Download Fliud_Electrolyte_Acid_Base - Berlin: Reviews in Internal Medicine

Dr. Sakarn Bunnag
Osmol receptor
(hypothalamus)
Thirst center
(hypothalamus
AVP secretion
(Post.pituitary)
Baro receptor
•Aortic arch
•Carotid body
•Afferent arteriole
(kidney)
•Lt atrium
Renin
(juxta apparatus of kidney)
AngiotensinII
Aldosterone
Water intake
Water reabsorption
Na and water
reabsorption
Na
reabsorption
Na, water
reabsorption
=isotonic
Na
reabsorption
isotonic
50-100
mosmol/kg
(free water)
Water
Reabsorption
If AVP +
~1200
Mosmol/kg
V2-R
AVP
Aquarporin II
urea
Aquarporin III or IV
50-100
mosmol/Kg
lumen
water
1200 mosmol/Kg
Hypotonic Hyponatremia
• Na+ < 135,
• effective serum osmol <275)
Intact diluting ability
Impair diluting ability
Urine osmol 50-100 mosmol/Kg
Urine osmol >50-100 mosmol/Kg
(May be + too much water intake)
Low GFR?
•Psychogenic polydipsia
•Beer protomania
AD effect +
(10-20 ml/min)
No
Yes
•renal failure
(may be + others)
AD effect +
Low ECV
Yes
No
Appropriate ADH
•Volume deplesion
•U Na+ > 20 meq/l: Renal
•U Na+ < 10 meq/l: extrarenal, 3rd space loss)
•Edematous stage
(cirrhosis, CHF, hypo albuminemia)
•Others
(hypothyroid, adrenal insuff.)
Inappropriate AD
•N/V
•Severe stress
•Drug induced
•SIADH
•Mutation of V2R
•Free water formation defect
Hypernatremia
High ECF volume
administration
of
hypertonic sodium solutions
• salt water drowning
• NaHCO3 replacement
Diuretic
with water
replacement
Low or normal ECF volume
loss of free water
• central DI
• nephrogenic DI
• reset osmostat upward
(essential hypernatremia)
• osmotic diuresis
• osmotic diarrhea
• excessive insensible
or sweat loss
Inappropriate
Replacement
of free water
• disorder of
thirst center
• unable to
access water
Water replacement
with
correction of specific cause.
K+ < 3.5 meq/l
R/O pseudo hypo K+  WC > 100,000
R/O redistribution 
• TTKG < 2 or
• 24 hour urine K+ < 10 meq
No
• diarrhea
• sweating
• remote diuretic use
•
•
•
•
•
•
Periodic paralysis
Insulin, B2 agonist
refeeding
Rx neutropenia with G-CSF
Rx anemia with B12, folate
Ba poisoning, acute chloroquine toxic
• TTKG > 4 or
• 24 hour urine K+ > 20 meq
= renal loss
Renal K+ loss
normal
Metabolic acidosis
High gap
• DKA
• ketoacidosis
• methanal
• ethylene glycol
•
•
•
•
•
Non-oligulic ATN
Diuretic phase ATN
low serum Mg
high dose PGs
TI disease
Metabolic alkalosis
Urine Cl-
Normal gap
• RTA
• CA inhibitor
• glue sniff
< 10 meq/l
(hypo-volumemia)
• vomiting
• NG suction
>20 meq/l
(hyper-volumemia
or
Cl- losing)
Normal BP
• resent diuretic use
• Barter
• Gitelman
High renin
High aldosterone
•
•
•
•
RAS
malignant HT
scleroderma
renin producing tumor
High BP
R/O HT with diuretic use
low renin
High aldosterone
low renin
low aldosterone
• 1o hyper
aldosteronism
• Liddle (mutation
of Na channel
increase Na reabsorption)
•Increase mineralocorticoid
• Very high cortisol
• 11 B-OH def
• Licorice
• fludocortisone
• 17 a-OH def
K+ > 5.5 meq/l
R/O pseudo hyper K+ 
• TTKG > 7 or
• 24 hour urine K+ > 200 meq
• Hemolysis
• WC > 70,000
• Plt > 1,000,000
If > 6.0 EKG should be done
yes
K+ load
External source
• diet
• IV fluid
• old blood > 5 day
Internal source
• intravascular hemolysis
•
•
•
•
•
•
rhabdomyolysis
tumor lysis syndrome
UGIB
absorb hematoma
major trauma or Sx
severe sepsis
no
Redistribution
• beta-block (esp.
nonselective beta 1)
• metabolic acidosis
• periodic paralysis
• severe exercise
• Digitalis toxic
• fluoride toxic
Defect of renal excretion
Principal cell
Collecting tubule
ClNa+
Aldosterone
+
3Na+
ATP
2K+
Aldosterone
negative
lumen
+
K+
+
Aldosterone
basolateral
Defect of renal excretion
site
cause
Low distal Na
delivery
low ECV, low GFR(<15), Gordon syndrome
(psudohypoaldosterone type II)
Defect of Na
channel (ENAC)
triamterene, amiloride
Defect of Clchannel
heparin, cyclosporine
Defect of K+
channel (ROMK)
cyclosporine
Defect of
aldosterone
ACE-I, ARB, spironolactone, NSAIDs, heparin, cyclosporine
DM,1o hypoaldosterone,1o adrenal insuff
Frequent Urine
Polyuria
Water diuresis
• primary polydipsia
• DI
•CDI
•NDI
Non-polyuria
Solute diuresis
• organic
• glucose
• Urea
• osmotic agent
• radiocontrast
• salt
• increase salt intake
• renal salt loss
• diuretic
•
UTI
• hyperactive bladder
• anxiety
Primary polydipsia
CDI
NDI
cause
Psychiatric problem
Psychiatric drug
Female puberty
Trauma, Sx, Tumor,
Infarction, infiltrative
(hypothal, pituitary)
Hyper Ca, Hypo K
Litium toxic, AmphoB, renal D
onset
gradual
abrupt
gradual
Volume
Day
vs.
night
vary
constant
constant
severity
Vary
on sign of
volumedepletion
Suggestive if severe
± sign of
volumedepletion
Rare to be severe ±
sign of
volumedepletion
P Na
Low normal
To
normal
High normal
To
high
High normal
To
high
Polyuria
SpGr > 1.010 or
Urine osmol > 300 or
U osmol/P osmol > 0.9
SpGr < 1.005 or
Urine osmol < 150 or
U osmol/P osmol < 0.9
Solute diuresis
Water diuresis
2(U Na + U K)/U osmol
< 0.4
Water deprivation test
> 0.6
Organic diuresis
Salt diuresis
Urine glucose
4+
glucose
<4
Urine osmolal gap
> 200
• osmotic agent
• radiocontrast
< 200
• urea
U osmol
DDAVP
1200
1000
800
600
400
200
normal
partial CDI
partial NDI
complete CDI
complete NDI
End point (Posmol>295)
Water deprivation test
ตรวจ serum osmol และ PNa+
• BW ลดลง> 3%
• urine osmolality มีกำรเปลี่ยนแปลง
<10% ติดต่อกัน 2-3 ครัง้
end
point
start
• งดน ้ำและของเหลวต่ำงๆ
• ตรวจ plasma และ urine osmolality,
serum electrolytes และ
ระดับ plasma AVP
serum osmolality > 295-300 mOsm/kg H2O หรื อ PNa+ > 145 mEq/L
DDAVP 1-2 mcg SC or IV
• วัด BP, HR ผู้ป่วยเป็ นระยะ
เพื่อป้องกันกำรเกิดภำวกำรณ์ขำดสำรน ้ำรุนแรง
• urine osmolality ทุกครัง้ ที่ปัสสำวะ
• ชัง่ น ้ำหนักตัวและวัดปริมำณปั สสำวะต่อ 1 ชัว่ โมงทุกชัว่ โมง
2 hr
urine osmolality ทุกครัง้ ที่ปัสสำวะ
Fixed Acid
A- + H+
Volatile acid
(from CO metabo)
Lung
Gluconeogenesis
Anionic Amino acid
H+ + HCO3-
Renal
H2CO3
NH4+ excretion(HCO3- regeneration)
Tritratable acid excretion
HCO3-reclamation
H2O + CO2
Intracellular (Hb, protein)
and
Bone Buffering (carbonate)
Unmeasured cation
K+, Ca2+ , Mg2+
Unmeasured anion
alb , phosphate , sulphate,
organic cation ( M protein )
Anion gap
+
Na - ( Cl + HCO3 )
Measured cation
Na+
Measured anion
Cl-, HCO3-


Delta gap in met.acidosis ; due to A( HA  H+ + A- )
Delta HCO3◦ 60% H+ buffer in intracellular and bone pure
met.acidosis delta gag/delta HCO3- may be 1:1 to 2:1
◦ Resp.acidosis  decrease delta HCO3◦ Resp.alk  increase delta HCO3-



1-2  pure wide gap acidosis
<1  wide gap + normal gap met.acidosis
 wide gap met.acidosis + resp.alk.
>2  wide gap met.acidosis + met.alk.
 wide gap met.acidosis + resp.acido.





=Measured osmol – calculated osmol
Calculated osmol
= 2(Na+K) + BUN/2.8 + Glu/18
In wide gap met.acidosis if > 25 suggest methanol
or ethylene glycol ingestion
Wide P osmolol gap can be found in lactic or keto
acidosis
Rarely elevated in salicylic acidosis
because toxic level is very low.
Urine anion gap (urine net charge)
Unmeasured cation
NH4+
Unmeasured anion
Anion gap
(Na+ + K+) - Cl-
Measured cation
Na+ + K+
Measured anion
Cl-

NH4+ is U unmeasured cation

Urine is neutral.

When acidemia  high urine NH4+  high
U unmeasured cation  neg urine net charge




=Measured osmol – calculated osmol
Calculated osmol
= 2(Na+K) + UUN/2.8 + Glu/18
More than half of urine osmolol gap is
ammonium.
Unmeasured anion are already included in
2(Na+K)
Low serum HCO3Met acidosis ?
R/O resp. alkalosis
Or
Mixed acid-base
ABG
Serum anion gap (collected with alb)
Wide gap
Delta gap/Delta HCO3-
Normal gap
Wide gap met.acidosis
With ?
Wide gap met. Acidosis
Lactic acidosis
Ketoacidosis (dibetes/starvation/alcoholic)
Toxic (methyl or ethyl alcohol/ethylene glycol/salicylate
Normal gap hyperchloremic met. acidosis
Fe HCO3->15
CA-I
Fe HCO3-<15
Proximal RTA (type 2)
Isolated type
Fanconi synd.
Fe HCO3- <15
Negative urine net charge
Or
Urine osmolar gap > 100 mmol/l
Or
Urine ammonium >50 mmol/day
yes
High ammonium excretion
(diarrhea, acid load)
no
Low ammonium excretion
RTA type 1 (low serum K+) or
RTA type 4 (high serum K+)
Generation
•
•
•
•
H+ loss (renal, extrarenal)
H+ shift in to cells
Retention of HCO3Contraction Alkalosis
Correction
• Increase HCO3- filtration
• Decrease HCO3- reabsorption
• Decrease HCO3- regeneration
(=decrease NH4+ secretion)
• Increase HCO3- secretion
◦ H+loss
 GI; vomiting, NG tube suction, antacid
 Renal; thiazide or loop diuretic, 1o mineralocorticoid
excess, Bartter or Gitelman synd., post hypercapnia
◦ H+shift in to cell
 Hypo K+
◦ HCO3- Gain; administration of NaHCO3, organic
anion(citrate, acetate)
◦ Contraction alkalosis; loss CL- > HCO3 Cl- losing diarrhea
Generation
Maintenance
Correction
•
•
•
•
H+ loss (renal, extrarenal)
H+ shift in to cells
Retention of HCO3Contraction Alkalosis
•
•
•
•
decrease ECF volume
Cl- depletion
K+ depletion
renal failure
Case 1
 55 y/o female presented with UGIB
 Blood transfusion : WB 10 U, PRC 6 U
 BP 100/80 mmHg BUN/Cr 50/2
 Serum Na 140 K 3.0 Cl 88 HCO3 40 mEq/L
ABG: pH 7.53 PCO2 50 PaO2 80 mmHg
Q? Why does the patient have metabolic alkalosis?
Q? What is the expected value of urine pH and urine
Na?
Q? What is the appropriate treatment?
Case 2
 45 y/o female presented with PU and persistent
vomiting 2 days
 BP 100/60 mmHg, poor skin turgor
 Serum Na 140 K 2.2 Cl 80 HCO3 42 mEq/L
 BUN 80/1.9
 ABG: pH 7.53 PCO2 53 PaO2 80 mmHg
 Urine pH 5 Una 2 Uk 21 Ucl 3 mEq/L
Q? Why does the patient have metabolic alkalosis
and hypokalemia?
Q? Why does the patient have aciduria ?
Q? What is the appropriate treatment?
Case 3
 65y/o, COPD with pneumonia
ABG: pH 7.32 pCO2 70 mmHg HCO3 35
 post ET Intubation
ABG pH 7.52 pCO2 40 mmHg HCO3 32
Q? Why does the patient have metabolic alkalosis?
Q? What is the appropriate treatment?