SISAYAN | SISON | SONGCUAN 1 of 8 Page

ACID BASE BALANCE

Ma. Martina F. Alcantara, MD, FPCP,DPSN 02.07.2012
INTRODUCTION
Normal pH = 6.8 7.8 (pH compatible with life)
o [H+] =40 nEq/L
Extremely low concentration, that is why it is usually
expressed in negative logarithms pH
o [Na+]=140 mEq/L
All cellular, tissue, & organ processes are sensitive to pH
o At pH 6.8: 160 nanometers of H
o At pH 7.8: 16 nEq/L of H
Acid & alkali are ingested in diet to maintain life processes
o Aci d: adds H to body fluids
o Base: removes H to body fluids

Interstitial: more than plasma in a ratio of 70:30.

HCO
-
BUFFER SYSTEM
Main buffer system; important in the ECF
23 to 25 meq/L = normal pl asma HCO3 (ma am uses 24 for
uniformity s sake)
o ECF: 350 mEqs of HCO3 (70kg man, TBW=14L vol)
Regulated by both lungs & kidneys, and to some extent, the
liver
CO2 +H2O H2CO3 H
+
+HCO
-

(Enzyme: carbonic anhydrase; happens intracellularly)
Hydrogen is secreted going to the tubular area; excretion, then
HCO3 will be reabsorbed
Hendersson-Hassel bach eq
o [H
+
] =24 x pCO2 (CO2)RESPIRATORY A/B D/O
[HCO
-
] (HCO
-
) METABOLIC A/B D/O


OVERVIEW OF ACID-BASE BALANCE
Diet & cellular metabolism produce acids/ base with alkali
lost in feces
o Acidosis =acid addition >excretion
o Alkalosis =acid excretion >addition
Vol ati le aci d (Carbonic acid) comes from metabolism of
CHO & fats
o When tissue perfusion is adequate, and oxygen and insulin are
available, CHO and fats, which are the major constitution of
diet, are metabolized into CO2 +H2O
CO2 +H2O H2CO3 H
+
+CO3
o CO2 is a volatile acid. On a daily basis, 15-20 mmols of CO2
are generated on a process which is effectively eliminated by
the body by the lungs
Non-volati l e aci d (noncarboni c) derived from metabolism
of dietary amino acids (e.g. lactic acid; sulfuric acid; HCl
acid): more important
o Diet, cellular metabolism & fecal HCO
-
loss add
nonvolatile acid ~1 meq/L kg BW to the body (should
only generating 50-100 mEq/L/day) do not circulate
the body at all, but are immediately neutralized by the HCO3 in
the system; so if you have 350 meqs of HCO3 in the ECF as a
baseline, and you have 50-100 meqs to buffer, you have 5
days supply of HCO3 in the ECF (50 x 7 =350)
Excess amino acids, excess acid burden in the body
HCO production from some amino acids (aspartate &
glutamate), and organic anions (citrate: anticoagulant in the
blood bag) immedi atel y neutral i zes NVA (nonvolatile
acids) in the ECF
Kidneys play an important role in maintaining acid-base
balance by replenishing HCO3 in the ECF

NET ACID EXCRETION BY THE KIDNEYS
Under normal conditions, the kidneys: (3 Functions)
1. Excrete H
+
equal to NVA production with urinary buffers
(phosphate, creatinine): once H gets out of the tubules, it
interacts with PO4, proteins, hemoglobins, citrates, etc. called
the TITRATABLE ACIDS
2. Reabsorb filtered HCO3: the ultrafiltrate of plasma goes to
kidney at a rate of 180 L/day, so the kidneys can reabsorb
4320 meqs of HCO3 because the kidneys can secrete H
almost at the same amount; H goes out to be secreted, HCO3
goes into the blood
3. Creates new HCO3 through ammonium
Both excretion of acid and reabsorption of HCO3 are
accomplished by H+secretion.
H+ secretion: drives the reabsorption of filtered HCO3
Moreover, synthesis and excretion of ammonium (NH4+)
helps acid-base balance
o Ki dneys synthesi ze NH4 (ammoni agenesi s)
1 NH4+excreted : 1 HCO3- returned to ECF
Unused ammonium goes to the liver = Cori cycle
NAE = (Urinary NH4+ + Uri nary TA) (Uri nary HCO3 x V)
NAE: Net Acid Excretion, V: Volatile acids TA: Titratable acids
Ti tratabl e Aci ds urinary buffers (amino acids, citrates,
phosphates, sulfates) excreted with H; but is insufficient to
balance daily nonvolatile acid load ~50-100meq/L/d
-kidneys synthesize ammoni um (ammoniagenesis) and
excess goes to liver
Uri nary HCO3 very little lost in the urine because most are
effectively reabsorbed by the kidneys; not contributory to NAE

HCO3 REABSORPTION ALONG THE NEPHRON
HCO3 is freely filtered at the glomerulus with 4,320
meqs/day being reabsorbed (24 meqs/L x 180L/day)
o PCT: 80%; TAL: 10%; DT: 6%; CCD:4%
Thus, very little or no HCO3 is excreted in the urine

REGULATION OF H
+
SECRETION
Increased Decreased
pH pH
a PCO2 (ie. COPD) a PCO2
Cortisol, endothelin
(both stimulate the H+ secretion and the
HCO3 reabsorption in the PCT and the
collecting ducts)

HCO3 filtered load HCO3 filtered load
ECFV contraction (stimulates RAA) ECFV expansion
AII (acts on the PCT and the distal tubule to
secrete H+ and reabsorb the HCO3),
Aldosterone (1.stimulates Na reabsorption in
terms of volume contraction, 2. excretes K,
and 3. stimulates H+ secretion), K
Hypoaldosteronism, K
PTH (chronic) PTH ( acute)

FORMATION OF NEW HCO3
PCT produces NH
4+
from the metabolism of glutamine
TAL (ascending loop) reabsorbs NH
4+
accumulates in
medullary interstitium with NH3, CD secrete NH
4+
and
eliminated in the urine. This process adds HCO
3-
nto the
body.
Secretion adds bicarbonate
Assessing NH4+excretion is done indirectly


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Uri ne ani on gap = Uri ne (Na + K) Uri ne Cl
o Negative value adequate NH4+excreted; more Cl
excreted; kidneys are normal (ie. diarrhea)
o Posi ti ve val ue renal defect in NH4+production and
excretion (ie. RTA: defect in acidification of urine)
NOTE: Chloride: only reabsorbable ion; negative is favorable

BUFFERING: RESPONSE TO A/B DISORDERS
ECF maintains a very narrow range pH 7.35-7.45 (ideal
whether diseased or normal state)
pH =6.1 + log HCO
3-
metabolic d/o kidneys
0.03PCO2 respiratory d/o lungs
3 compensatory mechani sms:
1. ECF and ICF buffering
2. Respiratory
3. Renal

1. ECF AND ICF BUFFERING:
ECF buffering is virtually INSTANTANEOUS
o HCO
3-
, phosphates and plasma proteins buffer 50-70%
of nonvolatile acids & alkali (most in diet)
o Demineralization of Bones in acidosis (CKD, renal
osteodystrophy) because buffers are overuse
ICF buffering takes SEVERAL MINUTES
o Movement of H+into cells (nonvolatile acids)
o Movement of H+out of cells (nonvolatile alkali)
o Responsible for virtually all respiratory a/b d/o
H+goes in or out depends on what is needed

2. RESPIRATORY COMPENSATION:
MINUTES to SEVERAL HOURS to complete
Chemoreceptors sense blood PCO2 & pH RR
o brainstem (medulla)
o periphery (carotid/aortic bodies)
Metabolic acidosis [H
+
] pH RR PCO2
o Note: maximal PCO2=10 mmHg
o RR to attempt to decrease acid (hyperventilate)
Metabolic alkalosis [H
+
] pH RR PCO2
o Note: maximal PCO2=60 mmHg (at this level, theres
also hypoxia going on along with retained CO2 at 60 )
o In the presence of hypoxia, the brain is being stimulated
to start breathing

3. RENAL COMPENSATION
SEVERAL DAYS to complete; very responsive to acidosis
Acidosis ( [H+] or PCO2) H+ secretion
HCO3 reabsorption
T.Acid excretion
NH4 prod. &excretion
o *new HCO3 added to body
Alkalosis ( [H+] or PCO2) H+ secretion
HCO3 reabsorption
T.Acid excretion
NH4 prod. & excretion
o HCO3 appears in the urine
o Kidneys are the last organ to buffer the system

SIMPLE ACID-BASE DISORDERS
Di sorder Plasma pH Primary Al terati on Defense Mechani sm
Metabolic
Acidosis
ECF [HCO3] ICF & ECF buffers
Hyperventilation
(PCO2); Renal NAE
Metabolic
Alkalosis
ECF [HCO3] ICF & ECF buffers
Hypoventilation(PCO2);
Renal NAE
Respiratory
acidosis
PCO2 ICF buffers
Renal NAE
Respiratory
alkalosis
PCO2 ICF buffers
Renal NAE

Simple acid-base disorders
- pH is acidotic or alkalotic
- uncompensated
- one disorder
PREDICTION OF COMPENSATORY RESPONSE
ON SIMPLE ACID-BASE DISORDERS
Di sorder Predi cti on of Compensati on
Metabolic
Acidosis
PaCO2 = (1.5 x HCO3) + 8 OR PaCO2 = [ HCO3] +15
PaCO2 1.25 : 1 mmol/L in [ HCO3]
Metabolic
Alkalosis
PaCO2 0.75 mmHg : 1 mmol/L in [ HCO3]
PaCO2 = [ HCO3] +15
R. Alkalosis
Acute
Chronic

[ HCO3] 2 mmol/L : 10 mmHg PaCO2
[ HCO3] 4 mmol/L : 10 mmHg PaCO2
R. Acidosis
Acute
Chronic

[ HCO3] 1 mmol/L : 10 mmHg PaCO2
[ HCO3] 4 mmol/L : 10 mmHg PaCO2

MIXED ACID-BASE DISORDERS
Independently coexi sti ng di sorders, not merely
compensatory responses are often seen in patients in
critical care units
o Ex. Diabetic ketoacidosis (metabolic acidosis) with an
independent respiratory problem leading to respiratory
acidosis or alkalosis; metabolic acidosis or
alkalosis+pneumonia
o Cl ue: normal i zi ng pH
Acid-base nomograms

DIAGNOSIS OF ACID-BASE DISORDERS
1. Obtain ABGs and electrolytes (Na, K, Cl-) simultaneously.
2. Compare [HCO3] on ABGs and electrolytes to verify
accuracy.
3. Calculate ANION GAP (AG).
4. Know 4 causes of hi gh AG aci dosi s.
a. Ketoacidosis
b. Renal acidosis
c. Lactic acidosis
d. toxins
5. Know 2 causes of hyperchloremic or Non Ani on Gap
aci dosi s.
a. Bicarbonate loss from GI tract (diarrhea)
b. Renal tubular acidosis
6. Estimate compensatory response (see table)
7. Compare AG and HCO3
8. Compare change in [Cl] with change in [Na+]

ANION GAP
All evaluations of acid-base disorders should include a
simple calculation of the anion gap; represents the
unmeasured anions in plasma (normally 10-12 mmol/L)
Unmeasured anions in plasma (10-12mmol/L)
1. Anion proteins 3. Phosphate


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2. Sulfate 4. Organic anions

AG = [Na+] ([Cl ] + [HCO3])
[Na+] +[unmeasured cations] =[Cl] +[HCO3] +[unmeasured
anions]

HIGH-ANION GAP ACIDOSIS
May come from accumulation of acid anions (acetoacetate
and lactate), more commonly increased in the unmeasured
anions rather than decrease in the unmeasured cations, or
increase in anionic albumin
o Increased unmeasured anion/decrease in unmeasured
cations (calcium, magnesium, potassium) (20-30)
High-AG acidosis low [HCO3] and elevated AG
Usually due to non-Cl-contai ni ng acids that contain:
o inorganic (phosphate, sulfate)
o organic (ketoacids, lactate, uremic organic anions)
o exogenous (salicylate) anions
*Recall: Chloride is the only reabsorbable ion; others are non-
reabsorbable, so they remain in the blood
AG additional a-b disorder is present that modifies the
[HCO3 ] independently
o e.g. Met acidosis +chronic respi acidosis

DECREASED ANION GAP
unmeasured cations
Addition of abnormal cations (lithium intox) or cationic Ig
(plasma cell dyscrasia)
in plasma anion albumin (nephrotic syndrome)
in effective anionic charge on albumin (acidosis)
Hyperviscosity & severe hyperlipidemia
o ( al bumin by 1g/dl from 4.5 g/dl: AG 2.5 meq/L)


Metabolic acidosis because bicarbonate level is low.
a. Normal anion gap (A=10), hyperchloremic (Cl= 126)
b. High anion gap (A=30), normochloremic (Cl=106)

METABOLIC ACIDOSIS
Can occur in the following situations:
o in endogenous acid production (lactate/ketoacids)
o Loss of bicarbonate (diarrhea)
o Accumulation of endogenous acids (renal failure)
Has profound effects on:
o Respiratory (Kussmaul respiration: fast, shallow
breathing)
o Cardiac (depressed cardiac contractility)
o Nervous system (peripheral arterial vasodilation &
(central venoconstriction)
o CNS depression
o Glucose intolerance




TWO TYPES OF METABOLIC ACIDOSIS
A. HIGH AG ACIDOSIS:
METABOLIZABLE NON-METABOLIZABLE
lactic acidosis
ketoacidosis
- diabetic
- alcoholic
- starvation
drugs/toxin
- ethylyne glycol
- methanol
- salicylates
- renal failure
*Think of only four in high AG (normochloremic) acidosis
: 1. Lactic acidosis, 2. Ketoacidosis, 3. Toxins from drugs, 4. Toxins from
renal failure

B. NON-AG/ HYPERCHLOREMIC ACIDOSIS:
GI bicarbonate loss
o Diarrhea
o External pancreatic or small-bowel drainage
o Ureterosigmoidostomy, jejunal loop, ileal loop
o Drugs CaCl, MgSO4, cholestyramine
Renal Acidosis/Renal Tubular Acidosis
o RTA 2 (proximal)
o RTA 1 (classic/distal)
o RTA 4 (hyperkalemic)
Drug-induced hyperkalemia (with renal insufficiency)
o K-sparing diuretics
o trimethoprim
o pentamidine
o ACE or AT-II receptor blockers
o CYA

TREATMENT OF METABOLIC ACIDOSIS
Alkali treatment in severe acidemia to slowly increase the
plasma [HCO3 ] to 20 to 22 mmol/L range
Severe acidemia, pH <7.20, needs 50-100 meq of Na HCO3
(1-2 vials) over 30-45 mins during the initial 1 to 2 hrs of
therapy
Fluids, inotropes
Treat underlying disorders; determine if acid is
metabolizable or nonmetabolizable


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A. HIGH-AG ACIDOSIS:
1. LACTIC ACIDOSIS
Type A poor ti ssue perfusi on
o Circulatory insufficiency (shock/ failure)
o Severe anemia
o Mitochondrial enzyme defects & inhibitors (Carbon
monoxide, cyanide)
Type B - anaerobi c disorders
o Malignancies, DM, hepatic or renal failure, severe
infections, seizures, AIDS, drugs or toxins, bowel
ischemia or infarctions

Treatment:
o Restore good tissue perfusion
o Avoid vasoconstrictors
o Alkali therapy in severe acidosis (pH<7.15) to raise pH
to 7.2 over 30-40 mins
o Note that overshoot alkalosis can occur causing fluid
overload & hypertension (1 vial of NaHCO3 can invite
fluid in lungs and cause congestion)

2. KETOACIDOSIS
DM ketoacidosis - fatty acid metabolism and
accumulation of ketoacids (acetoacetate &
hydroxybutyrate)
o This condition is caused by increased fatty acid
metabolism and accumulation of ketoaicds,
acetoacetate and beta hydroxybutyrate
o It occurs in i nsul i n-dependent DM with cessation of
insulin or an intercurrent illness
infection,gastroenteritis, pancreatitis, or myocardial
infarction which increases insulin reqt acutely and
temporarily. The accumulation of ketoacids accounts
for the increment in the AG accompanied by
hyperglycemia.
Cl i ni cal l y - AG & hyperglycemia (>300mg/dl)
o Because insulin prevents ketoacidosis, bicarbonate
therapy is only indicated with severe acidemia
Al cohol i c ketoaci dosi s - abrupt cessation of alcohol
consumption with accumulation of - hydroxybutyrate
o Accompanied by UGIB, pancreatitis, pneumonia
o Clinically, AG & hypophospahtemia, hypokalemia &
hypomagnesemia
o Typically, insulin levels are low, with high triglycerides,
cortisol, glucagon & growth hormones



3. DRUG/TOXIN- INDUCED ACIDOSIS
(1) Salicylates
(2) Ethylyne glycol
(3) Methanol
(4) Renal failure
*very uncommon

DRUG-INDUCED-SALICYLATE ACIDOSIS
a/b disorders:
o Respi ratory al kal osi s
o Mi xed metabol i c aci dosi s and respi ratory al kal osis,
or pure hi gh-AG met aci dosi s
Treatment:
o Vigorous gastric lavage with saline (not NaHCO3)
immediately, followed by activated charcoal per NG
tube
o In acidotic patients: NaHCO3 per IV, for alkaline
diuresis and maintain urine output (urine pH >7.5)
o Precautions for hypokalemia, hyponatremia and
hypoglycemia
Alkalemic patients should not receive NaHCO3
Acetozolamide in the face of alkalemia when alkaline
diuresis cannot be achieved or to ameliorate volume
overload associated with NaHCO3 administration
Glucose-containing fluids administered due to danger of
hypoglycemia
Excessive insensible fluid losses severe volume
depletion and hypernatremia

DRUG-INDUCED-ETHELYNE GLYCOL
Commonly used in anti -freeze
a/b disorder: metabol i c aci dosis + severe damage to
CNS, heart, lung & kidney
Di agnosti c:
o AG acidosis and osmolar gap attributable to
ethylene glycol & its metabolites, oxalic acid, glycolic
acid, lactic acid
o oxal ate crystals i n the uri ne


SISAYAN | SISON | SONGCUAN 5 of 8 |Page

o what is osmolar gap? We measure osmolarity base on
Na, etc. We also submit plasma to the lab for
measurement. If the 2 measurements are different then
there is a GAP which may be due to INTOXICATION
Treatment:
o Saline/osmotic diuresis
o Thiamine & pyridoxine supplements
o Fomepizole or ethanol
IV Administration of alcoholic dehydrogenase inhibitor to
achieve level of 22mmol/L serves to lessen toxicity
because compete with ethylene glycol for metabolism of
alchol dehydrogenase
o Hemodialysis
Indicated when arterial pH is <7.3, or osmolar gap
exceeds 20mOsm/kg

DRUG-INDUCED-METHANOL
Ingestion of methanol ( wood alcohol)
Di agnosti c:
o metaboli c acidosis +optic nerve & CNS damage
Caused by metabolites formaldehyde and formic acid
o osmolar gap
Treatment: same as ethylene glycol acidosis (general
supportive measures, fomepizole, hemodialysis)

4. TOXIN-INDUCED- RENAL FAILURE
Accumulation of endogenous toxin
Hyperchloremic acidosis of moderate renal insufficiency eventually
will convert to high-AG acidosis
Advanced renal failure due to poor filtration and
reabsorption of organic anions
o Number of functioning nephrons becomes insufficient to keep
pace with net acid production
Uremi c aci dosi s NH4+ production and excretion
Metaboli c aci dosi s characterized by HCO3 15mmol/L;
AG 20 mmol/L
o Also increases calcium excretion, proportional to cumulative
acid retention
Acid retention in chronic renal failure is buffered by
al kal i ne sal ts from bone recall renal osteodystrophy
o HCO3- does not decreased further despite significant acid
retention (up to 20mmol/d) indicates participation of buffers
outside the extracellular comp.
Treatment: NaHCO3 at 1.0-1.5 mmol/kg/day
o Conservative vs renal replacement therapy


B. HYPERCHLOREMIC (NONGAP) METABOLIC ACIDOSIS
Alkali can be lost from the GIT (diarrhea) or from the kidneys
(renal tubular acidosis). In these disorders, reciprocal
changes in Cl and HCO3 result in normal anion gap.
in [Cl] above the normal value ~ in [HCO3] thus
resulting in a normal AG
o Absence of this relationship suggests mixed disturbance

DIARRHEA VS RENAL TUBULAR ACIDOSIS (RTA)
Loss of HCO3 in di arrhea metabolic acidosis +volume
depletion
o But, despite the met. acidosis, urine pH is ~6, due to
the renal synthesis & excretion of NH4+ (serving as
urinary buffer that increases urine pH)
In contrast, in RTA, there is urinary excretion of NH4+
o RTA: the tubules itself could not acidify; hypokalemic, very
severe metabolic acidosis but patient does not present with
tachypnea; urine is alkaline, blood acidic

Uri nary Ani on Gap = [Na+ + K] u - [Cl ]u
UAG = negati ve (extrarenal cause/di arrhea)
=[Cl ]u >[Na++K]u [ NH4]u
Kidneys are doubling up in production of ammonia
UAG = posi ti ve (renal cause)
=[Cl ]u <[Na++K]u [ NH4]u
Kidneys fail in acidification
Renal causes:
o RTA
o Chronic Kidney Ds, GFR 20-50 ml/min
RTA l ow pl asma [HCO3 ] / (+)UAG
1. RTA 2 (proximal): reabsorpti on problem i n PCT
80%-Glucosuria, aminoaciduria, phosphaturia
(Fanconis syndrome), hypokalemia, urine pH
<5.5, low serum K
Since HCO3 is not reabsorbed normally in the proximal
tubule, therapy with NaHCO3 enhanced renal
potassium wasting and hypokalemia
2. RTA 1 (di stal): aci di fi cati on defect
hypokalemia, urine pH > 5.5, nephrolithiasis,
nephrocalsinosis & bone disease (hypocitraturia,
hypercalciuria), low serum K
most common
3. RTA 4 (hyporeninemi c hypoal dosteroni sm)
Hyperkalemia, older pts, DM or tubulointerstitial ds,
CKD with Hypertension, CHF
Never mind daw!


NONGAP METABOLIC ACIDOSIS RTA2
Everything goes in: bicarbonates, amino acids, phosphates, glucose
found in urine = Fanconis syndrome
Distal tubule intercalated alpha cells-responsible for secretion of H. but
there is a failure of acidification and secretion


NONGAP METABOLIC ACIDOSIS RTA1



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METABOLIC ALKALOSIS
pH, serum [HCO3] with compensatory PaCO2; often
with hypochl oremia & hypokal emia
Pathophysi ol ogy:
o How do patients become alkalotic?
o Why do they remain alkalotic, since renal excretion of
the excess HCO3- should rapidly restore normal acid-
base balance?
o Generative and maintenance phase
Rarely find patients with metabolic alkalosis
Ssx are similar with acidosis but with hypoventil ati on
instead



CAUSES OF METABOLIC ALKALOSIS
A. LOSS OF H+
1. GIT Hydrogen l oss: vomiting, nasogastric suction, antacid,
Cl-losing diarrhea
o Gastric juice has high HCl concentration; its entry into
the duodenum is matched by pancreatic HCO3-. Thus,
plasma rise in HCO3 is only transient.
o In vomiting and NG suction, tendency for alkalosis is
enhanced with hypokalemia; HCl is lost; in duodenum
buffered by pancreatic HCO3 where it gets reabsorbed by
blood
o In antacid use (Mg OH): OH buffers H+, while Mg
combines with pancreatic HCO3 and some fats and
PO4; thus some HCO3 becomes reabsorbed in the GI
tract
2. Renal Hydrogen Loss
o Loop or thiazide-type diuretics
Volume contraction
(-) NaCl & water reabsorption inc flow to the the
distal tubule (+) aldosterone in distal
tubulehypokalemia
Note: Hypokalemia K moves out of the cellH+
(and Na+) shifts inside the cell
o Mineralocorticoid excess
Aldosterone: (+)H secretion (intercalated cells )
and (+) Na reabsorption
Concomitant Hypokalemia plays impt role in
maintenance of metabolic alkalosis
o Postchronic hypercapnia
Chronic respi alkalosis compensatory H
secretion renal reabsorption of HCO3
o Low chloride intake
o Carbenicillin
o Hypercalcemia (increase milk alkali syndrome)
3. H+ movement i nto cell s: hypokalemia, refeeding

B. RETENTION OF HCO3-
massive blood transfusion (due to citrate preservative),
NaHCO3, milk-alkali syndrome
Organic anions (lactate, acetate, citrate, ketoacids in
presence of insulin) are rapidly metabolized as HCO3 in the
body.
Citrate used as anticoagulant by blood banks; >8 units of
blood to cause significant plasma rise in HCO3
Human plasma protein fractions used as plasma expanders
also use acetate and citrate

C. CONTRACTION ALKALOSIS
(1) loop or thiazide-type diuretics
(2) gastric losses in achlorhydria
(3) sweat losses in cystic fibrosis

NaCl and water is lost w/o HCO3
Whereas, it is mainly the H+loss that causes met alkalosis
in vomiting and diuretic use, volume contraction contributes
to the maintenance of met alkalosis
Diuretics cause: 1. Volume contraction, 2. Enhances free water
clearance, kidneys would have to double up absorption of water
with Na and Cl, fluid going to the distal tubule is increased,
aldosterone is stimulated, hypokalemia moving out of the cell invites
H+to shift inside the cell
Aldosterone: potentiates H+secretion by the intercalated cells and
Na reabsorption
Chronic respiratory alkalosis: compensation is reabsorption of
HCO3


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Lactate, acetate, citrate, ketoacids: metabolized as HCO3 in the
body; so in excess blood transfusion, expect alkalosis; also human
plasma protein fractions such as plasma expanders
Reverse of dilutional acidosis

TREATMENT OF METABOLIC ALKALOSIS
Saline-responsive Alkal osi s:
o Reversal of contracti on component: mainstay of
treatment
o Give NSS, not LRS, because lactate will also become HCO3
o Removing stimulus to Na retention; allowing NaHCO3
excretion in the urine
o Increasing distal Cl delivery to promote HCO3 secretion
in the CC tubule
o Examples
Vomiting, nasogastric suction
Diuretics
Posthypercapnia
Low chloride intake
Saline-Resi stant:
o Edematous states
o Mineralocorticoid excess
o Severe hypokalemia
o Renal failure



ACID BASE DISORDERS:
pH = 7.4 [ HCO3] = 24
(mEq/L)
P CO2 = 40
(mm Hg)
Di sorder
7.23 10 25 Metabolic Acidosis
7.46 30 44 Metabolic Alkalosis
7.37 28 50 Respiratory Acidosis,
Chronic
7.34 26 50 Respiratory Acidosis,
Acute
7.40 11 19 Metabolic Acidosis
+Respi Alkalosis
7.14 17 45 Metabolic acidosis
+respi acidosis

Sample computati ons:
1. pH is low; metabolic because the change in HCO3 is far
greater than the change in pCO2 =metabolic acidosis
Compute for compensation:
PaCO2 =(1.5 x HCO3) +8
=(1.5 x 10) +8
=15 +8
=23 +/-2 (21-25)
pCO2 of the patient is 25, so this is simple metabolic acidosis.

2. pH is a little bit high, HCO3 is high, pCO2 is high
Compute for compensation:
PaCO2 0.75 mmHg: 1 mmol/L in [HCO3]
HCO3 of the patient is 30; difference from normal is 6.
So, 0.75 x 6 =4.5 +40 (pCO2) =44.5 ~44, so this is
simple metabolic alkalosis
3. pH is normal, HCO3 is low, pCO2 is low: so there are two
problems. For sure there is a metabolic problem because the
HCO3 is used up.
Compute for compensation:
PaCO2 =(1.5 x HCO3) +8
=(1.5 x 11) +8
=16.5 +8
=24.5 +/- 2 (22.5-26.5)
But the pCO2 did not fall in that range, still it is low (19), so there
must be an existing respiratory problem that is using the HCO3,
respiratory system is compensating but not at predicted level, so
there is respiratory alkalosis

4. pH is acidic, HCO3 is low, and pCO2 slightly increases
Compute for compensation:
PaCO2 =(1.5 x HCO3) +8
=(1.5 x 17) +8
=25.5 +8
=33.5 +/- 2 (31.5-35.5)
But HCO3 is 45, there is retention of pCO2, so there is metabolic
acidosis and respiratory acidosis




LECTURE Sources
Normal Font from ppt, italics from recording
Harrisons Principle of Internal Medicine vol. 1 17
th
ed
Renal Physiology 4
th
ed., Bruce M. Loeppen,MD, PhD & Bruce A. Stanton, PhD
Comprehensive Clinical Nephrology 3
rd
ed., Richard J . J ohnson, MD
Accdg to maam she may give short histories to help with computation.
Some Tips(Paulet ulet??):
Blood has to always maintain this pH= 7.35-7.45
Helpful from pH formula:
pH = HCO3-(/H) metabolic d/o kidneys
PaCO2 respiratory d/o lungs
There is always an interplay of lungs and kidney to maintain blood ph.
Bicarb is metabolic, CO2 =respiratory
bicarb pH= metab alkalosis (compensation is done by lungs=
PaCO2 to pH hypoventil ation)

bicarb pH=metab aci dosis (compensation i s done by l ungs=
PaCO2 to pH hyperventi lat ion). Check if compensation is
adequate via Wint er s formula: PaCO2 = (1.5 x HCO3) + 8 +/-2

PaCO2, pH (i nverse rel ati onship from the above formula)-
respirat ory acidosis probmetaboli c compensat ion of the ki dneys,
bicarb to pH

PaCO2 pH respiratory al kal osis probmetabolic
compensati on of kidneys= bi carb to pH)

In metabolic acidosis (low bicarb,low pH) distinguish between:
1. High AG met acidosis (MUDPILES)

M-ethanol
U-remia
D-KA
P-araldehyde
I-Iron, INH ingestion
L-actic acidosis
E-thanol (alcohol)
S-alicylate

2. Normal AG met acidosis (includes hyperchloremic acidosis) (HARD)

H-hyperventilation/hyperalimentation
A-cetazolamide
R-enal tubular acidosis
D-iarrhea



SISAYAN | SISON | SONGCUAN 8 of 8 |Page

Pathophysio of metabolic acidosis: ischemia, dec tissue perfusion, dec
normal oxygen exchange on alveoli and blood vesselanaerobic
metabolism (lactic acidosis, ketoacidosis,etc)

In metabolic alkalosis, increased bicarb and ph always check Urine
chloride, to det if saline responsive (<10 caused by vomiting, NGT,
diuretics) or saline unresponsive (>20, caused by alkali administration
with dec GFR, unilateral adrenectomy)
Tx: NSS (due to loss of fluids)
For saline unresponsive primary aldosteronism: give potassium
(Al-K-l ow-sis)

MEGA SHOUT-OUT!!!
This is our first and last shout-out ever (pagbigyan na!) Hi sa mga
naging groupmates ko from year 1 to year 3.. Love you guys, all! Sana di pa rin
tayo mag-away-away sa JIship. Hehehe.. Special shout-out to small boy,
makibaka/miss black, glaucoma, incompetent leader (thanks sa Rebisco! ),
absentee, mission impossible, four eyes, bathroom tissue, amboy, miss
violet/lawyer, and dr.E (please pakuhanin mo na kami ng exam!).. Hi sa mga
artistahing boys of medisinasss Franz, Leo, Kim the lantern queen escorts!
Hi na rin to all members of uerm3bics yg, especially to Reg Santos. Hi Mark
Tecson, alam na.. To starbucks tomas people, I so miss those days! Hi Anglo
people: rooms 222, 223, 302, 315, 324, 325, 326, 420, 428, and 526.. Hi Jeanie,
love you girlie! And last but not the least, hi to my beloved girls: Tet, Berna,
Claire, Nix, Pam, Golda, and Dap (I know youll read this). Are you all prepared
for our epic group pic??
2013B meds finest!..
~ Crystal (aka mother butler/blue sky/aquadel) ~

Thank You Lord. tinapay lang hiningi ko..binigyan Nyo ko ng hamburger, may
fries pa!
Cast all your cares upon Him for He cares for you. 1Peter 5:7
Heres to 2013B^^ <3

Tal ang toxic nga talaga ng recording nato. Malapit na ako masuka. Buti na lang
natapos ko,hehe. I added some info for clarification.GOD BLESS US GUYS.
Malapit na JI. Let us entrust everything to HIM. ---- CAT