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Foundations 2 > Unit 2-Acid/Base > Flashcards

Unit 2-Acid/Base Flashcards

1
Q

acid base balance

A

•homeostasis of H+ concentration in body fluids
•maintained by shift of H+ b/t extra/intra cellular fluids
•maintained by H+ ion production matching H+ ion loss
*minor [H+] changes have major cellular fxn effects

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2
Q

[H+] and pH relationship

A
  • lower pH -> more free H+
  • inversely proportional
  • 1 pH unit represents tenfold change in free H+
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3
Q

changes in pH causes…

A
  • change of shape/fxn of hormones and NZs
  • change of distribution of electrolytes (-> imbalances)
  • changes in excitable membranes (nerves less or more active)
  • decreasing effectiveness of drugs
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4
Q

acids

A

•substances that release H+ when dissolved in H2O
•produced from metab of protein (sulfuric acid), carbohydrates (CO2) and fatty acids (fatty acids and ketoacids)
*CO2 (carbonic acid) most important regulated by LUNGS

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5
Q

volatile acid

A
  • can be converted to gases
  • CO2 (acid component in blood) produced as aerobic carb metabolism
  • CO2 binds w/ H2O to form carbonic acid (H2CO3)
  • H2CO3 excreted from LUNGS during breathing in gaseous form of CO2
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6
Q

nonvolatile acid

A

•fixed acids that can’t be converted to gases
•excreted by kidneys
•3 metab products
1. sulfuric and phosphoric acid produced by protein metabolism
2. ketoacids produced by incomplete lipid metabolism
3. lactic acids produced by anaerobic carb metab

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7
Q

lactic acid

A
  • nonvolatile
  • produced when incomplete breakdown of glucose occurs when cells metabolize under anaerobic conditions
  • produced during hypoxia, sepsis, and shock
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8
Q

base

A

•substance that binds to free H+ in H2O
•less H+ -> more basic
•strong bases bind to H+ easily
*bicarbonate most important regulated by KIDNEY

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9
Q

body acid base ratio

A

•1 (H2CO3) : 20 HCO3

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10
Q

fatal ECF pH

A
  • below 6.9

* above 7.8

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11
Q

normal PCO2

A

35-45 mmHg

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12
Q

normal HCO3

A

22-26 mEq/L

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13
Q

3 regulators of acid base

A
  • chemical/protein buffers
  • respiratory
  • renal
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14
Q

chemical buffers

A
  • 1st of defense against abnormal pH fluctuations
  • bind/release H+ rapidly
  • bicarbonate (primary)- ECF and ICF
  • phosphate- ICF
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15
Q

bicarbonate (HCO3)

A

•most common/important (weak) base in blood

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16
Q

protein buffers

A
  • most common chemical buffers
  • albumin/globulins- ECF
  • Hgb- ICF
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17
Q

Hgb as buffer

A
  • when amount free H+ is high, Hgb within RBCs binds to H+ ions
  • results in fewer H+ ions in blood -> pH back up
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18
Q

respiratory system as regulator

A
  • 2nd line of defense
  • lungs control amnt of free H+ by controlling amnt of CO2 in arteriole blood
  • chemoreceptors in medulla increase/decrease rate of breathing based on CO2 levels
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19
Q

CO2 production/excretion

A

•produced by aerobic carb metabolism
•converted to H+ when combines w/ H2O to form H2CO3 (carbonic acid)
•lungs excrete H2CO3 in gaseous from of CO2
*pH determined by how much CO2 produced by cells during metabolism vs how rapidly CO2 is removed by lungs during breathing
*CO2 level directly r/t H+ level

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20
Q

respiratory fxn in regards to pH

A
  • response in minutes
  • TEMPORARY changes
  • regulates blood CO2 by varying rate/depth of breathing
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21
Q

low HCO3

A
  • quicker, deeper breathing
  • high H2CO3 (free H+)
  • high CO2 -> exhaled
  • hyperventilation (decrease H+)
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22
Q

high HCO3

A
  • slower, shallow breathing
  • low H2CO3 (free H+)
  • low CO2 -> retained
  • hypoventilation (increase H+)
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23
Q

kidney as regulator

A
  • 3rd line of defense
  • act hrs to days
  • reabsorb/excrete acids/bases
  • replenishes bicarbonate
  • form acids
  • form ammonium
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24
Q

kidney response to high PaCO2 (high H2CO3)

A
  • bicarbonate retained

* acid excreted

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25
Q

kidney response to low PaCO2 (low H2CO3)

A
  • bicarbonate excreted

* acid retained

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26
Q

compensated

A

•pH normal
•acid/base components may be abnormal, but they are balanced
*most abnormal is reason

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27
Q

uncompensated

A
  • pH abnormal and one other value

* buffer/regulatory mechanisms have not begun to correct imbalance

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28
Q

partially compensated

A
  • all values abnormal abnormal (CO2 and HCO3 in same direction)
  • evidence buffer/regulatory mechanisms have begun to respond
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29
Q

acid-base imbalances

A
  • result of insufficient compensation

* resp./renal fxn play major role

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30
Q

respiratory compensation

A

•more sensitive to changes
•rapid
•usually corrects imbalances due to metabolic problems
Ex: prolonged running -> lactic acid build-up -> H+ in ECF increase -> breather faster/deeper

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31
Q

kidney compensation

A
  • occurs when resp. comp isn’t enough
  • more powerful than resp.
  • Ex: CO2 levels in COPD high -> kidney excrete H+ and reabsorb HCO3
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32
Q

respiratory acidosis labs

A
  • pH < 7.35
  • CO2 > 45
  • HCO3 normal (22-26)
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33
Q

respiratory acidosis causes

A
  • area of resp fxn impaired, reducing exchange of O2 and CO2

* impairment leads to increase in CO2 (hypercapnia), thus increase in H+

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34
Q

respiratory acidosis etiology (4)

A
  1. respiratory depression
  2. inadequate chest expansion
  3. airway obstruction
  4. reduced alveolar capillary diffusion of gases
35
Q

respiratory acidosis s/s

A
  • dyspnea, tachypenic
  • anxiety/irritability/disorientation
  • hypoventilation -> hypoxemia (b/c no where for O2 to bind)
  • hyPOtension
  • tachycardia
  • headache
  • hypERkalemia -> dysrhythmias
36
Q

hypoventilation

A 
•not breathing enough (getting rid of enough CO2)
•rapid/shallow breaths
•vasodilation
•hypercapnia
*blood becomes ACIDIC
37
Q

why does acidosis cause hyperkalemia

A
  • The body tries to maintain electro-neutrality during buffering by moving H+ move from blood (to decrease the amount of acids) into cells
  • which causes excess positive ions so the positively charged K+ ions must move out of cells and into blood
38
Q

respiratory acidosis tx

A
  • The body tries to maintain electro-neutrality during buffering by moving H+ move from blood (to decrease the amount of acids) into cells
  • which causes excess positive ions so the positively charged K+ ions must move out of cells and into blood
39
Q

respiratory alkalosis labs

A
  • pH > 7.45
  • PaCO2 < 35 mmHg
  • HCO3 normal (22-26)
40
Q

respiratory alkalosis etiology

A 
•hypoxemia stimulated hyperventilation 
-emphysema; pneumonia
•impaired lung expansion (ascites, scoliosis, preggo)
•Salicylates (aspirin) OD
•CNS trauma/tumor
•excessive exercise/stress/pain
•anxiety
•diabetes
41
Q

respiratory alkalosis s/s

A
  • Tachypnea; hyperpnea, tachycardia
  • Giddiness, dizziness, syncope, convulsions, or coma
  • Weakness, paresthesias, tetany
  • Hypokalemia
  • Hypocalcemia
42
Q

hyperventilation

A 
•deep, labored, rapid breathing
•vasconstriction
•hypocapnia 
•Kussmaul respirations
*blood becomes BASIC
43
Q

respiratory alkalosis tx

A
  • treat cause
  • increase CO2 retention
  • CO2 rebreathing
  • sedation
44
Q

metabolic acidosis labs

A

•pH < 7.35
•PaCO2 normal (35-45)
•HCO3 < 22
*fixed acid excess and base deficit

45
Q

metabolic acidosis etiology

A 
•renal failure
•DMKA
•lactic acidosis
•ingested toxins (aspirin, antifreeze)
•carbonic anhydrase inhibitors (Diamox)
*over-production/under-elimination of H+
*underproduction/over-elimation HCO3
46
Q

metabolic acidosis s/s

A
  • Tachypnea (hyper) “Kussmaul’s”
  • Hypotension- poor tissue perfusion as condition worsens
  • Drowsiness,confusion, or coma
  • Headache, dec. DTRs & muscle tone
  • Altered GI: anorexia, N/V
  • Hyperkalemia
47
Q

why diabetes ketoacidosis contributes to metabolic acidosis

A
  • insulin drives glucose into cells, which is necessary for metabolism
  • if no glucose, metabolism of other products, increasing acid production
48
Q

metabolic acidosis tx

A
  • treat cause
  • correct electrolytes
  • IV NaHCO3
49
Q

metabolic alkalosis labs

A

•pH > 7.45
•PaCO2 normal (35-45)
•HCO3 > 26
*fixed acid deficit or base excess

50
Q

metabolic alkalosis etiology

A 
•hypokalemia (diuresis, steroids)
•gastric fluid loss
•overcorrection of acidosis w/ NaCO3
•massive transfusion w/ whole blood
•hyperaldosteronism
•licorice intoxication
*base excess and acid deficit
51
Q

metabolic alkalosis s/s

A
  • Tachycardia, Hypoventilation (compensatory)
  • Dysrhythmias
  • Paresthesias, muscle weakness, confusion
  • Hypokalemia
  • Hypocalcemia
52
Q

diuretics and alkalosis

A
  • diuretics cause loss of fluid not containing HCO3
  • ECF reduction results in hypovolemia (diuresis), which stimulates vomiting and aldosterone release
  • there is then an increase in HCO3 and increased H+/K+ secretion
53
Q

metabolic alkalosis tx

A
  • diuretics causes loss of fluid not containing HCO3
  • ECF reduction results in hypovolemia (diuresis), which stimulates vomiting and aldosterone release
  • there is then an increase in HCO3 and increased H+/K+ secretion
54
Q

mixed acid-base disorders

A

•two primary acid-base imbalances coexist

55
Q

cardiac arrest

A
  • mixed acid base disorder
  • lactic acid accumulation
  • elevated H2CO3 (resp. arrest)
56
Q

COPD

A
  • mixed acid base disorder
  • resp. acidosis
  • metabolic alkalosis secondary to diuretic/steroid tx
57
Q

arterial blood gas draw

A
  • mixed acid base disorder
  • resp. acidosis
  • metabolic alkalosis secondary to diuretic/steroid tx
58
Q

normal PaO2 levels

A
  • 80-100 mmHg

* amount of O2 dissolved in arterial blood

59
Q

normal SaO2 levels

A

96-100%

*amnt O2 dissolved in blood

60
Q

anion gap levels

A

•10-14 mEq/L

61
Q

compensation present

A
  • PaCO2 and HCO3 abnormal in opposite directions

* one acidotic and other alkalotic

62
Q

compensation absent

A

•PaCO2 or HCO3 abnormal, while the other is normal

63
Q

pH as primary disorder

A

•if pH is clearly abnormal

64
Q

deviant component as primary disorder

A
  • if pH is normal or near normal

* more deviant component should be consistent with pH (acidotic or alkalotic)

65
Q

analysis of ABG

A
  1. classify pH
  2. assess PaCO2
  3. assess HCO3
  4. compensation present?
  5. ID primary disorder
  6. classify degree of compensation
66
Q

nursing interventions respiratory acidosis

A

•O2; patent airway; enhance gas exchange via…

  • positioning
  • breathing technique
  • vent support
  • bronchodilators
  • mucolytics
67
Q

nursing interventions respiratory alkalosis

A
  • O2 therapy
  • anxiety interventions
  • rebreathing techniques
68
Q

nursing interventions metabolic acidosis

A
  • DKA- admin insulin
  • GI losses- admin antidiarrheals; rehydrate
  • low serum HCO3- admin NaHCO3
69
Q

nursing interventions metabolic alkalosis

A
  • GI loses- antiemetics, fluids, electrolytes

* K+ depletion- discontinue causative agent (diuretic)

70
Q

COPD pt. considerations

A

•tend to have chronic resp. acidosis
•if exacerbate, need O2
•their drive to breathe is when O2 drops, rather than higher CO2
*have to be careful when giving O2 b/c their drive to breathe will be decreased and you can put them into resp. failure

71
Q

complications of acid-base imbalances

A
  • convulsions
  • coma
  • respiratory arrest
  • important to implement seizure precautions and provide life support if necessary
72
Q

characteristic symptoms of acidosis

A
  • hyperkalemia

* hyperreflexia

73
Q

characteristic symptoms of alkalosis

A
  • hypokalemia

* muscle weakness

74
Q

metabolic acidosis –>

A
  • respiratory system tries to compensate
  • CO2 blown off
  • Kussmaul’s deep rapid breaths
75
Q

hyperventilation is a cause of ____ and a symptom of ____

A
  • respiratory alkalosis

* metabolic acidosis

76
Q

good indicator of metabolic acidosis during hyperventilation

A

•severe diarrhea

77
Q

good indicator of respiratory acidosis during hyperventilation

A

•anxiety

78
Q

partially comp. resp. acidosis

A
  • pH down

* CO2 and HCO3 up

79
Q

partially comp. resp. alkalosis

A
  • pH up

* CO2 and HCO3 down

80
Q

partially comp. met. acidosis

A

•all down

81
Q

partially comp. met. alkalosis

A

•all up

82
Q

combined acid-base balance

A
  • pH abnormal

* CO2 and HCO3 in opposite directions

83
Q

high HCO3 during compensated

A
  • problem is resp. acidosis

* high HCO3 is usually comp. mechanism

Foundations 2 (10 decks)

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