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
respiratory acidosis
excessive retention of CO2 due to hypoventilation leading to a decrease in pH below 7.35
26
respiratory acidosis causes
COPD pneumonia atelectasis neuromuscular disease post-op recovery narcotics
27
metabolic acidosis
decreased HCO3 and decrease in pH below 7.35
28
metabolic acidosis causes
diabetic acidosis starvation impending shock ASA OD diarrhea
29
respiratory alkalosis
low PCO2 due to hyperventilation (excess amount of CO2 exhaled) resulting in pH above 7.45
30
respiratory alkalosis causes
hysteria fear anxiety head injury pain fever ventilator
31
metabolic alkalosis
increased HCO3 and an increase in pH above 7.45
32
metabolic alkalosis causes
diuretics prolonged NG suction without electrolyte replacement excessive vomiting overuse of antacids
33
shift to the left
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
effects of shift to the left
low CO2 low body temp high CO high pH decreased 2,3-DPG
35
shift to the right
Hgb loses its affinity harder to bind, easier to release
36
shift to the right effects
high CO2 high temp low CO low pH increased 2,3-DPG
37
normal V/Q
4:5
38
V/Q > 0.8
ventilation exceeds perfusion
39
V/Q < 0.8
poor ventilation
40
pulmonary perfusion
distribution of perfusion is gravity dependent preferential blood flow to gravity dependent areas
41
causes of impaired perfusion
decreased Hgb: anemia, CO poisoning decreased flow: hemorrhage, PE, pulmonary vasoconstriction physiologic shunt: anatomic left to right cardiac shunt
42
alveolar dead space
occurs in diseased states when alveoli are ventilated but not perfused only occurs with PE ventilation with no perfusion
43
pulmonary absolute shunt
anatomic shunt + intrapulmonary shunt
44
pulmonary anatomic shunt
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
intrapulmonary shunt
perfusion but no ventilation no diffusion no surface area aka right to left shunt
46
shunt-like effect
not a true shunt excess of perfusion in relation to alveolar ventilation alveolar ventilation is reduced
47
obstructive lung disease
difficulty exhaling all the air from the lungs abnormally high amount of air still lingers in lungs (air trapping)
48
types of obstructive lung disease
COPD asthma bronchiectasis cystic fibrosis
49
restrictive lung disease
cannot fully fill their lungs with air lungs are restricted from fully expanding from conditions causing stiffness in lungs
50
types of restrictive lung disease
interstitial lung disease (idiopathic pulmonary fibrosis) sarcoidosis obesity scoliosis neuromuscular disease (Muscular dystrophy, ALS0
51
signs of impaired gas exchange
tachypnea restlessness anxiety confusion crackles decreased PaO2, SaO2 increased PaCO2, pH intrapulmonary shunt infiltrates by CXR
52
acute respiratory distress syndrom
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
clinical definition of ARDS
acute onset bilateral infiltrates on CXR PAWP < 18 mmHg or no clinical evidence of left ventricular failure hypoxemia refractory to O2 tx
54
direct causes of ARDS
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
indirect causes of ARDS
sepsis severe massive trauma acute pancreatitis anaphylaxis cardiopulmonary bypass DIC opioid drug overdose severe head injury shock states transfusion-related
56
signs and symptoms of ARDS
severe shortness of breath dyspnea labored breathing tachypnea low O2 levels in blood cough and fever hypotension confusion extreme tiredness
57
pathophysiology of ARDS
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
release of mediators: what causes increase in capillary membrane permeability
alveolar flooding damage to alveolar epithelial cells type 1 and 2 loss of surfactant alveolar collapse or filling
59
release of mediators: change in small airway diameter
increased airway resistance decreased lung compliance
60
release of mediators: injury to pulmonary vasculature
pulmonary vasoconstriction microemboli formation (DIC) pulmonary hypertension alveolar dead space increased PVR decreased CO
61
effects of increased work of breathing
alveolar hypoventilation V/Q mismatching intrapulmonary shunting causes hypoxemia refractory to oxygen therapy
62
tests and diagnostics for ARDS
imaging: CXR, CT, bronchoscopy labs: ABG, BMP, CBC, blood/urine/sputum CX heart tests: electrocardiogram, echocardiogram
63
collaborative management ARDS
treat underlying cause promote pulmonary gas exchange fluids: NS, LR meds: abx, vasopressors, anti-clots, pain meds
64
ARDS complications
pulmonary fibrosis, barotrauma, PE, VAP pneumothorax cardiac dysfunctions blood clots acute renal failure memory, cognitive, and emotional problems