Unit 2-Acid/Base Flashcards
(83 cards)
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
2
Q
[H+] and pH relationship
A
- lower pH -> more free H+
- inversely proportional
- 1 pH unit represents tenfold change in free H+
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
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
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
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
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
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
9
Q
body acid base ratio
A
•1 (H2CO3) : 20 HCO3
10
Q
fatal ECF pH
A
- below 6.9
* above 7.8
11
Q
normal PCO2
A
35-45 mmHg
12
Q
normal HCO3
A
22-26 mEq/L
13
Q
3 regulators of acid base
A
- chemical/protein buffers
- respiratory
- renal
14
Q
chemical buffers
A
- 1st of defense against abnormal pH fluctuations
- bind/release H+ rapidly
- bicarbonate (primary)- ECF and ICF
- phosphate- ICF
15
Q
bicarbonate (HCO3)
A
•most common/important (weak) base in blood
16
Q
protein buffers
A
- most common chemical buffers
- albumin/globulins- ECF
- Hgb- ICF
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
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
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
20
Q
respiratory fxn in regards to pH
A
- response in minutes
- TEMPORARY changes
- regulates blood CO2 by varying rate/depth of breathing
21
Q
low HCO3
A
- quicker, deeper breathing
- high H2CO3 (free H+)
- high CO2 -> exhaled
- hyperventilation (decrease H+)
22
Q
high HCO3
A
- slower, shallow breathing
- low H2CO3 (free H+)
- low CO2 -> retained
- hypoventilation (increase H+)
23
Q
kidney as regulator
A
- 3rd line of defense
- act hrs to days
- reabsorb/excrete acids/bases
- replenishes bicarbonate
- form acids
- form ammonium
24
Q
kidney response to high PaCO2 (high H2CO3)
A
- bicarbonate retained
* acid excreted
25
kidney response to low PaCO2 (low H2CO3)
* bicarbonate excreted
| * acid retained
26
compensated
•pH normal
•acid/base components may be abnormal, but they are balanced
*most abnormal is reason
27
uncompensated
* pH abnormal and one other value
| * buffer/regulatory mechanisms have not begun to correct imbalance
28
partially compensated
* all values abnormal abnormal (CO2 and HCO3 in same direction)
* evidence buffer/regulatory mechanisms have begun to respond
29
acid-base imbalances
* result of insufficient compensation
| * resp./renal fxn play major role
30
respiratory compensation
•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
31
kidney compensation
* occurs when resp. comp isn't enough
* more powerful than resp.
* Ex: CO2 levels in COPD high -> kidney excrete H+ and reabsorb HCO3
32
respiratory acidosis labs
* pH < 7.35
* CO2 > 45
* HCO3 normal (22-26)
33
respiratory acidosis causes
* area of resp fxn impaired, reducing exchange of O2 and CO2
| * impairment leads to increase in CO2 (hypercapnia), thus increase in H+
34
respiratory acidosis etiology (4)
1. respiratory depression
2. inadequate chest expansion
3. airway obstruction
4. reduced alveolar capillary diffusion of gases
35
respiratory acidosis s/s
* dyspnea, tachypenic
* anxiety/irritability/disorientation
* hypoventilation -> hypoxemia (b/c no where for O2 to bind)
* hyPOtension
* tachycardia
* headache
* hypERkalemia -> dysrhythmias
36
hypoventilation
```
•not breathing enough (getting rid of enough CO2)
•rapid/shallow breaths
•vasodilation
•hypercapnia
*blood becomes ACIDIC
```
37
why does acidosis cause hyperkalemia
* 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
respiratory acidosis tx
* 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
respiratory alkalosis labs
* pH > 7.45
* PaCO2 < 35 mmHg
* HCO3 normal (22-26)
40
respiratory alkalosis etiology
```
•hypoxemia stimulated hyperventilation
-emphysema; pneumonia
•impaired lung expansion (ascites, scoliosis, preggo)
•Salicylates (aspirin) OD
•CNS trauma/tumor
•excessive exercise/stress/pain
•anxiety
•diabetes
```
41
respiratory alkalosis s/s
* Tachypnea; hyperpnea, tachycardia
* Giddiness, dizziness, syncope, convulsions, or coma
* Weakness, paresthesias, tetany
* Hypokalemia
* Hypocalcemia
42
hyperventilation
```
•deep, labored, rapid breathing
•vasconstriction
•hypocapnia
•Kussmaul respirations
*blood becomes BASIC
```
43
respiratory alkalosis tx
* treat cause
* increase CO2 retention
* CO2 rebreathing
* sedation
44
metabolic acidosis labs
•pH < 7.35
•PaCO2 normal (35-45)
•HCO3 < 22
*fixed acid excess and base deficit
45
metabolic acidosis etiology
```
•renal failure
•DMKA
•lactic acidosis
•ingested toxins (aspirin, antifreeze)
•carbonic anhydrase inhibitors (Diamox)
*over-production/under-elimination of H+
*underproduction/over-elimation HCO3
```
46
metabolic acidosis s/s
* 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
why diabetes ketoacidosis contributes to metabolic acidosis
* insulin drives glucose into cells, which is necessary for metabolism
* if no glucose, metabolism of other products, increasing acid production
48
metabolic acidosis tx
* treat cause
* correct electrolytes
* IV NaHCO3
49
metabolic alkalosis labs
•pH > 7.45
•PaCO2 normal (35-45)
•HCO3 > 26
*fixed acid deficit or base excess
50
metabolic alkalosis etiology
```
•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
metabolic alkalosis s/s
* Tachycardia, Hypoventilation (compensatory)
* Dysrhythmias
* Paresthesias, muscle weakness, confusion
* Hypokalemia
* Hypocalcemia
52
diuretics and alkalosis
* 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
metabolic alkalosis tx
* 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
mixed acid-base disorders
•two primary acid-base imbalances coexist
55
cardiac arrest
* mixed acid base disorder
* lactic acid accumulation
* elevated H2CO3 (resp. arrest)
56
COPD
* mixed acid base disorder
* resp. acidosis
* metabolic alkalosis secondary to diuretic/steroid tx
57
arterial blood gas draw
* mixed acid base disorder
* resp. acidosis
* metabolic alkalosis secondary to diuretic/steroid tx
58
normal PaO2 levels
* 80-100 mmHg
| * amount of O2 dissolved in arterial blood
59
normal SaO2 levels
96-100%
| *amnt O2 dissolved in blood
60
anion gap levels
•10-14 mEq/L
61
compensation present
* PaCO2 and HCO3 abnormal in opposite directions
| * one acidotic and other alkalotic
62
compensation absent
•PaCO2 or HCO3 abnormal, while the other is normal
63
pH as primary disorder
•if pH is clearly abnormal
64
deviant component as primary disorder
* if pH is normal or near normal
| * more deviant component should be consistent with pH (acidotic or alkalotic)
65
analysis of ABG
1. classify pH
2. assess PaCO2
3. assess HCO3
4. compensation present?
5. ID primary disorder
6. classify degree of compensation
66
nursing interventions respiratory acidosis
•O2; patent airway; enhance gas exchange via...
- positioning
- breathing technique
- vent support
- bronchodilators
- mucolytics
67
nursing interventions respiratory alkalosis
* O2 therapy
* anxiety interventions
* rebreathing techniques
68
nursing interventions metabolic acidosis
* DKA- admin insulin
* GI losses- admin antidiarrheals; rehydrate
* low serum HCO3- admin NaHCO3
69
nursing interventions metabolic alkalosis
* GI loses- antiemetics, fluids, electrolytes
| * K+ depletion- discontinue causative agent (diuretic)
70
COPD pt. considerations
•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
complications of acid-base imbalances
* convulsions
* coma
* respiratory arrest
* important to implement seizure precautions and provide life support if necessary
72
characteristic symptoms of acidosis
* hyperkalemia
| * hyperreflexia
73
characteristic symptoms of alkalosis
* hypokalemia
| * muscle weakness
74
metabolic acidosis -->
* respiratory system tries to compensate
* CO2 blown off
* Kussmaul's deep rapid breaths
75
hyperventilation is a cause of ____ and a symptom of ____
* respiratory alkalosis
| * metabolic acidosis
76
good indicator of metabolic acidosis during hyperventilation
•severe diarrhea
77
good indicator of respiratory acidosis during hyperventilation
•anxiety
78
partially comp. resp. acidosis
* pH down
| * CO2 and HCO3 up
79
partially comp. resp. alkalosis
* pH up
| * CO2 and HCO3 down
80
partially comp. met. acidosis
•all down
81
partially comp. met. alkalosis
•all up
82
combined acid-base balance
* pH abnormal
| * CO2 and HCO3 in opposite directions
83
high HCO3 during compensated
* problem is resp. acidosis
| * high HCO3 is usually comp. mechanism
