gas exchange Flashcards

1
Q

purpose of ABG’s

A

to measure acid-base balance in the body

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2
Q

oxygenation

A

the process of getting O2 into the body

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3
Q

ventilation

A

the process of eliminating CO2 from the body

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4
Q

respiratory failure as an indication for ABG

A
  • evaluates efficiencty of oxygenation and ventilation
  • helps determine if intubation and mechanical ventilation are necessary
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5
Q

mechanical ventilation as an indication for an ABG

A
  • ongoing monitoring of a patients response to the ventilation
  • helps guide ventilator settings
  • evaluates pt response and readiness to be weaned from ventilator
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6
Q

critical illness as an indication for ABG

A
  • evaluates pt response to treatment and interventions
  • assists in prognosing patients condition
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7
Q

pH

A

normal is 7.35-7.45
- lower than 7.35 is considered acidotic
- greater than 7.45 is considered alkalotic

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8
Q

CO2

A

lungs/respiratory; normal is 45-35
- greater than 45 is acidotic
- less than 35 is alkalotic

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9
Q

HCO3

A

carbonic acid; metabolic/kidneys; normal range is 22-26; excreted in lungs; considered a base
- lower than 22 is acidotic
- higher than 26 is alkalotic

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10
Q

H+

A

metabolic acid; metabolic/kidneys; excreted in kidneys

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11
Q

respiratory acidosis

pH and CO2

A

increased CO2, decreased pH

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12
Q

respiratory alkalosis

pH and CO2

A

decreased CO2, increased pH

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13
Q

metabolic acidosis

pH and HCO3

A

decreased HCO3, decreased pH
- may be caused by a-fib as there is poor perfusion leading to anaerobic metabolism causing lactic acid buildup

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14
Q

metabolic alkalosis

pH and HCO3

A

increased HCO3, increased pH

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15
Q

respiratory acidosis patho

A

too much CO2 or carbonic acid caused by hypoventilation
- renal compensation through excretion of H and retention of HCO3
- can be seen in asthma, COPD, pneumonia, pulmonary edema, sleep apnea

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16
Q

respiratory alkalosis patho

A

too little CO2 (blowing off more than being produced) caused by hyperventilation
- renal compensation by decreased H production and increased HCO3 secretion
- can be seen in MI, asthma, anxiety, COPD, sepsis, DKA, PE

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17
Q

metabolic acidosis patho

A

too much metabolic acid and get rid of too much base (HCO3); too much acid in body
- increased secretion of H and increased retention of HCO3
- respiratory compensates by hyperventilation
- can be caused by DKA, excessive diarrhea or vomiting, lactic acidosis, HF, seizures, liver failure

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18
Q

metabolic alkalosis patho

A

too little metabolic acid
- correct through decreased secretion of H and increased secretion of HCO3
- respiratory compensates through hypoventilation
- can be caused by overuse of diuretics, large loss of potassium or sodium in short amount of time

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19
Q

chloride responsive alkalosis

metabolic alkalosis

A

loss of H by vomiting or dehydration

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20
Q

chloride-resistant alkalosis

metabolic alkalosis

A

body retains too much HCO3 or shift of H from blood to cells

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21
Q

respiratory acidosis s/s

A
  • hypoxia d/t hypoventilation
  • shallow/rapid breathing
  • decreased BP
  • pale
  • hyperkalemia –> dysrhythmias
  • dizzy
  • muscle weakness
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22
Q

respiratory alkalosis s/s

A
  • seizures
  • deep breathing/rapid
  • hyperventilation
  • tachy
  • decrease or normal BP
  • hypokalemia
  • numbness
  • lethargy
  • light headed
  • n/v
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23
Q

metabolic acidosis s/s

A
  • decreased BP
  • hyperkalemia
  • muscle twitching
  • vasodilation (warm/flush skin)
  • n/v
  • decreased muscle tone and reflex
  • hyperventilation
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24
Q

metabolic alkalosis s/s

A
  • restlessness followed by lethargy
  • dysrhythmias (tachy)
  • hypoventilation
  • confusion
  • n/v
  • tremors, tingling, muscle cramps
  • hypokalemia
25
Q

full compensation

A

pH presents as normal
- body is correcting the imbalance

26
Q

partial compensation

A

all 3 values (pH, CO2, HCO3) are abnormal
- body is attempting to correct the imbalance

27
Q

uncompensation

A

CO2 or HCO3 is within normal limits and the other value
(CO2 or HCO3) is abnormal ‘
- body has made no attempt to correct

28
Q

outcomes when compensatory mechanisms fail

A
  • altered cell function, esp in brain
  • change in intracellular enzyme activity causing cell dysfunction
  • decreased LOC caused by acidosis
  • decreased LOC and other neuro manifestations caused by alkalosis
29
Q

potassium and acidosis

A

shifts out of cell into blood (swaps with H) and causes hyperkalemia

30
Q

potassium and alkalosis

A

H switches to ECF and K moves in to cell or becomes excreted causing hypokalemia
- remember “K-low sis”

31
Q

treatment/intervention for metabolic acidosis

A

hemodialysis, NaHCO3 admin

32
Q

treatment/intervention for metabolic alkalosis

A
  • sodium chloride in chloride responsive alkalosis
  • diamox which increases HCO3 excretion
  • hemodialysis
33
Q

preventative interventions for respiratory acidosis (hypoventilation)

A
  • bronchodilators
  • CPAP/BiPAP, give O2, ventilator
34
Q

prevention of respiratory alkalosis (hyperventilation)

A

breathe into paper bag to re-breath CO2, pursed lip breathing

35
Q

left lung

36
Q

right lung

37
Q

lung anatomy

A

bronchi –> bronchioles –> alveoli
- apex: top of lungs
- base: bottom of lungs

38
Q

parietal pleura

A

covers body wall

39
Q

visceral pleura

A

covers lungs

40
Q

pleural fluid

A

between the 2 pleura to decrease friction

41
Q

Asthma

A

exaggerated hypersensitivity response to allergens, exercise, etc..

42
Q

COPD

A

airway obstruction due to hyperinflation, mucus hypersecretion, gas exchange abnormalities

43
Q

pneumothroax

A

presence of air in the lungs
- common in young, tall, thin males
- closed: air moves from alveoli into pleural space
- open: air enters in inspiration and exits during expiration

44
Q

tension pneumothroax

A

pleura acts as one way valve where air can enter but cannot exit
- look for mediastinal shift to their left side

45
Q

PE

A

caused by DVT
- s/s are chest pain, SOB, low O2
- need CT to diagnose

46
Q

crackles

A

popping sounds; more
- common during inspiration
- can be coarse or fine

47
Q

wheezing

A

continuous; high or low
- more pronounced on expiration

48
Q

DKA

A

no insulin in the body and breaks down fats which releases ketones; glucose stays in blood
- hyperglycemia
- keotsis
- acidosis

49
Q

acute pancreatitis

A

does not lead to chronic unless complications develop
- can be caused by alcohol abuse or gallstones

50
Q

chronic pancreatitis

A

inflammatory disorder caused by progressive destruction on pancreas

51
Q

cholecystitis

A

inflammation of gallbladder which can be caused by bacteria, alterations in fluid and electrolytes, and bile stasis
- increase in WBC will be seen

52
Q

gallbladder location

A

right side of abdomen just beneath liver

53
Q

sepsis

A

innapropriate and extreme systemic response to infection; pathogen in organ or blood leads to extreme vasodilation and hypoperfusion –> can lead to activation of coagulation system which then forms clots whether or not there is bleeding due to cytokines
- can be a product of respiratory alkalosis

54
Q

atelectasis

A

collapse of alveoli where there is not enough ventilation but perfusion is adequate
- increased risk for hypoxia

55
Q

chronic bronchitis

type of COPD

A

chronic productive cough greater than 3 months
- inflammation and secretions of bronchioles

56
Q

emphysema

type of COPD

A

airspace in alveoli is increased and alveoli walls are stiff leading to trapped air

57
Q

cardiogenic pulmonary edema

A

increase in capillary hydrostatic pressure and pulmonary circulation backs up into the lungs
- leading and related to left sided heart failure

58
Q

ARDS

A

occurs within 1 week of respiratory changes from original event relating to inflammation
- increased CO2 in blood, decreased O2 inhalation leading to hypoxemia and hypercapnia