1 - Acid/Base Disorders Flashcards
(91 cards)
1
Q
Henderson Hasselbach eqn for physiological pH
A
pH = 6.1 + log (HCO3-/H2CO3)
=(HCO3-/(0.3xpCO2)
2
Q
normal PaCo2
A
35-45 mmHg
3
Q
normal HCO3
A
22-26 mEq/L
4
Q
normal PaO2
A
95-100 mmHg
5
Q
normal SaO2
A
> =95%
6
Q
What are the adverse CV effects of acidemia?
A
decr CO
imp’d contractility
incr PVR
arrhythmias
7
Q
What are the metabolic effects of acidemia?
A
insulin resis
inhib of anaerobic glycolysis
hyperkal
8
Q
What are the CNS effecs of acidemia?
A
coma or AMS
9
Q
What are misc effects of acidemia?
A
decr resp musc strength
hypervent
SOB
10
Q
What are the adverse CV effects of alkalemia
A
decr coronary BF
arteriolar constriction
decr anginal threshold
arrhytmias
11
Q
What are the metabolic effects of alkalemia?
A
decr K, Ca, Mg
stim of anerobic glycolysis
12
Q
What are the CNS effects of alkemia?
A
decr cerebral BF
Szs
13
Q
What are the nonvolatile acids and how are they formed?
A
anaerobic metab: lactic & pyruvic acid
TG ox: acetoacetic and beta-hydroxybutyric acid
AA metb: sulfuric and phosphoric acids
14
Q
Describe the buggering capacity of bicarb.
A
rapid onset w intermediate capacity
15
Q
Describe the phosphates as a buffer.
A
intermed onset and capacity.
EC Pi limited actvity
bone relativey inaccessible
16
Q
Describe proteins as buffer.
A
alb/hbg: rapid onset, limited: more effective IC
17
Q
What are the mechanisms by which the kidney regulations acid/base status?
A
- reabsorb filtered bicarb
- excrete hydrogen ions released from nonvolatile acids
- ammoniagenesis, titratable acidity
18
Q
most bicarb is reabosbed at the
A
PCT
19
Q
limiting H+ secretion into the PCT results in
A
bicarb losses
20
Q
How can carbonic anhydrase inhibitors affect a/b status?
A
cause metabolic acidosis as HCO3- excretion increases
21
Q
Where does H+ secretion take place?
A
DCT
22
Q
H+ secretion in the DCT results in generation of
A
NEW Bicarb
23
Q
Describe vent reg of a/b status.
A
rapid and large cap
chemoreceptors detect incrin PaCO2 and incr rate and depth of vent.
24
Q
Which chemoreceptors are activated by arterial acidosis, hypercapnia, and hypoxia?
A
peripheral chemoreceptors in carotid arteries and aorta
25
Which chemoreceptors are activated by CSF acidosis?
central chemoreceptors in medulla
26
Describe hepatic regulation of A/b status
Oxidation of protein generations bicarb and ammonium that can be elim's via urea synthesis or renal ammoniogenesis.
if liver decr urea synthesis--> incr pH
27
**comp in met acidosis
PaCo2 falls by 1-1.5 x HCO3 fall
28
**comp in met alk
PaCO2 incr by 0.4-0.6 x rise in plasma HCO3-
29
**comp in resp acid
acute: HCO3- rise by 0.1 x incr in PaCO2 +/- 3
chronic: 0.4x +/-4
30
**comp in resp alk
acute: HCO3- fall by 0.1-0.3 x decr in PACO2 but usually not less than 18 mEq/L
chronic: 0.2-0.5, 14 mEq/L
31
normal anion gap
3-11 mEq/L
32
anion gap eqn
AG=Na-Cl-HCO3-
33
nother name of non-anion gap met acidosis
hyperchloremia acidosis
34
Causes of non-anion gap acidosis
GI bicarb loss
renal wasting/imp'd H+ secr
acid/Cl gain
35
Examples of GI bicarb loss
diarrhea
pancreatic fistula
biliary drainage
36
Explain renal bicarbonate loss
type II RTA (PCT)
- cannot reabs
- -incr'd Na and fluid loss --> RAAS
- -2* hyperaldosteronism-->hypokalemia
--> able to acidify urine pH <5.3
37
what are the causes of reduced renal H+ excretion?
type I RTA (hypokalemia)
type IV RTA (hypoaldosteronism / hyperkalemia)
chronic renal failure
38
Explain type I RTA
caused by tubule defect, SLE, myeloma, toluene (OD)
H+ cannot be pumped into DCT
- ->urine cannot be acidified
- ->incr K+ excretion d/t Na exchange
39
Explain type IV RTA
hypoaldosteronism
- ->decr H+ and K+ excretion
- ->acidosis and hyperkalemia
40
Explain how CRF can cause a metabolic acidosis.
decr H+ secr.
| less ammonia production. (less bicarb made)
41
MULEPAK
```
methanol
uremia
lactic acidosis
ethylene glycol
paraldehyde ingestion
aspirin (salicylates)
ketoacidosis
```
42
MUDPILES
```
methanol
uremia
DKA
poisoing/propylene glycol ingestion
intox/infx
lactic acidosis
etylene glycol
salicylate/sepsis
```
43
delta gap
for AG met acidosis add to measured HCO3-
--> if high for HCO3- then mixed disorder (also metabolic alkalosis)
44
What causes lactic acidosis?
- decr clearance of lactate
- shock (hypoxia, decr hep fxn)
- DRUGs
45
How does ethanol cause lactic acidosis?
incr lactate and hypoglycemia - impaired gluconeogenesis
46
How does metformin cause lactic acidosis?
we don't know
47
How do NRTIs cause lactic acidosis?
inhibit DNA Pol for mitochondrial DNA synthesis
48
How do linezolid, isoniazid, and propofol cause lactic acidosis?
simply increase lactic acid
49
How do Sz cause lactic acidosis?
enhanced met act
| self-limiting
50
How does leukemia cause metabolic acidosis?
packed porly perfused bone marrow caviity
51
How does hep/RF cause lactic acidosis?
imp'd metab and excr
52
How does DM cause lactic acidosis?
formation of ketones/lactate; use of metformin
53
How does ketoacidosis cause met acid?
increase acetoacetic acid and beta-hydroxy butyric acid (KETONE BODIES)
54
How do salicylates cause AG met acid?
resp alkalosis from stim of resp drive
| met acid from accumulation of organic acids
55
How do methanol/ethylene glycol cause AG met acid?
methanol-->formaldehyde-->formic acid
ethylene glycol-->glycoaldehyde-->glycolate-->glycoxylate-->oxalate
56
Wht are the Sx of lactic acidosis?
```
Kussmaul respiration
periph vasodil causes flushing and tachycardia --> arrhythmias, decr contractility
hyperkalemia
lethary/coma
N/V
bone demineralization if chronic
```
57
When to use bicarb therapy?
pH <7.1-7.15
ind: hyperkalemia, pH <7.1 w/ cardiac arrest after defib, vent, and meds have been utilized, ODs
58
How to dose bicarb
dose (mEq)=[0.5L/kg x IBW] x (goal bicarb - actual bicarb)
use 12 mEq/L for goal
give 1/3-1/2 calc'd dose
monitor ABG
59
Tips for bicarb therapy
monitor ABG
supplement K+, if needed
don't overalk-->left shift hypoxia, hypernatremia, CSF acidosis
60
What electrolyte shifts can bicarb therapy cause?
K+ --> shifts IC --> hypokalemia
| Ca2+-->decr Cai so decr contractility
61
Dose of chronic bicarb therapy.
1-3 mEq/kg/d (up to 10+)
62
What is tromethamine?
Tx for acidosis
combines with H+ from H2CO3 to form bicarb
--osmotic diuretic
63
What are some drugs to treat met acidosis?
bicarb
tromethamine
carbicarb
dichloroacette (DCA): lactate metab
64
What are the mechanisms of metabolic alk?
loss of acid
admin of HCO3- or precursor
contraction alkalosis
65
What the heck does contraction alkalosis mean?
loss of Cl- rich, HCO3- poor fluid
66
How do volume and chloride depletion maintain a met alk?
decr in blood vol
decr ability to excr bicarb
incr reabs of PCT reabs of bicarb
67
What are the two types of met alkalosis?
```
saline responsive
saline resistance (Cl in urine >20 mEq/L)
```
68
What are the causes of saline responsive met alk?
diuretic therapy
vomting and NG suction
exogenous HCO3- admin or blood transfusions
69
How is a saline responsive met alk maintained?
reduced GFR (incr HCO3 reabs w Na+)
- incr PCT HCO3- abs w Na+ (hypochloremia)
- hypokalemia: more H+ secreted and new bicarb
70
How does diuretic therapy cause saline responsive met alk?
volume contraction --> ALDOSTERONE --> incr Na reabs in DCT
- -> incr H+/K+ sec
- -> incr BICARB made
-->HYPOKALEMIA--> K+ moves EC --> H+ moves IC --> basic EC
-->HYPOCHLOREMIA (d/t diuresis) --> increase bicarb reabs
71
Why do blood products cause alkalosis?
contain citrate-->breaks down into bicarb
72
What is the pathology of saline resistant met alk?
enhanced renal H+ excr and bicarb reabs
urinary chloride >20 mEq/L
--> no Cl depletion or there is inability to reabsorb Cl
73
What are the causes of saline res mmet alk?
incr mineralcorticoid activity
hypokalemia
renal tubular chloride wasting (Bartter's syndrome)
74
How does increased mineralcorticoid acitivyt cause saline res met alk?
stim CD H+ secr
| -->incr ammoniagenesis
75
How does hypokalemia cause saline res met alk?
incr H+ secr w bicarb reabs and ammoniagenesis
76
How does Bartter's syndrome cause saline res met alk?
chloride wasting:
imp's NaCl reabs
-->fluid loss --> RAAS --> incr aldosterone
77
What are the Sx of metabolic alkalosis?
msucle cramps, weakness, paresthesias
cellular hypoxia, confusion, coma, Sz
myocardial suppression, CV collapse, arrhytmias (low K)
78
How to treat saline responsive alkalosis?
fluid/elyte replacement w NaCl or KCl
- -> less bicarb reabs
- ->increase volume
- ->increase K+ --> decr H+ secr
or CAI
79
Example fluid treatment for saline responsive met alk
0.9% NaCl w 20-40 mEq/L KCl over 4-6 hrs
80
What to monitor for met alk?
```
I/O
BP
HR
lung sounds
elyes
edema
```
81
How do carbonic anhydrase inhibitors help treat saline resp met alk?
decr bicarb reabs in PCT
SE: K+ wasting
82
carbonic anhydrase inhibitor dose
acetohexamide 250-375 once or bid
83
Rare therapeutic options of met alkalosis
HCl acid
Ammonium chloride
arginine monohydrochoride
84
adjunct therapy for pts for met alk d/t NG suctioning or vomitting
H2 antagonists or PPIs
85
How to treat saline resistant alkalosis?
correct hypokalemia w K-sparing diuretic or KCl supplementation
- decrease mineralcorticoids
- spironolactone (mincortR antag, inhib aldosterone-stim of H+ secr)
--correct hyperaldosteronism-> give fluids but not first line
86
What are the causes of respiratory acidosis?
```
airway obstruction
reduced stimulatus for resp from CNS (OD, sleep apnea, CNS infx)
-failture of heart or lungs
-neuromusc defects (can't breathe)
-mech vent
```
87
Sx of resp alk?
SOB
CNS: HA, drowsy, confusion, coma, Sz
CV: tachycardia, arrhythmias, hypoTN
88
Tx of resp acidosis
underlying cause
- mech vent or O2 (caution in COPD)
- avoid rapid correction (alk)
- rarely use bicarb (only high arrhythmia risk)
89
What are the causes of resp alk?
```
central stim of resp
periph stim of resp
mech vent
pulmonary
salicylate intox
```
90
What are the Sx of resp alk?
CNS: lightheadedness, confusion, Sz
decr cerebral BF
tetany/cramps
N/V
91
How is resp alk treated?
correct underlying cause
| vent, sedate, paralyze
