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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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