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‫بسم ا الرحمن‬
‫الرحيم‬
‫” رب اشرح لي‬
‫صدري‬
‫ويسر لي أمري‬
‫واحلل عقدة من‬
‫لساني‬

APPROACH TO
ACID-BASE
DISORDERS

Definitions
Acid: a substance that may donate protons
(hydrogen ions)
Base: a substance that may receive protons
pH: the negative logarithm of protons
concentration
Strong acids vs. weak acids
Volatile (Co2) vs. nonvolatile acids
Buffers

40 neq = 0.00000004 meq = pH 7.4

0.00000020= pH 6.7
0.00000010 = pH 7.0
0.00000008 = pH 7.1
0.00000006 = pH 7.2
0.00000005 = pH 7.3
0.00000004 = pH 7.4
0.00000003 = pH 7.5
0.00000002 = pH 7.7
0.00000001 = pH 8.0

ACID-BASE DISORDERS
DEFINITIONS
 ACIDEMIA VS ALKALEMIA
 ACIDOSIS VS ALKALOSIS
 RESPIRATORY VS METABOLIC
 COMPENSATORY RESPONSES
 SIMPLE (SINGLE) VS MIXED

ACID-BASE DISORDERS
DIAGNOSIS BASED ON:

SUGGESTIVE HISTORY

SUGGESTIVE PHYSICAL EXAM

SUGGESTIVE CO2, K+, CL-

SUGGESTIVE pH, PCO2, HCO3-, AG

APPROACH TO THE DIAGNOSIS
OF ACID-BASE DISORDERS
Suspicious clinical or lab findings
Identify the major Acid-base disorder
Determine if it is simple or mixed
Establish the cause of the disorder
Direct treatment to the underlying cause unless
the pH is in a dangerous range
(7.10 < or > 7.60)

ACID-BASE DISORDERS

FORMULAS:
HENDERSON-HASSELBALCH
 pH = pK + log ([HCO3-]/[0.03* PCO2])

pH = 6.10 + log (24/0.03*40) = 7.40
MODIFIED HENDERSON
 [H+] = 24* PCO2/[HCO3-]

[H+] = 24* (40/24) = 40 neq/L (pH=7.4)

Simplified Henderson -
Hasselbach equation
(H+) = 24 x PaCO2
HCO3
Shows relationship between 3 major
factors:

H+
 CO2
 HCO3

SIMPLE ACID-BASE DISORDERS

Primary Disorder pH HCO3- PCO2
Met. Acidosis ↓ ↓↓ ↓
Resp. Acidosis ↓ ↑ ↑↑
Met. Alkalosis ↑ ↑↑ ↑
Resp. Alkalosis ↑ ↓ ↓↓

FREQUENCY OF SIMPLE ACID-
BASE DISORDERS
Metabolic

Acidosis 10%

Alkalosis 40%
Respiratory

Acidosis 20%

Alkalosis 20%

Consequences of acidosis vs. alkalosis
Impaired cardiac
contractility
Arteriolar dilation
Venoconstriction
Centralization of blood
volume
Increased pulmonary Arteriolar constriction
vascular resistance Reduced coronary blood flow
Cardiovascular Decreased cardiac output Reduced anginal threshold
Decreased systemic BP Decreased threshold for
Decreased hepatorenal cardiac arrhythmias
blood flow
Decreased threshold for
cardiac arrhythmias
Attenuation of
responsiveness to
catecholamines

Insulin resistance Stimulation of anaerobic
Inhibition of anaerobic glycolysis
glycolysis Formation of organic acids
Reduction in ATP Decreased oxyhemoglobin
Metabolic synthesis dissociation
Hyperkalemia Decreased ionized Ca
Protein degradation Hypokalemia
Bone demineralization Hypomagnesemia
(chronic) Hypophosphatemia

Tetany
Inhibition of metabolism
Seizures
and cell-volume
Neurologic Lethargy
regulation
Delirium
Obtundation and coma
Stupor
Compensatory
Compensatory
hyperventilation with
Respiratory hypoventilation with
possible respiratory
hypercapnia and hypoxemia
muscle fatigue

RESPONSE TO SIMPLE
ACID-BASE DISORDERS
Disturbance Equation Interval Level
Met. Ac. 1 = 1.2 12-24 hr 10
Met. Al. 1 = 0.7 24-36 hr 55
Ac. Resp. Ac. 1 = 0.1 5-10 min 43
Ch. Resp. Ac. 1 = 0.3 72-120 hr 45
Ac. Resp. Al. 1 = 0.2 5-10 min 18
Ch. Resp. Al. 1 = 0.4 48-72 hr 13

Calculation of appropriate compensation

Or
In metabolic disorders add 15 to HCO3:
Example: if HCO3=10 + 15 = 25 then the PCO2
should be 25, and the last two digits of pH 25

pH=7.25

HCO3=10

PCO2=25

Normal Anion Gap
AG = Na – (HCO3+Cl) = 8-12
A-10
HCO3- PaCO2 40
25 pH 7.40

Na
140 CL
105

METABOLIC ACIDOSIS
AG = 10 AG = 10
AG = 25
HCO3 =15
HCO3 =25
HCO3 =10
- HCO3 - HCO3
CL- =115
+ CL- CL- =105 + A- CL- =105

HYPERCHLOREMIC NORMAL HIGH AG

THE SERUM ANION GAP

AG = Na+ - (HCO3- + CL-), NL = 10 ± 2
AG ≥ 27 INDICATE ORGANIC MET. AC.
AG + HCO3 ≥ 42 INDICATE MET. AL.
AG DECREASED WITH PARAPROTEIN
AG DECREASED WITH LOW ALBUMIN

Increased anion gap
metabolic acidosis

ketones, lactate, sulfates, or metabolites of methanol,
ethylene glycol, and salicylate
hyperalbuminemia and uremia (increased
anions)
hypocalcemia or hypomagnesemia (decreased
cations)

The effect of low albumin can be
accounted for by adjusting the
normal range for the anion gap
2.5 mEq/L for every 1 g/dL fall in
albumin.

Decreased anion gap
hypoalbuminemia
hypercalcemia
hypermagnesemia
Lithium intoxication
hypergammaglobulinemia
bromide or iodide intoxication

ACID-BASE DISORDERS
EXAMPLE OF A SIMPLE DISORDER
pH (7.55) = C * [HCO3-] (18 mmol/L)
PCO2 (21 mm Hg)

Step 1: pH , indicates alkalemia (Met. or Resp)
 Step 2: HCO3- , indicates Resp. Alkalosis
 Step 3: PCO2 , confirms Resp. Alkalosis

The delta gap
The difference between the patient's anion gap
and the normal anion gap is termed the delta gap
considered an HCO3 − equivalent, because for
every unit Rise in the anion gap, the
HCO3 − should lower by 1
The delta gap is added to the measured HCO3 − , the
result should be in the normal range for HCO3 −;
elevation indicates the additional presence of a
metabolic alkalosis

ACID-BASE DISORDERS
EXAMPLE OF A MIXED DISORDER
pH (7.55) = C * [HCO3-] (30 mmol/L)
PCO2 (35 mm Hg)

Step 1: Alkalemia
 Step 2: HCO3- , indicates Met. alkalosis
 Step 3: PCO2 , indicates Resp. alkalosis
 Step 4: ∆ HCO3- (25%) > ∆ PCO2 (12.5%)

Step 5: The major disorder is metabolic alkalosis

MIXED ACID-BASE DISORDERS
DOUBLE

Metabolic and respiratory acidosis (serious)

Metabolic and respiratory alkalosis (serious)

Metabolic acidosis & respiratory alkalosis

Metabolic alkalosis & respiratory acidosis
TRIPLE

Metabolic acidosis & alkalosis + resp. disorder

EXAMPLE OF DOUBLE DISORDER
Health Emphysema + Diarrhea
pH 7.40 7.32 7.10
PCO2 40 80 80
HCO3 24 40 24

EXAMPLE OF DOUBLE DISORDER
Health Emphysema + Diuretic
pH 7.40 7.32 7.40
PCO2 40 80 80
HCO3 24 40 48

EXAMPLE OF TRIPLE DISORDER
Health NG + Sepsis + Endotox.
pH 7.40 7.49 7.14 7.44
PCO2 40 44 24 12
HCO3 24 32 8 8
AG 9 11 33 35
∆ AG 0 2 24 26

Masked disorder
A vomiting, ill-appearing diabetic patient has
laboratory results showing:

Na, 137; K, 3.8; Cl, 90; HCO3 −, 22;

pH, 7.40; Pco2, 41; Po2, 85
anion gap = 137 − (90 + 22) = 25 (normal :10)
Respiratory compensation is evaluated by Winter's formula
Predicted Pco2 = 1.5 (22) + 8 ± 2 = 41 ± 2
delta gap = 15 + 22 = 37

Normal ABG?
A diabetic patient presented with gastroentritis
found to have:

pH: 7.4

HCO3: 24

PCO2: 40

Na: 144, K: 4, CL: 95, TCO2: 24, RBS: 520,

Positive test for ketons
What is the acid-base status of this patient?

METABOLIC ACIDOSIS
P R IM A R Y : D E C R E A S D H C O 3
RESPO NSE: D EC RESED PC O 2

C AU SES

NO RM A L A G H IG H A G
1 0 m E q /L > 1 5 m E q /L

G I HC O 3 LO SS K E T O A C ID O S ID
RENA L HC O 3 LO SS L A C T IC A C ID O S IS
H Y P O A L D O S T E R O N IS M R E N A L F A IL U R E
TPN IN T O X IC A T IO N

METABOLIC ACIDOSIS
HIGH ANION GAP
Ketoacidosis (DM1, ETOH, Starvation)
Lactic acidosis (A, B, D)
Intoxication

Ethylene glycol

Methanol

Salicylic acid
Advanced renal failure

METABOLIC ACIDOSIS
INTOXICATION:
HIGH OSMOLAR GAP

ETHYLENE GLYCOL

METHANOL
SALICYLATE

RESPIRATORY ALKALOSIS

METABOLIC ACIDOSIS

MIXED

METABOLIC ACIDOSIS
KETOACIDOSIS
Diabetes 1 (Insulin lack) leads to fatty acids
oxidation and production of acetoacetate (2) and
B-OH-butyrate (5), which is buffered by HCO 3-,
causing high AG
ETOH (altered cell metabolism)
Starvation (use of fatty acids), usually mild

METABOLIC ACIDOSIS
LACTIC ACIDOSIS (Dx by exclusion)
Type A: O2 delivery to cells is inadequate

Shock, mesenteric vascular events, and pulmonary
edema)
Type B: Cells cannot use O2

Hepatic failure, sepsis, acute pancreatitis
Anaerobic glycolysis of glucose to pyruvate and
then lactate (buffered by HCO3-)

METABOLIC ACIDOSIS

RENAL FAILURE:
Unable to excrete the daily acid load
Bone buffers keep HCO3-> 15 in CRF

In ARF HCO3- falls by 0.5 mmol/L/day
Retention of sulfate, phosphate, and organic
anions causes the increase in AG

METABOLIC ACIDOSIS
NORMAL ANION GAP
 GI HCO3- LOSS (Diarrhea, fistula)

 RENAL HCO3- LOSS
 RTA (Proximal, Distal, Hyperkalemic)
 Acetazolamide, hypoaldostironism
 Miscellaneous
 NH4Cl ingestion, Sulfur ingestion
 Pronounced dilution

METABOLIC ACIDOSIS
GI. BICARBONATE LOSS
NORMAL AG, HYPERCHLOREMIC
CAUSES

DIARRHEA

EXTERNAL FISTULA

URETEROSIGMOIDOSTOMY OR ILEAL LOOP
CONDUIT

METABOLIC ACIDOSIS
RENAL BICARBONATE LOSS
TYPE I RTA (DISTAL, CLASSICAL)

PROTON SECRETION DEFECT
TYPE II RTA (PROXIMAL, FANCONOI)

BICARBONATE REABSORPTION DEFECT
TYPE IV RTA (HYPERKALEMIC)

HYPORENINEMIC HYPOALDOSTERONISM

METABOLIC ACIDOSIS
URINARY ANION GAP
UAG = (Na+ + K+) - Cl-
UAG is an estimate of urinary ammonium
 Elevated in GI HCO3- loss

Low in distal RTA
UAG: NEGATIVE -20 mEq/L IN GI LOSS
UAG: POSITIVE + 23 mEq/L IN RTA

RENAL TUBULAR ACIDOSIS
K+ Tubular Aldo Proximal
HCO3- + + + ++
K+ ↓ ↑ ↑ ↓
Urine pH >5.4 >5.4 <5.5 <5.5
FE HCO3- <5% <5% <5% >15%
Calculi +++ - + -
Bone ++ - + ++

CAUSES OF DISTAL RTA

Primary

Hypercalcemia and nephrocalcinosis

Multiple myeloma

Cirrhosis

SLE

Amphotericin B

Lithium

Transplant rejection

Medullary sponge kidney

CAUSES OF
HYPERKALEMIC RTA

Hypoaldosteronism

Obstructive nephropathy

Sickle cell nephropathy

SLE

Cyclosporine A nephropathy

CAUSES OF PROXIMAL RTA

Primary

Cystinosis

Wilson’s disease

Lead toxicity

Multiple myeloma

Nephrotic syndrome

Early transplant rejection

Medullary cystic disease

Outdated tetracycline

METABOLIC ALKALOSIS
P r im a r y : IN C R E A S E D H C O 3
R E S P O N S E : IN C R E A S E D P C O 2

A p p r o p r ia te r e s p o n s e ?
P C O 2 = 0 .7 H C O 3

U R IN A R Y C H L O R ID E

< 2 0 m E q /L > 2 0 m E q /L

N o rm a l E C V D e c re a s e d E C V N o rm a l E C V D e c re a s e d E C V
A lk a li lo a d G I lo s s E xcess B a r tte r 's
D iu r e tic s M in e r a lo c o r tic o id s H y p o k a le m ia

Effects of Metabolic Alkalosis
Decreased serum potassium
Decreased serum ionized calcium
Dysrhythmias
Hypoventilation / hypoxemia
Increased bronchial tone / atelectasis
Left shift of the Oxygen curve

METABOLIC ALKALOSIS
Volume - depleted type:

Gastric acid loss
 Vomiting

 NGT suction

Renal chloride loss
 Diuretics

 Hypercapnia correction

METABOLIC ALKALOSIS
Volume - repleted type:
Mineralocorticoid excess
 Hyperaldosteronism

 Bartter’s syndrome
 Cushing’s syndrome
 Licorice excess
Profound potassium depletion

RESPIRATORY ACIDOSIS
P r i m a r y : IN C R E A S E D P C O 2
R E S P O N S E : IN C R E A S E D H C O 3

A p p ro p ria te re s p o n s e ?
A c u te : H C O 3 (1 ) = P C O 2 (1 0 )
C h ro n ic : H C O 3 (3 ) = P C O 2 (1 0 )

CAUSES

P u lm o n a ry N e u ro m u s c u la r

P n e u m o th o ra x COPD C N S d e p re s s a n t P rim a ry h y p o v e n tila tio n
P n e u m o n ia P u lm o n a ry fib ro s is B ra in s te m le s io n s P o lio m y e litis
P u lm o n a r y e m b o lu s S p in a l c o rd le s io n s
P u lm o n a r y e d e m a

P rim a ry : D E C R E A S E D P C O 2
RESPONSE: DECREASED HCO3

A p p ro p ria te re s p o n s e ?
A c u te : H C O 3 (2 ) = P C O 2 (1 0 )
C h ro n ic : H C O 3 (4 ) = P C O 2 (1 0 )

CAUSES

P E R IP H E R A L CENTRAL

ACUTE C H R O N IC ACUTE C H R O N IC
P n e u m o n ia P u lm o n a ry fib ro s is S a lic y la te o v e rd o s e B ra in tu m o r
P u lm o n a ry e m b o lu s CHF P a in P re g n a n c y
S e p s is C irrh o s is A n x ie ty P a in

RESPIRATORY ACIDOSIS
PaCO2 40 PaCO2 60 PaCO2 60
pH 7.40 pH 7.26 pH 7.30
A-12 A-11 A-12
HCO3- HCO3- HCO3-
24 26 29

Na+ Na+ Na+
140 Cl- 141 Cl- 140 Cl-
104 104 99

Normal Ac. resp. acidosis Ch. resp. acidosis

PaCO2 40 PaCO2 20 PaCO2 20
pH 7.40 pH 7.62 pH 7.49
A-12 A-14 A-14
HCO3- HCO3- HCO3-
24 20 15

Na+ Na+ Na+
140 Cl- 138 Cl- 140 Cl-
104 104 111

Normal Ac. resp. alkalosis Ch. resp. alkalosis

↓ CO2
SaO2 Right shift—
↓ 2,3 DPG better tissue
oxygenation
↑ pH
↑ CO2
Left shift—
worse tissue ↑ 2,3 DPG
oxygenation
↓ pH

pO2

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