Bicarb Flashcards
(66 cards)
1
Q
normal pH
A
7.35-7.45
2
Q
incompatible with life
A
<6.7 or >7.7
3
Q
acidemia pH
A
< 7.35
4
Q
alkalemia pH
A
> 7.45
5
Q
Henderson Hasselbach
A
pH = pKa + log (B/A)
6
Q
HCO3- acid or base?
A
base
7
Q
CO2 acid or base?
A
acid
8
Q
normal paCO2
A
35-40 mmHg remember 40
9
Q
normal HCO3
A
22-26 mEq/L remember 24
10
Q
normal PaO2
A
95-100 mmHg
11
Q
normal SaO2
A
> 95%
12
Q
consequences of acidemia (cardiovascular)
A
Cardiovascular:
decreased cardiac output
impairment of cardiac contractility
^ pulmonary vascular resistance and arrhythmias
13
Q
consequences of acidemia (metabolic)
A
insulin resistance (^ BG)
inhibition of anaerobic glycolysis (decreased O2)
hyperkalemia
14
Q
consequences of acidemia (CNS)
A
- coma or altered mental status
15
Q
consequences of acidemia (other)
A
decreased respiratory muscle strength
*hyperventilation- trying to get rid of CO2
dyspnea
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)
17
Q
consequences of alkalemia (metabolic)
A
decreased K, Ca & Mg
stimulation fo anaerobic glycolysis
18
Q
consequences of alkalemia (CNS)
A
decreased cerebral flow (lethargy, stupor, delirium)
seizures
19
Q
consequences of alkalemia (other)
A
decreased respirations (wanting to reserve CO2)
20
Q
mechanisms of acid regulation
A
buffering
renal regulation
ventilatory regulation
21
Q
main buffers for acid regulation
A
bicarbonate/carbonic acid, phosphate, and protein
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
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)
24
Q
proteins (as buffer for acidosis)
A
albumin/hemoglobin- rapid onset, limited capacity (intracellular acidosis in particular)
25
renal system regulation (acidosis)
kidney serves to main purposes:
reabsorb filtered HCO3 (prepares to absorb H+)
excrete H+ ions released from nonvolatile acids (get rid of acid)
26
bicarbonate reabsorption
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
27
carbonic anhydrase inhibitors
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
bicarb generation/ H+ excretion
delayed onset but large capacity
H+ excretion takes places primary in distal tubule
29
ventilatory regulation of acidosis
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
hepatic regulation of acidosis
new mech, significance unknown
31
compensation characteristics for acid-base disorders
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
met acidosis (cause and compensation)
decreased HCO3
compensation: decreased paCO2
33
met alkalosis (cause and compensation)
increased HCO3
compensation: increased paCO2
34
res acidosis
increased PaCO2
compensation: increased HCO3 (synthesis)
35
res alkalosis
decrease PaCO2
compensation: decreased HCO3 synthesis
36
met acidosis
low pH, low serum HCO3 (<24), and a compensatory decrease in CO2
37
met acidosis non-anion gap
wnl: 3-11
38
met acidosis anion gap
> 3-11
39
non-anion gap acidosis
loss of plasma HCO3 replaces by Cl-
40
causes of non-anion gap acidosis
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
causes of anion gap acidosis****
```
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
anion gap acidosis
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
treatment of anion gap acidosis
treat underlying cause
ACUTE bicarb therapy
> if pH < 7.10-7.15
44
dosing bicarb
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
hazards of bicarb therapy
over alkalization can reduce cerebral flow and impair O2 release from HgB tissues
can result in hypernatremia/ hyperosmolality
can result in electrolyte shifts
46
bicarb therapy and potassium
bicarb pushes K+ back into cells creating a more severe hypokalemia
47
bicarb therapy and calcium
results in hypocalcemia
decrease ionized Ca --> decreased myocardial contractility
48
met alkalosis
pH > 7.45 and increased HCO3 ( >30) and a compensatory hypoventilation resulting in increased CO2
49
causes of alkalosis
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
low chlorine results in
more HCO3 reabsorption
51
causes of saline responsive alkalosis ( urinary Cl < 10-20 mEq/L)
- 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
normally Cl- is absorbed with Na, but w/out Cl-
Na is resorbed w/ HCO3
53
saline resistant alkalosis
urinary Cl- >20 mEq/L
** no chloride depletion or inability to reabsorb Cl-
54
causes of saline resistant alkalosis
increased mineralocorticoid activity
hypokalemia
renal tubular chloride wasting
55
symptoms of saline resistant alkalosis
-muscle cramps, weakness (due to low K)
postural dizziness
-cellular hypoxia; mental confusion; coma; seizures
-direct myocardial suppression; CV collapse; arrhythmias (low K)
56
treatment of saline resistant alkalosis
correct underlying cause!!!
not as urgent --> rapid correction unnecessary
57
treatment of saline responsive alkalosis
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
treatment for saline resistant alkalosis
- 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
respiratory acidosis
high pH, hypercapnia ( >45 mmHg), and compensatory increase in HCO3
usually a result from failure of excretion vs. overproduction
60
causes of respiratory acidosis
- 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
symptoms of respiratory acidosis
dyspnea, SOB, HA, drowsiness, confusion, coma, seizures, tachycardia, arrhythmias, and/or hypotension
62
treatments of respiratory acidosis
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
respiratory alkalosis
increased pH, decreased PaCO2 (<40), and compensatory decrease in HCO3 concentration
64
causes of respiratory alkalosis
>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
symptoms of respiratory alkalosis
- CNS: lightheaded
- decreased cerebral blood flow
- tetany/muscle cramps
- N/V
66
treatment of respiratory alkalosis
correct underlying cause
| >ventilation, sedation, paralysis
