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PHRM 825 > Bicarb > Flashcards

Bicarb Flashcards

1
Q

normal pH

A

7.35-7.45

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2
Q

incompatible with life

A

<6.7 or >7.7

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3
Q

acidemia pH

A

< 7.35

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4
Q

alkalemia pH

A

> 7.45

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5
Q

Henderson Hasselbach

A

pH = pKa + log (B/A)

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6
Q

HCO3- acid or base?

A

base

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7
Q

CO2 acid or base?

A

acid

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8
Q

normal paCO2

A

35-40 mmHg remember 40

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9
Q

normal HCO3

A

22-26 mEq/L remember 24

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10
Q

normal PaO2

A

95-100 mmHg

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11
Q

normal SaO2

A

> 95%

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12
Q

consequences of acidemia (cardiovascular)

A

Cardiovascular:
decreased cardiac output
impairment of cardiac contractility
^ pulmonary vascular resistance and arrhythmias

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13
Q

consequences of acidemia (metabolic)

A

insulin resistance (^ BG)
inhibition of anaerobic glycolysis (decreased O2)
hyperkalemia

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14
Q

consequences of acidemia (CNS)

A
  • coma or altered mental status
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15
Q

consequences of acidemia (other)

A

decreased respiratory muscle strength
*hyperventilation- trying to get rid of CO2
dyspnea

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16
Q

consequences of alkalemia (cardiovascular)

A

decreased coronary blood flow (b/c heart constricting)
arteriolar contraction
decreased anginal threshold
arrhythmias (can be metabolic related)

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17
Q

consequences of alkalemia (metabolic)

A

decreased K, Ca & Mg

stimulation fo anaerobic glycolysis

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18
Q

consequences of alkalemia (CNS)

A

decreased cerebral flow (lethargy, stupor, delirium)

seizures

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19
Q

consequences of alkalemia (other)

A

decreased respirations (wanting to reserve CO2)

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20
Q

mechanisms of acid regulation

A

buffering
renal regulation
ventilatory regulation

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21
Q

main buffers for acid regulation

A

bicarbonate/carbonic acid, phosphate, and protein

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22
Q

bicarbonate- principle buffer (acidosis)

A

*rapid onset w/ intermediate capacity

present in largest concentration

supply of CO2 is unlimited

acidity can be regulated by CO2 or HCO3

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23
Q

phosphate buffer (acidosis)

A

*intermediate onset and capacity

calcium phosphates in bones relatively inaccessible (can be broken down for use in prolonged acidosis- BAD)

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24
Q

proteins (as buffer for acidosis)

A

albumin/hemoglobin- rapid onset, limited capacity (intracellular acidosis in particular)

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25
Q

renal system regulation (acidosis)

A

kidney serves to main purposes:

reabsorb filtered HCO3 (prepares to absorb H+)

excrete H+ ions released from nonvolatile acids (get rid of acid)

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26
Q

bicarbonate reabsorption

A

4-45k mEq filtered daily

85-90% reabsorbed by proximal tubule (if damaged become very acidic)

10-15% reabsorbed by distal

virtually no HCO3 in urine

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27
Q

carbonic anhydrase inhibitors

A

inhibit activity of carbonic anhydrase

decrease entry of CO2 and H2O –> decreased HCO3 reabsorption

metallic acidosis occurs with ^ HCO3 excretion

treatment for metabolic acidosis

28
Q

bicarb generation/ H+ excretion

A

delayed onset but large capacity

H+ excretion takes places primary in distal tubule

29
Q

ventilatory regulation of acidosis

A

rapid onset and *LARGE capacity

chemoreceptors detect an ^ in PaCO2 and ^ the rate and depth of ventilation

peripheral chemoreceptors in carotid arteries and aorta (activated by arterial acidosis, hypercapnia, and hypoxia)

central chemoreceptors in medulla (activated by CSF acidosis)

30
Q

hepatic regulation of acidosis

A

new mech, significance unknown

31
Q

compensation characteristics for acid-base disorders

A

respiratory compensation very rapid

renal compensation takes 3-5 days for max effect

compensation moves pH towards normal, but rarely corrects pH to normal

32
Q

met acidosis (cause and compensation)

A

decreased HCO3

compensation: decreased paCO2

33
Q

met alkalosis (cause and compensation)

A

increased HCO3

compensation: increased paCO2

34
Q

res acidosis

A

increased PaCO2

compensation: increased HCO3 (synthesis)

35
Q

res alkalosis

A

decrease PaCO2

compensation: decreased HCO3 synthesis

36
Q

met acidosis

A

low pH, low serum HCO3 (<24), and a compensatory decrease in CO2

37
Q

met acidosis non-anion gap

A

wnl: 3-11

38
Q

met acidosis anion gap

A

> 3-11

39
Q

non-anion gap acidosis

A

loss of plasma HCO3 replaces by Cl-

40
Q

causes of non-anion gap acidosis

A

A.) GI HCO3 losses
- diarrhea (can’t reabsorb bicarb b/c moving through too fast)

  • pancreatic fistulas/ biliary drainage (rich in HCO3)

B.) renal bicarb loss: type II renal tubular acidosis (proximal)

-causes: heavy metal toxicity, carbonic anhydrase inhibitor therapy (topamax),

C.) reduced renal H+ excretion (distal tub RTA)
- type I RTA
> H+ cannot be pumped into tubule lumen by cells of collecting duct
>increase in K+ excretion –> H+ can’t be secreted in response to Na+ reabsorption

-type IV RTA
>low aldosterone
>aldosterone stimulates H+ excretion –> decreased aldosterone results in H+ retention
>hyperkalemia also results in H+ retention

-chornic renal failure:
>decreased H+ secretion
> less ammonia production –> less HCO3 production

-acid & chloride admin:
> TPN admin
>HCl or Ammonium Cl admin

41
Q

causes of anion gap acidosis**

A 
M ethanol intoxication
U remia
D diabetic ketoacidosis
P poisoning/ propylene glycol ingestion
I intoxication/ infection
L actic acidosis 
E thylene glycol 
S alicylate (aspirin)/ sepsis
42
Q

anion gap acidosis

A

overall HCO3 losses are replaced w/ another anion besides Cl

delta gap- if present tells you there is also presence of met alkalosis on top of acidosis

43
Q

treatment of anion gap acidosis

A

treat underlying cause

ACUTE bicarb therapy
> if pH < 7.10-7.15

44
Q

dosing bicarb

A

dose (mEq) = [0.5 L/kg (IBW)] x (desired HCO3 - actual HCO3)

desired = 12

**once you calculate dose give 1/3 - 1/2 that dose and monitor ABG

can give ~ 1 mEq/kg during cardiac arrest

45
Q

hazards of bicarb therapy

A

over alkalization can reduce cerebral flow and impair O2 release from HgB tissues

can result in hypernatremia/ hyperosmolality

can result in electrolyte shifts

46
Q

bicarb therapy and potassium

A

bicarb pushes K+ back into cells creating a more severe hypokalemia

47
Q

bicarb therapy and calcium

A

results in hypocalcemia

decrease ionized Ca –> decreased myocardial contractility

48
Q

met alkalosis

A

pH > 7.45 and increased HCO3 ( >30) and a compensatory hypoventilation resulting in increased CO2

49
Q

causes of alkalosis

A

loss of acid from GI tract or urine

admin of bicarb or its precursor

contraction alkalosis (loss of Cl rich, HCO3 poor fluid)

often V and Cl depletion contribute:
> decreased arterial blood V
> decreased ability of kidney to excrete bicarb
> w/ V depletion, capacity of proximal tubule to reabsorb HCO3 increased

50
Q

low chlorine results in

A

more HCO3 reabsorption

51
Q

causes of saline responsive alkalosis ( urinary Cl < 10-20 mEq/L)

A
  • diuretic therapy
    >enhances NaCl and H2O excretion

-vomiting and NG suction
>1 L/ day, 1 L contains 200 mEq Cl and 25-100 mEq H+

-exogenous HCO3 admin or blood transfusions
>citrate in blood breaks down HCO3

-maintenance of alkalosis
>reduced GFR
>enhanced proximal tubular HCO3 reabsorption
> effects of hypokalemia
-w/ less K+, H+ is secreted while Na is reabsorbed

52
Q

normally Cl- is absorbed with Na, but w/out Cl-

A

Na is resorbed w/ HCO3

53
Q

saline resistant alkalosis

A

urinary Cl- >20 mEq/L

** no chloride depletion or inability to reabsorb Cl-

54
Q

causes of saline resistant alkalosis

A

increased mineralocorticoid activity

hypokalemia

renal tubular chloride wasting

55
Q

symptoms of saline resistant alkalosis

A

-muscle cramps, weakness (due to low K)
postural dizziness
-cellular hypoxia; mental confusion; coma; seizures
-direct myocardial suppression; CV collapse; arrhythmias (low K)

56
Q

treatment of saline resistant alkalosis

A

correct underlying cause!!!

not as urgent –> rapid correction unnecessary

57
Q

treatment of saline responsive alkalosis

A

fluid/electrolyte replacement w/ KCl or NaCl

> allows more Na to be reabsorbed w/ Cl vs getting exchanged w/ H+ or reabsorbed w/ HCO3
reduces V stimulus for Na retention, permitting HCO3 excretion in urine
reduces plasma K concentration –> reducing renal H+ secretion
use caution in its w/ HF or hepatic/renal failure

carbonic anhydrase inhibitors
>for pts who can’t tolerate excess Na or fluid

58
Q

treatment for saline resistant alkalosis

A
  • correct hypokalemia w/ K-sparing diuretic or KCl supplementation
  • decrease dose of mineralocorticoid or change steroids to one w/ less activity
  • administer spironolactone
  • correct hyperaldosteronism
59
Q

respiratory acidosis

A

high pH, hypercapnia ( >45 mmHg), and compensatory increase in HCO3

usually a result from failure of excretion vs. overproduction

60
Q

causes of respiratory acidosis

A
  • airway obstruction (asthma, foreign body, aspiration)
  • reduced stimulus for respiration from CNS (drug overdose, sleep apnea, CNS infections, trauma)
  • failure of heart or lungs (PE or cardiac arrest)
  • neuromuscular defects affecting nerves or skeletal muscles required for ventilation (ALS or Guallian- Barre)
  • mechanical ventilation
61
Q

symptoms of respiratory acidosis

A

dyspnea, SOB, HA, drowsiness, confusion, coma, seizures, tachycardia, arrhythmias, and/or hypotension

62
Q

treatments of respiratory acidosis

A

correct underlying cause!

mechanical ventilation or oxygen (use caution w/ COPD its b/c low drive to breathe and even lower w/ O2)

avoid rapid correction to prevent alkalemia

63
Q

respiratory alkalosis

A

increased pH, decreased PaCO2 (<40), and compensatory decrease in HCO3 concentration

64
Q

causes of respiratory alkalosis

A

> central stimulation of respiration- anxiety, pain, injury, trauma
peripheral stimulation of respiration- hypoxemia, hypotension, high altitude, CHF
mechanical ventilation
pulmonary (PE, edema, pneumonia)
salicylate intoxication

65
Q

symptoms of respiratory alkalosis

A
  • CNS: lightheaded
  • decreased cerebral blood flow
  • tetany/muscle cramps
  • N/V
66
Q

treatment of respiratory alkalosis

A

correct underlying cause

>ventilation, sedation, paralysis

PHRM 825 (1 decks)

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