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    Clinical Pathology Med School, Padjadjaran University

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    Jenadi Binarto
    This document provides an overview of acid-base, electrolyte, and water disturbances. It defines key terms and lists normal values. It describes compensatory mechanisms like buffer systems and kidney and lung functions. The Henderson-Hasselbalch equation is shown. Four types of acid-base disturbances are defined: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Methods for blood collection for analysis and various nomograms are also outlined.

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    Clinical Pathology Med School, Padjadjaran University

    Uploaded by

    Jenadi Binarto
    71 views38 pages
    This document provides an overview of acid-base, electrolyte, and water disturbances. It defines key terms and lists normal values. It describes compensatory mechanisms like buffer systems and kidney and lung functions. The Henderson-Hasselbalch equation is shown. Four types of acid-base disturbances are defined: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Methods for blood collection for analysis and various nomograms are also outlined.

    Original Description:

    keseimbangan asam basa, elektrolit, analisa gas darah

    Original Title

    Asam Basa

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    This document provides an overview of acid-base, electrolyte, and water disturbances. It defines key terms and lists normal values. It describes compensatory mechanisms like buffer systems and kidney and lung functions. The Henderson-Hasselbalch equation is shown. Four types of acid-base disturbances are defined: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Methods for blood collection for analysis and various nomograms are also outlined.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    71 views38 pages

    Clinical Pathology Med School, Padjadjaran University

    Uploaded by

    Jenadi Binarto
    This document provides an overview of acid-base, electrolyte, and water disturbances. It defines key terms and lists normal values. It describes compensatory mechanisms like buffer systems and kidney and lung functions. The Henderson-Hasselbalch equation is shown. Four types of acid-base disturbances are defined: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Methods for blood collection for analysis and various nomograms are also outlined.

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    © All Rights Reserved
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    of 38

    Clinical Pathology

    Med School, Padjadjaran


    University

    ACID BASE, ELECTROLYTES AND WATER


    DISTURBANCES
    I. GLOSSARY OF TERMS :
    1.
    2.
    3.
    4.
    5.
    6.

    Acid
    Base
    Buffer
    Buffer Base (BB)
    Normal Buffer Base (NBB)
    Base, Negative (-)

    13.
    14.
    15.
    16.
    17.
    18.

    Hypocapnia
    Hypoxemia
    Hypoxia
    Oxygen content (ct O2)
    Oxygen saturation
    pO2 (pressure-O2)

    7. Base, Positive (+)

    19. pO2 (0,5) or P50

    8. Bicarbonate (HCO3-)

    20. Total-CO2 (TC02)

    9.
    10.
    11.
    12.

    Henderson-Hasselbalch Equation 21. pCO2


    Dalton's law
    22. pH
    Henry's law
    23. pKa
    Hypercapnia

    II. Normal values


    1. pH
    : 7.40 + 0.05
    2. pCO2
    : 40
    +
    5 mmHg
    3. pO2
    : 80
    - 100 mmHg
    4. (HCO3-)
    : 24
    +
    2 mmol/L
    5. TCO2
    : 25,2 +
    2 mmol/L
    6. O2 - saturation: 95 - 98 %
    7. Base, Negative (Base, deficient) : - 2,5
    8. Base, positive (Base, Excess)
    : + 2,5

    III. Compensatory Mechanisms


    1. Buffer System :
    a. Carbonic acid
    CO2 + H20

    Bicarbonate Buffer System :


    H2CO3
    H+ + HCO3-

    b. Non Bicarbonate Buffer System :


    Hbuf
    H+ + Buf -

    2. Lungs :
    Compensate by altering the acid or respiratory
    component during :
    a. Hypoventilation
    b. Hyperventilation
    3. Kidneys : Na+ - H+ Exchange
    The kidneys tend to correct for primary
    abnormalities in the basic or metabolic (HCO3-)
    component.

    Henderson-Hasselbalch Equation :
    pH = 6.1 + Log [HCO3-] / [H2CO3]
    6.1 + Log [HCO3-] / 0.03 x pCO2
    6.1 + Log 24/1.2

    24/1.2
    24/1.2

    = 6.1 + Log 20/1


    = 6.1 + 1.3
    = 7.40

    The mechanism for bicarbonate synthesis reabsoption


    ( Na + - H+ exchange ) is illustrated in Fig.1,2,3

    ECF

    TUBULE
    Na+ + HCO3-

    Na+ Active Transport Na+


    Na+
    +
    + Active Transport
    HCO
    +H
    H+
    HCO3
    3
    H2CO3

    H2CO3

    Carbonic anhydrase

    CO2

    H2 O
    +
    CO2

    HCO3-

    CO2

    H 2O

    ECF

    TUBULE
    Na+ + Na+ + HPO4=

    Na+ Active Transport Na+


    Na+
    +
    + Active Transport
    HCO
    +H
    H+
    HCO3
    3

    H2PO4-

    H2CO3
    Carbonic anhydrase

    CO2

    H2 O
    +
    CO2

    Na+ H2PO4-

    ECF

    TUBULE
    Na+

    Cl-

    Na+ Active Transport Na+


    Na+
    +
    + Active Transport
    HCO
    +H
    H+
    HCO3
    3
    H2CO3
    Carbonic anhydrase

    NH3 Diffusion NH3

    CO2

    H2 O
    +
    CO2 Glutamine

    NH4+ + Cl-

    IV. Types of Acid - Base Disturbances:


    There are four types of Acid-Base disturbances:
    1. Respiratory Acidosis
    2. Respiratory Alkalosis
    3. Metabolic Acidosis
    4. Metabolic Alkalosis

    pH = 6.1 + log [HCO3-] / 0.03 X pCO2

    NaHCO3
    H2CO3

    Na+ + HCO3- ( I )
    H+

    + HCO3- ( II)

    1. Respiratory Acidosis
    Henderson - Hasselbalch Equation :
    pH = 6.1 + log [HCO3-] / 0.03 X pCO2
    a. Primary Defect
    CO2 excess

    pH

    HCO3-

    20

    20

    H2CO3

    < 7,35)

    CO2 retention

    H2CO3

    (hypercapnea)
    pH
    ( < 7,35)
    Pa CO2 > 45 mmHg
    PaO2 rendah
    HCO3-

    (< 30 mEq/L)

    Etiology:
    *Inhibition on resp center in OM
    A Medicine : opiat, sedatives
    B. O2 therapy
    C. Cardiac arrest
    D Apnea during asleep
    *Resp muscle and thorax
    A Muscle disease : myastenia gravis,
    GuillainBarre syndrome
    B Thoracal deformity : kiphoscoliosis
    C Overt obesity
    D Thoracal injury

    2. Respiratory Alkalosis
    Henderson - Hasselbalch Equation :
    pH = 6.1 + log [HCO3-] / 0.03 X pCO2
    a. Primary Defect
    Alveolar hypervent
    PaCO2
    pH

    CO2 excretion
    (>45 mmHg)

    B Hypoxia :
    1. Pneumonia, bronchiale asthma,
    pulmonary oedem
    2. Congestive heart failure
    3. Pulmonary fibrosis
    4. Live in high place
    C. Overt mechanical ventilation
    D. Unexplained mechanism :
    .Gram negative sepsis
    .Hepatic cirrhosis
    .Physical training

    Compensation
    a. Buffer :
    HCO3- ( react II & I)
    b. Renal :
    No reabsorp HCO3No prod H+ & NH4+
    No exchange Na+
    base urine
    pH Normal

    3. Metabolic Acidosis
    Henderson - Hasselbalch Equation :
    pH = 6.1 + log [HCO3-] / 0.03 X pCO2
    a. Primary Defect
    * Noncarbonic acid accumulation
    * HCO3- loss
    HCO3

    pH

    Renal failure : acid excretion


    accumulation
    DM: Insulin
    Starvation
    keton

    Cardio pulm

    O2

    acid

    ketosis
    (H+)

    unaerob metab

    sepsis
    lactate acidosis

    lactate

    Etiology:
    Increased production of nonvolatile metabolic
    acids
    # Excess production of metab acids: Lactic
    acidosis, diabetic ketoacidosis, fasting and
    starvation, poisoning (salicylate,
    methanol)
    # Impaired elimination: failure or dysfunction
    Excessive loss of bicarbonate
    *Loss of intestinal secretions : diarrhea,
    intestinal suction,
    intestinal or biliary fistula
    * Increased renal losses: RTA, th/ with
    carbonic anhydrase inhibitor,
    hyperaldosteronism

    Compensation
    a. Buffer :
    H2CO3 ( X) (end prod)
    HCO3b.Resp
    CO2 expirate (Kussmaul)
    H2CO3
    c. Renal :
    HCO3- reabsorp
    H+ & NH4+ prod
    replaced Na+

    acid urine

    4. Metabolic Alkalosis
    Henderson - Hasselbalch Equation :
    pH = 6.1 + log [HCO3-] / 0.03 X pCO2
    a. Primary Defect
    * noncarbonic acid loss
    * HCO3- excess
    pH

    HCO3

    pCO2

    Etiology
    Excess loss of hydrogens ions :
    Vomiting, gastric suction
    Potassium defisit (diuretic th/ ,
    hyperaldosteronism)
    Milk-alkali syndrome

    Excess gain of bicarbonate or alkali :


    Ingestion or administ of NaHCO3
    Administ of citrate-containing blood
    transfusions

    H+ , Na+ , Cl- , K+ loss


    NaHCO3

    Na+ + HCO3- ( I )

    H2CO3

    H+

    re II : HCO3-

    + HCO3- ( II)
    , H2CO3

    Compensation
    a. Buffer:
    H2CO3

    HCO3b. Resp :
    pH

    carotid body

    CO2 retention , H2CO3

    hypoventil
    hypoxia

    Vol ECF
    dehydration
    renin-angiotensin-aldosteron
    Na+ reabsorp
    KHCO3 loss
    K+ secretion

    K+ def

    H+ & NH4+ (tub secr)


    HCO3-

    acid urine

    severe metab alkalosis

    V. Collection of Blood for pH/Blood Gases


    Determination
    1. Unaerobic Collection : to avoid gas exchange
    2. Blood gas determination should be performed
    immediately (within 10 minutes)
    If the determination is delayed, the specimen
    should be placed in ice water or placed on
    crushed ice, but should be assayed within 1
    hour.
    3. Whole blood samples (using Lithium heparin
    as the anti-coagulant : 240 Unit / ml.

    4. The blood may be obtained from arteries (it is


    more uniform in composition): radialis, ulnaris,
    brachialis, femoralis.
    If the arterial blood cannot be obtained,
    capillary blood may be used as a substitute as
    long as moist heat is used before collection
    (=Arterialized blood is obtained by warming a
    limb to 450 C, 20 minutes.

    This method of collection is routinely used


    when samples are obtained from infants.
    Heparinized - capillary tubes are used for
    collecting
    arterialized
    blood.
    Before
    sealing, a small piece of wire is inserted
    into the capillary tube.
    The wire may be moved with a magnet to
    allow mixing of the blood prior to analysis.

    Delay without cooling > 10 mnt


    pH
    pCO2
    pO2 (lactic ac)
    Sampling aerobic (air contaminattion)
    pH
    pCO2
    pO2
    Condition: hyperventilation
    pH
    pCO2
    pO2
    Temp :
    hyperthermia : pH
    hypotermia

    : pH

    pCO2

    pO2

    pCO2

    pO2

    pH
    pH

    HCO3-/pCO2
    / N : metab alkalosis without compensation
    /
    part comp
    N
    /
    complete comp

    pH
    N
    pH

    /N
    /
    /

    : metab acidosis without compensation


    part comp
    complete comp

    N /
    /
    /

    : resp alkalosis without compensation


    part comp
    complete comp

    N /
    /
    /

    : resp acidosis without compensation


    part comp
    complete comp

    pH

    VI.

    NORMOGRAM :
    1. Siggaard - Andersen Alignment
    2. pO2 - Oxygen Saturation

    Inspired Air

    Expired Air
    pO2
    pCO2
    pH2O

    pO2
    pCO2
    pH2O

    = 115 mmHg
    = 30 mmHg
    = 47 mmHg

    = 152
    mmHg
    = 0.25 mmHg
    = variable

    TRACHEAL OR BRONCHIAL AIR


    pO2 = 149 mmHg
    pCO2 = 0.25 mmHg
    pH2O = 47 mmHg

    ALVEOLAR AIR

    Arterial Blood
    pO2 = 100 mmHg
    pCO2 = 40 mmHg
    O2

    pO2
    pCO2
    pH2O

    = 102 mmHg
    = 36 mmHg
    = 47 mmHg

    LUNG CAPILLARY
    TISSUE CAPILLARY
    CO2

    pO2 = 20 mmHg
    pCO2 = 60 mmHg
    surface of tissue cell

    pO & pCO in air, blood & tissue

    CO2
    Venous Blood
    pO2 = 40 mmHg
    pCO2 = 46 mmHg

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