

signs and symptoms of ARDS

A

severe shortness of breath
dyspnea
labored breathing
tachypnea
low O2 levels in blood
cough and fever
hypotension
confusion
extreme tiredness

57
Q

pathophysiology of ARDS

A

increase in permeability of the alveolar-capillary barrier, leading to an influx into the alveoli
type 1 and type 2 epithelial cell destruction
initiation of inflammatory-immune response
activation of cytokines

58
Q

release of mediators: what causes increase in capillary membrane permeability

A

alveolar flooding
damage to alveolar epithelial cells type 1 and 2
loss of surfactant
alveolar collapse or filling

59
Q

release of mediators: change in small airway diameter

A

increased airway resistance
decreased lung compliance

60
Q

release of mediators: injury to pulmonary vasculature

A

pulmonary vasoconstriction
microemboli formation (DIC)
pulmonary hypertension
alveolar dead space
increased PVR
decreased CO

61
Q

effects of increased work of breathing

A

alveolar hypoventilation
V/Q mismatching
intrapulmonary shunting

causes hypoxemia refractory to oxygen therapy

62
Q

tests and diagnostics for ARDS

A

imaging: CXR, CT, bronchoscopy
labs: ABG, BMP, CBC, blood/urine/sputum CX
heart tests: electrocardiogram, echocardiogram

63
Q

collaborative management ARDS

A

treat underlying cause
promote pulmonary gas exchange
fluids: NS, LR
meds: abx, vasopressors, anti-clots, pain meds

64
Q

ARDS complications

A

pulmonary fibrosis, barotrauma, PE, VAP
pneumothorax
cardiac dysfunctions
blood clots
acute renal failure
memory, cognitive, and emotional problems

NURS 470 (28 decks)

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