acid-base imbalance Flashcards

1
Q

molecule that releases H+

A

Acid

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2
Q

molecule that accepts H+

A

base

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3
Q

degree to which an acid or base dissociates into ions

A

dissociation constant (pK)

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4
Q

the scale we use to measure the amount of H+ in a solution

A

pH

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5
Q

pH of ECF in the body

A

7.35-7.45

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6
Q

4 chemical buffer systems

A

bicarbonate buffer system
proteins
H+/k+ transcellular exchange
bone buffer system

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7
Q

3 systems for pH regulation

A

chemical buffer systems
respiratory acid/base control
renal acid/base control

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8
Q

describe the bicarbonate buffer system

A

HCO3- can accept H+ to reduce pH
H2CO3 can contribute H+ ions if needed
body can eliminate the components that are not needed

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9
Q

what is the largest buffering system in the body

A

proteins

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10
Q

____ have binding sites for acid and base molecules

A

amphoteric

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11
Q

why do proteins have a delayed onset

A

due to transmembrane movement of acid/base

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12
Q

describe h+/k+ transcellular exchange

A

both ions move freely across the membrane
cells can exchange H+ for K+ as needed to attain equilibrium

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13
Q

which is not a not considered a “buffering system”

A

bone

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14
Q

how does bone help with buffering

A
  • excess H+ can be exchanged for Na+ and K+ on the bone surface
  • can be broken down to release NaHCO3 and CaCO3
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15
Q

when is the bone buffering system mainly active

A

during acute acid loads and chronic acidemia

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16
Q

what system is managed through control of extracellular CO2

A

respiratory acid/base control

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17
Q

where are chemoreceptors in the body to sense changes in pH and pCO2 and alter respiratory rate

A

brainstem, carotids, aorta

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18
Q

this system causes rapid changes in pH
starts within minutes, maximum effect in 12-24hrs

A

respiratory

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19
Q

respiratory acid/base control is not as effective at managing pH as ___

A

kidneys

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20
Q

lungs respond by increasing ventilation rate during ___

A

acidemia
low pCO2 = low formation of carbonic acid

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21
Q

lungs respond by lowering ventilation rate during ____

A

alkalemia
high pCO2 = high formation of carbonic acid

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22
Q

what system is managed through control of H+ and HCO3- excretion

A

renal acid/base control

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23
Q

describe the renal acid/base control

A
  • kidneys excrete h+ ions freely and through creation of H-containng molecules
  • kidneys reabsorb HCO3- as needed for pH balance
  • takes several HOURS - DAYS to reach full effect!! - can be sustained for longer periods
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24
Q

Kidneys excrete H+ and reabsorb HCO3- during ___

A

acidemia

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25
Q

kidneys reabsorb H+ and excrete HCO3- during ___

A

alkalemia

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26
Q

describe the relationship between H+ and K+ in renal acid/base control

A

H+ and K+ excretion are dependent on each other
- kidneys struggle to excrete or reabsorb high amounts of both H+ and K+ simultaneously

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27
Q

increased k+ secretion, impaired H+ secretion

A

hyperkalemia

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28
Q

increased K+ reabsorption, impaired H+ reabsorption

A

hypokalemia

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29
Q

inappropriate excess of HCO3- and loss of Cl-

A

hypochloremic alkalosis

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30
Q

inappropriate excess of Cl- and loss of HCO3-

A

hyperchloremic acidosis

31
Q

4 tools to assess acid-base status

A
  1. hx
  2. PE
  3. BMP
  4. ABG
32
Q

which tool to assess acid-base status must be adjusted prior to interpretation

A

ABG

33
Q

why are BMP useful in detecting acid-base disorders

A

easy, at-a-glance check on bicarbonate status
can calculate anion gap

34
Q

what is an anion gap

A
  • difference between measured cations and anions in ECF
  • helps determine etiology of METABOLIC ACIDOSIS
  • [Na+] - ([Cl-] + [HCO3-])
35
Q

if the anion of the acid added to the plasma is Cl- then the anion gap will be __

A

normal

36
Q

if the anion of the acid is not Cl-, then the anion gap will ___

A

increase

37
Q

what gives more accurate measurements of oxygen, carbon dioxide, bicarbonate, and pH

A

ABG

38
Q

when can ABGs be useful

A
  1. establishing Dx/assessing severity
    - suspected hypercapnia
    - suspected severe hypoxemia
    - other suspected ventilatory difficulty
  2. guiding Tx/monitoring response
    - ventilated patients
    - dyspneic patients
    - O2 therapy
39
Q

change in normal value of extracellular pH that may result when: (2)

A
  1. renal or respiratory function is abnormal
  2. acid or base load overwhelms excretory capacity
40
Q

4 types of acid-base disorders

A
  1. metabolic acidosis
  2. respiratory acidosis
  3. metbaolic alkalosis
  4. respiratory alkalosis
41
Q

___ = decreased ventilation

A

respiratory acidosis

42
Q

causes of respiratory acidosis

A
  1. depression of CNS respiratory center
    - head trauma
    - drug overdose
  2. lung disease
    - COPD
    - asthma
    - pulmonary edema
    -pneumonia
  3. airway obstruction or msk disease
    - obesity
    - kyphoscoliosis
    - paralysis of rsp muscles
    - chest wall injury/flail chest
    tumor or foreign body in airway
  4. breathing air with high CO2 content
43
Q

symptoms of respiratory acidosis

A
  1. neuro
    - HA
    - confusion
    - weakness
    -drowsiness/stupor
    - muscle twitching
    - tremors
    - paralysis
    - coma
  2. CV
    - vasodilation
  3. signs of underlying disease
44
Q

patients with chronic hypercapnia often have ?

A

desensitized chemoreceptors for CO2 detection

45
Q

in patients who rely on hypoxic drive, ___

A
  • overzealous correction of hypoxemia with supplemental O2 may depress ventilation
46
Q

____ = increased ventilation

A

respiratory alkalosis

47
Q

causes of respiratory alkalosis

A
  1. excessive ventilation
    - pain
    - anxiety
    - mechanical ventilation
    - psychogenic
  2. increased stimulation of CNS respiratory center
    - encephalitis
    - fever
    - salicylate toxicity
    - elevated blood ammonia levels
    - hypoxemia
48
Q

symptoms of respiratory alkalosis

A
  1. neuro - increased neuronal excitability
    - dizziness
    - panic
    - light-headedness
    - tetany
    - numbness/tingling
    - seizures
    - chvostek and trosseau signs
  2. CV
    - arrhythmias
  3. signs of underlying disease
49
Q

4 ways metabolic acidosis can happen:

A
  1. increased production or ingestion of acids
  2. inability to renally excrete acid
  3. increased plasma Cl-
  4. excessive loss of HCO3-
50
Q

excessive loss of HCO3- through kidneys or GI tract = ___ anion gap

A

normal
kidneys preserve Cl- to keep balanced charge = hyperchloremic metabolic acidosis

51
Q

ingestion of exogenous acid or elevation of unmeasured endogenous acid = ____ anion gap

A

elevated
lactate, salicylate, B-hydroxybutyrate
larger gap = worse acidosis

52
Q

when can decreased anion gap be seen

A

decreased anions - hypoalbuminemia
increased IgG/cations - multiple myeloma, elevations in Ca, K, or Mg

53
Q

allows us to determine if a secondary, “hidden” acid-base disturbance is also prsent besides the anion gap metabolic acidosis

A

delta gap
= anion gap - normal AG (12)

54
Q

if metabolic acidosis value is <24, =

A

another metabolic acidosis process present

55
Q

if metabolic acidosis value >24, =

A

metabolic alkalosis process also present

56
Q

delta gap that is done without bicarbonate value

A

modified delta gap
- delta gap = (Na+) - (Cl-) - 36
- -6 or less = Mixed high and normal anion gap metabolic acidosis
- -6 to 6 = Only high anion gap metabolic acidosis
- 6 or greater = Mixed high anion gap metabolic acidosis and metabolic alkalosis

57
Q

causes of metabolic acidosis

A
  1. increased anion gap (MUDPILES)
    - excess production of metabolic acids
    – lactic acidosis
    – ketoacidosis
    – poisoning
    - renal failure
    – accumulation of renal wastes
  2. normal anion gap (HARDUP)
    - HCO3- losses
    – renal tubular acidosis
    – diarrhea
    – carbonic anhydrase inhibitors
    – urinary diversion/intestinal fistula
    - inability to excrete H+
    – adrenal insufficiency
    – renal failure
    - excess administration of Cl
    – IV infusions
    – ammonium chloride
58
Q

symptoms of metabolic acidosis

A
  1. neuro
    - confusion
    - weakness
    - drowsiness/stupor
    - coma
  2. CV
    - vasodilation
    -cardiac arrhythmias
  3. gastrointestinal
    - ABD pain
    - N/V and anorexia
  4. respiratory
    - increased depth and rate of respiration
  5. bone
    - decreased density/osteoporosis
  6. signs of underlying disease
59
Q

impaired HCO3- excretion frequently related to depletion of ___, ___, and ____, often due to _____ or ____

A

chloride, potassium, and sodium ions
vomiting or diuretics

60
Q

causes of metabolic alkalosis

A
  1. excess amounts of bicarbonate/alkali
    - NaHCO3 administration
    - administration of alkaline solutions
  2. excessive loss of hydrogen ions
    - vomiting
    - gastric suction (NG tube)
    - hypokalemia
    - milk-alkali syndrome
  3. increased bicarbonate retention
    - loss of chloride
  4. volume depletion
    - including diuretic therapy
61
Q

symptoms of metabolic alkalosis

A
  1. neuro - increased excitability
    - dizziness
    - panic
    - light-headedness
    - tetany
    - numbness/tingling
    - seizures
    - chvostek and trosseau signs
  2. CV
    - arrhythmias
  3. signs of underlying disease
62
Q

primary respiratory disturbance and primary metabolic disturbance occur simultaneously

A

mixed acid-base disorder

63
Q

process by which either kidneys or the lungs make automatic adjustments when the other system is overwhelmed

A

compensation

64
Q

what two organs work together to help maintain a normal pH level in the body

A

kidneys and lungs

65
Q

respiratory acidosis compensatory mechanism

A

kidney reabsorb more HCO3- in proximal tubule
kidneys excrete more H+ in disstal tubule

66
Q

respiratory alkalosis compensatory mechanism

A

kidneys excrete more HCO3- in proximal tubule
kidneys reabsorb more H+ in distal tubule

67
Q

metabolic acidosis compensatory mechanism

A

lungs increase ventilation

68
Q

metabolic alkalosis compensatory mechanism

A

lung decrease ventilation

69
Q

acute compensation for respiratory acidosis

A

↑ HCO3- = 0.1 x Δ pCO2

70
Q

chronic compensation for respiratory acidosis

A

↑ HCO3- = 0.35 x Δ pCO2

71
Q

acute compensation for respiratory alkalosis

A

↓ HCO3- = 0.2 x Δ pCO2

72
Q

chronic compensation for respiratory alkalosis

A

↓ HCO3- = 0.6 x Δ pCO2

73
Q

compensation formula for metabolic acidosis and alkalosis

A

↓ pCO2 = 1.2 x Δ HCO3-