‫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
Buffering System
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
MIXED ACID-BASE DISORDERS
EXAMPLE OF DOUBLE DISORDER
       Health   Emphysema + Diarrhea
pH      7.40         7.32        7.10
PCO2 40         80          80
HCO3    24      40          24
MIXED ACID-BASE DISORDERS
EXAMPLE OF DOUBLE DISORDER
       Health   Emphysema + Diuretic
pH      7.40         7.32        7.40
PCO2    40      80          80
HCO3    24            40          48
MIXED ACID-BASE DISORDERS
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
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
Metabolic
Alkalosis
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
Respiratory
Acidosis
RESPIRATORY ALKALOSIS
                                            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
Alkalosis
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
RESPIRATORY ALKALOSIS
  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
Acid - Base Nomogram
↓ CO2
SaO2                                   Right shift—
             ↓ 2,3 DPG                 better tissue
                                       oxygenation
             ↑ pH
                               ↑ CO2
   Left shift—
  worse tissue                 ↑ 2,3 DPG
  oxygenation
                               ↓ pH

                         pO2
Acid - Base Nomogram
Acid base disorders

Acid base disorders

  • 2.
    ‫بسم ا الرحمن‬ ‫الرحيم‬ ‫” رب اشرح لي‬ ‫صدري‬ ‫ويسر لي أمري‬ ‫واحلل عقدة من‬ ‫لساني‬
  • 3.
  • 4.
    Definitions Acid: a substancethat 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
  • 8.
    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
  • 13.
  • 14.
    ACID-BASE DISORDERS DEFINITIONS ACIDEMIA VS ALKALEMIA  ACIDOSIS VS ALKALOSIS  RESPIRATORY VS METABOLIC  COMPENSATORY RESPONSES  SIMPLE (SINGLE) VS MIXED
  • 15.
    ACID-BASE DISORDERS DIAGNOSIS BASEDON: SUGGESTIVE HISTORY SUGGESTIVE PHYSICAL EXAM SUGGESTIVE CO2, K+, CL- SUGGESTIVE pH, PCO2, HCO3-, AG
  • 16.
    APPROACH TO THEDIAGNOSIS 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)
  • 17.
    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)
  • 18.
    Simplified Henderson - Hasselbach equation (H+) = 24 x PaCO2 HCO3 Shows relationship between 3 major factors:  H+  CO2  HCO3
  • 19.
    SIMPLE ACID-BASE DISORDERS PrimaryDisorder pH HCO3- PCO2 Met. Acidosis ↓ ↓↓ ↓ Resp. Acidosis ↓ ↑ ↑↑ Met. Alkalosis ↑ ↑↑ ↑ Resp. Alkalosis ↑ ↓ ↓↓
  • 21.
    FREQUENCY OF SIMPLEACID- BASE DISORDERS Metabolic  Acidosis 10%  Alkalosis 40% Respiratory  Acidosis 20%  Alkalosis 20%
  • 22.
    Consequences of acidosisvs. 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
  • 23.
    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
  • 24.
    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
  • 25.
  • 29.
    Or In metabolic disordersadd 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
  • 30.
    Normal Anion Gap AG= Na – (HCO3+Cl) = 8-12 A-10 HCO3- PaCO2 40 25 pH 7.40 Na 140 CL 105
  • 31.
    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
  • 33.
    THE SERUM ANIONGAP 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
  • 34.
    Increased anion gap metabolicacidosis  ketones, lactate, sulfates, or metabolites of methanol, ethylene glycol, and salicylate hyperalbuminemia and uremia (increased anions) hypocalcemia or hypomagnesemia (decreased cations)
  • 35.
    The effect oflow 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.
  • 36.
    Decreased anion gap hypoalbuminemia hypercalcemia hypermagnesemia Lithiumintoxication hypergammaglobulinemia bromide or iodide intoxication
  • 37.
    ACID-BASE DISORDERS EXAMPLE OFA 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
  • 38.
    The delta gap Thedifference 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
  • 39.
    ACID-BASE DISORDERS EXAMPLE OFA 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
  • 40.
    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
  • 41.
    MIXED ACID-BASE DISORDERS EXAMPLEOF DOUBLE DISORDER Health Emphysema + Diarrhea pH 7.40 7.32 7.10 PCO2 40 80 80 HCO3 24 40 24
  • 42.
    MIXED ACID-BASE DISORDERS EXAMPLEOF DOUBLE DISORDER Health Emphysema + Diuretic pH 7.40 7.32 7.40 PCO2 40 80 80 HCO3 24 40 48
  • 43.
    MIXED ACID-BASE DISORDERS EXAMPLEOF 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
  • 44.
    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
  • 46.
    Normal ABG? A diabeticpatient 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?
  • 47.
  • 48.
    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
  • 50.
    METABOLIC ACIDOSIS HIGH ANIONGAP Ketoacidosis (DM1, ETOH, Starvation) Lactic acidosis (A, B, D) Intoxication  Ethylene glycol  Methanol  Salicylic acid Advanced renal failure
  • 52.
    METABOLIC ACIDOSIS INTOXICATION: HIGH OSMOLAR GAP  ETHYLENE GLYCOL  METHANOL SALICYLATE  RESPIRATORY ALKALOSIS  METABOLIC ACIDOSIS  MIXED
  • 53.
    METABOLIC ACIDOSIS KETOACIDOSIS Diabetes1 (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
  • 54.
    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-)
  • 55.
    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
  • 56.
    METABOLIC ACIDOSIS NORMAL ANIONGAP  GI HCO3- LOSS (Diarrhea, fistula)  RENAL HCO3- LOSS  RTA (Proximal, Distal, Hyperkalemic)  Acetazolamide, hypoaldostironism  Miscellaneous  NH4Cl ingestion, Sulfur ingestion  Pronounced dilution
  • 58.
    METABOLIC ACIDOSIS GI. BICARBONATELOSS NORMAL AG, HYPERCHLOREMIC CAUSES  DIARRHEA  EXTERNAL FISTULA  URETEROSIGMOIDOSTOMY OR ILEAL LOOP CONDUIT
  • 59.
    METABOLIC ACIDOSIS RENAL BICARBONATELOSS TYPE I RTA (DISTAL, CLASSICAL)  PROTON SECRETION DEFECT TYPE II RTA (PROXIMAL, FANCONOI)  BICARBONATE REABSORPTION DEFECT TYPE IV RTA (HYPERKALEMIC)  HYPORENINEMIC HYPOALDOSTERONISM
  • 64.
    METABOLIC ACIDOSIS URINARY ANIONGAP 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
  • 65.
    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 ++ - + ++
  • 66.
    CAUSES OF DISTALRTA  Primary  Hypercalcemia and nephrocalcinosis  Multiple myeloma  Cirrhosis  SLE  Amphotericin B  Lithium  Transplant rejection  Medullary sponge kidney
  • 67.
    CAUSES OF HYPERKALEMIC RTA  Hypoaldosteronism  Obstructive nephropathy  Sickle cell nephropathy  SLE  Cyclosporine A nephropathy
  • 68.
    CAUSES OF PROXIMALRTA  Primary  Cystinosis  Wilson’s disease  Lead toxicity  Multiple myeloma  Nephrotic syndrome  Early transplant rejection  Medullary cystic disease  Outdated tetracycline
  • 69.
    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
  • 72.
  • 75.
    Effects of MetabolicAlkalosis Decreased serum potassium Decreased serum ionized calcium Dysrhythmias Hypoventilation / hypoxemia Increased bronchial tone / atelectasis Left shift of the Oxygen curve
  • 76.
    METABOLIC ALKALOSIS Volume -depleted type:  Gastric acid loss  Vomiting  NGT suction  Renal chloride loss  Diuretics  Hypercapnia correction
  • 77.
    METABOLIC ALKALOSIS Volume -repleted type: Mineralocorticoid excess  Hyperaldosteronism  Bartter’s syndrome  Cushing’s syndrome  Licorice excess Profound potassium depletion
  • 79.
    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
  • 80.
  • 81.
    RESPIRATORY ALKALOSIS 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
  • 82.
  • 83.
    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
  • 84.
    RESPIRATORY ALKALOSIS 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
  • 85.
    Acid - BaseNomogram
  • 86.
    ↓ CO2 SaO2 Right shift— ↓ 2,3 DPG better tissue oxygenation ↑ pH ↑ CO2 Left shift— worse tissue ↑ 2,3 DPG oxygenation ↓ pH pO2
  • 87.
    Acid - BaseNomogram