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    Acid -Base BasicsDr. Fawzeya Aboul Fetouh

    Prof of anesthesiaCairo unversity

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    )1908(Hendersoncreate the familiar equilibrium equation:

    A H + BHenderson Equation:

    [H+] x [HCO3-] = K x [CO2] x [H2O]

    Simply this equation describes

    the power of Hydrogen ions and its relationship toundissociated acids and anion content.

    or pH which is -log H activity

    Aqueous

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    Hasselbalch (1916)complicated Henderson's simple equation byadopting Sorensen's pH notation.

    Henderson-Hasselbalch Equation:

    pH = pK + log ( [HCO3-])

    [CO2]

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    Astrup and Siggaard-Andersen (1958)introduced

    Base Excess to measure the metabolic componentof acid-base disturbances. This brilliant conceptallows us to predict the treatment required tocorrect metabolic disturbances.

    Metabolic acidosis is described as a "negative"base excess. How much easier to have printreports like: "There is a metabolic acidosis of 10mEq/L"; or "There is a metabolic alkalosis of 5mEq/L".

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    Terminology. Standard pH (Hasselbalch 1916) : pH at normal

    temperature and PCO2

    Standard Bicarbonate ( Jorgensen and Astrup,1957) :

    bicarbonate at normal temp. and PCO2 Base Excess (Astrup and Siggaard-Andersen 1958): Dose to

    return plasma to normal (mEq/L)

    Standard Base Excess (Siggaard-Andersen1960) : Dose toreturn E.C.F. to normal (mEq/L)

    Calculated Bicarbonate Dose : 0.3 x Wt x BE

    Treatable Volume :Treatable Volume = 30% of BodyWeight

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    Balance" and Status"

    The terms "balance" and "status" should be

    distinguished.

    Balance is generally used to describe therelationships between inputs and outputs or

    turn over of substances.

    Status or level are terms used to describe theinstantaneous activity or concentration of a

    substance

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    Values and regulation

    Arterial blood pH = 7.40

    Venous Blood pH = 7.35

    pH is regulated via chemical buffers (fraction of second)

    rate of respiration (1- 3 min.)

    renal mechanisms (several hours)

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    pH7.4

    CO2 HCO3-Respiratory Component(acid) Metabolic Component(base)

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    Fatal Limits of pH Imbalances

    Acidosis pH 7.0

    depression of CNS, coma, death

    Alkalosis pH 7.8

    over-excitation of nervous system,

    muscle tetany, extreme nervousness,convulsions, death due to

    respiratory arrest

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    Buffers

    Chemical substance that minimizes the pH change in asolution caused by the addition of either an acid or base.

    There are four main buffer systems in the body:

    Bicarbonate buffer system. (the MAIN one) 64%

    NaHCO3 H2CO3 Hemoglobin buffer system. 29%

    HbO2- HHb

    Protein buffer system. 6%

    Pr- HPr

    Phosphate buffer system. 1%

    Na2HPO4 NaHPO4

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    Respiratory Regulation of

    Acid-Base Balance

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    PaCO2 PCO2 is the partial pressure of carbon dioxide.

    The normal value in arterial blood is 40 mmHg (or 5.33kPa).

    The mixed venous PCO2 is approximately 46 mmHg (6.13kPa)

    To convert pressure in mmHg to kPa, divide the valuein mmHg by 7.5.

    The end-exhaled value is usually very similar. Underanesthesia, the end exhaled value is often lower thanarterial value,

    (ETCO2) PACO2 - PaCO2 = 5 mmHg

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    Kidney Regulation of Acid-Base

    Balance

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    Why is it important for the body

    to maintain a normal pH?

    To optimize enzyme activity.

    To allow hemoglobin to release O2 tothe tissues.

    To improve myocardial contractility.

    To allow for acceptable reaction

    rates for intracellular reactions

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    Acidosis may occur as a "normal" part of a

    surgical procedure.

    For example, reperfusion after bypass willnormally result in transient acidosis.

    Post successful CPR

    Also, keep in mind that as a tourniquetcomes off.

    Incidence

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    Respiratory Acidosis

    A decrease in the pH to less than 7.35 and a

    CO2 greater than 45

    Respiratory Alkalosis

    An increase in the pH to greater than 7.45 and

    a CO2 less than 35

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    .Metabolic Acidosis

    A decrease in the pH to less than 7.35 and a

    HCO3 less than 22.

    Metabolic Alkalosis

    An increase in the pH to greater than 7.45and a HCO3 greater than 26.

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    Mixed acid-base disordersTwo or more simple acid-base disorders coexist

    Metabolic Acidosis +Respiratory Acidosis

    pH usually very low

    Pa CO2 too high

    HCO3- too low

    Metabolic Alkalosis +

    Respiratory Alkalosis pH usually very high

    Pa CO2 too low

    HCO3- too high

    Metabolic Acidosis +Respiratory Alkalosis

    pH may be near normal

    Pa CO2 too low

    HCO3- too low

    Metabolic Alkalosis +

    Respiratory Acidosis pH may be near normal

    Pa CO2 too high

    HCO3- too high

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    Effect of pH on drug action Relative acidity of tissues, for example in the vicinity

    of an abscess, is recognized to reduce the efficacy of

    local anesthetic solutions.

    Conversely, relative alkalinity enhances the uptake of

    local anesthetic solutions.

    Alkalinity also potentiates drugs such as meperidine

    and morphine by increasing the availability oflipophilic, uncharged base, to cross the blood-brain

    barrier (Shulman et al 1984)

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    Anesthesia related Respiratory acidosis .

    1- Hypoventilationis of primary concern as a causerelated to anesthesia.

    Hypoventilation results from

    CNS depression.

    muscle paralysis.

    Pulmonary disease.

    Rebreathing of exhaled gas,exhausted CO2 absorber or a

    faulty one way valve. Inhalation agents (cause

    tachypnea and shallowrespirations)

    Opiods

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    2- Increased CO2 production

    Increased CO2 production

    Hyperthermia (MH, acute bacteremia)

    High dose catecholamine (inotropic)

    Increased glucose load

    (hyperalimentation )

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    Causes of metabolic acidosis include

    Decreased renal elimination of hydrogen

    ions as in renal failure or liver cirrhosis.

    Increased production of hydrogen ions:anaerobic metabolism, DKA, metabolism of

    aminoacids (TPN).

    Loss of base from the GI tract (diarrhea). Administration of large amounts of Normal

    Saline (hyperchloremic acidosis).

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    Increased serum potassium.

    This occurs as hydrogen ions enter the cell to compensate forexcess hydrogen in the extracellular space. Hydrogen ions areexchanged for potassium ions and hyperkalemia results.

    Decreases in CNS activity.

    Decreased myocardial activity, myocardial depression.

    Dysrrhythmias.

    Decreased vascular tone resulting in decreases in bloodpressure.

    Increased CNS blood flow.

    Decreased O2 binding to hemoglobin causing a right shift in theoxyhemoglobin dissociation curve.

    Effect of Metabolic Acidosis on Body Functions

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    Anion Gap (AG)

    AG is a measure of the relative abundance

    of unmeasured anions.

    Used to evaluate patients with metabolicacidosis.

    AG= [Na+]- {[Cl-] + [HCO3-]}

    140- {(104 +24) } = 12.

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    Determinants of the Anion Gap Unmeasured Anions

    Proteins (15 mEq/L)

    Organic Acids (5

    mEq/L)

    Phosphates (2

    mEq/L)

    Sulfates (1mEq/L)

    Unmeasured Cations

    Calcium (5 mEq/L)

    Potassium (4.5 mEq/L)

    Magnesium (1.5

    mEq/L)

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    Normal AG metabolic acidosis is caused by the loss ofHCO3

    - which is counterbalanced by the gain of Cl-(measured cation) to maintain electrical neutrality.

    ====Most likely caused by HCO3- wasting from

    diarrhea or urinary losses in early renalfailure.

    High AG metabolic acidosis is due to theaccumulation of [H+] plus an unmeasured anion inthe ECF.

    ====Most likely caused by organic acidaccumulation or renal failure with impaired[H+] excretion.

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    What are the problems

    associated with Alkalosis?

    Decreased potassium. serum.

    Increased CNS irritability.

    Coronary artery spasm. Decreased oxygen delivery to the tissues, a

    left shift in the oxyhemoglobin dissociationcurve.

    Dysrythmias.

    Increased airway resistance.

    Decreased CNS blood flow. .

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    Respiratory Alkalosis : Causes include

    Hyperventilation,

    pain, anxiety,

    decreased barometric pressure,

    arterial hypoxemia,

    pulmonary receptor stimulation (asthma ,Pul.

    Edema) pulmonary vascular disease,

    cirrhosis of the liver, sepsis, hyperthermia

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    Metabolic Alkalosis : Causes include

    Excessive loss of hydrogen ions(vomiting, GI suction).

    Chloride and potassium loss(diuretics).

    Hypovolemia.

    Hyperaldosteronism.

    Steroid administration.

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    Hypovolemia

    This is one of the first factors that should be

    considered in the intraoperative andpostoperative patient that develops metabolic

    alkalosis.

    Lack of Hemoglobin buffer system. 29%

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    Stepwise approach to diagnosing

    base disorders-acid

    Is the patient Acidemic or Alkalemic

    Identify the primary Acidbase disorder byevaluating HCO3 and PaCO2

    What is the [HCO3]

    Elevated------Metabolic alkalosis if alkalotic

    Decreased ---- Metabolic acidosis if acidotic

    What is the PaCO2 Elevated ---Respiratory acidosis if acidotic

    Decreased --- Respiratory alkalosis if alkalotic

    What is the anion gap (to determine etiology of

    Metabolic acidosis)

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    Treatment Metabolic Acidosis

    The treatment for a metabolic acidosis is

    judged largely on clinical grounds.

    Bicarbonate therapy is justified when

    metabolic acidosis accompanies difficulty in

    resuscitating an individual or in maintainingcardiovascular stability.

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    The dose calculated

    The dose calculated will be sufficient to returnthe metabolic disturbance to about zero.

    This complete dose is very rarely recommended.

    A typical dose of bicarbonate might be 1 mEqper kilogram of body weight followed by repeatblood gas analysis

    As described above, it is customary to either givea small standard dose and reevaluate; or give

    about half the calculated dose.

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    The effect of a dose of bicarbonate

    can be anticipated

    by calculating the dose required for complete

    correction.

    This calculation is based on BE and the size of the

    treatable space (0.3 x weight, e.g., 21 liters,

    Dose (mEq) = 0.3 x Wt (kg) x BE (mEq/L)

    (- 4 BE is accepted)

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    There are several reasons for the

    partial correction

    1. Bicarbonate is, initially, injected intothe plasma volume, about 3 liters,instead of into the calculated treatablespace, 21 liters.

    2. When bicarbonate is added to acid it,the majority of the bicarbonate isconverted to carbon dioxide and has tobe eliminated.

    3. The carbon dioxide which isproduced enters the cells freely, unlikethe bicarbonate ions which have beenadministered.

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    Continued;

    4. The bicarbonate is accompanied by sodium ions

    which will increase the osmolality of the

    extracellular fluid. (hypernatremia, and

    hyperosmolality.)

    In neonates, rapid infusion of bicarbonate may

    cause intracranial hemorrhage.

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    Treating Metabolic Alkalosis

    As with metabolic acidosis, ideal treatment is thecorrection of the underlying abnormality.

    A common transient cause is iatrogenic; correctionof acute metabolic acidosis with sodium bicarbonateleaves a residual metabolic alkalosis.

    hydration, and renal function should graduallycorrect this.

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    Contraction Alkalosis

    "Further from Neutral"

    Dehydration concentrates the body'selectrolytes.

    As the extracellular fluid (pH = 7.4) is on thealkaline side of neutral (pH = 6.8), the relativealkaline mixture of electrolytes is concentratedand shifts the pH to more alkaline value.

    Rehydration, e.g., with oral fluids or intravenousRinger's lactate or acetate restores the normal

    electrolyte concentration and, pH.

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    This "strong ion difference" is

    commonly abbreviated "SID").

    the relationship between SID and

    [H ]+as well as [ OH -],

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    Dilutional Acidosis

    "Further from Neutral"

    The reverse ofcontraction alkalosis. Diluting

    the normal slightly alkaline mixture of

    extracellular electrolytes, also dilutes thealkalinity.

    This moves the pH closer to neutral at bodytemperature (6.8)

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    ConclusionIdentify the main disorder: Disorder

    pH PaCO2 HCO3

    (mmHg) (mEq/L)

    respiratory alkalosis > 7.40 < 40respiratory acidosis < 7.40 > 40metabolic alkalosis > 7.40

    > 24

    metabolic acidosis < 7.40 < 24

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    ALGORITHM FOR ACID-

    BASE DISORDERS Establish database: ABG,, anion gap (remember

    to correct anion gap for hypoalbuminemia.

    For every 1 g/dl decline in serum albumin, a ~2.5

    mEq/L decrease in anion gap will occur).

    Evaluate compensation using formulas For

    respiratory disorders, this will determine chronicity.If compensation does not match expected values,

    there is a mixed acid-base disorder.

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    Determine the anion gap (AG, normal = 12). Ifthe AG is 20 or greater, then a metabolic acidosis

    almost certainly exists regardless of pH or HCO3.AG= [Na+]-([Cl-] + [HCO3

    -])

    If there is an AG, determine whether this alone

    accounts for the change in HCO3.

    Calculate the patients anion gap = 12

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