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Acid -Base Basics

Dr. Fawzeya Aboul Fetouh Prof of anesthesia Cairo unversity

Henderson (1908)
create the familiar equilibrium equation: Aqueous A H + B Henderson Equation: [H+] x [HCO3-] = K x [CO2] x [H2O] Simply this equation describes the power of Hydrogen ions and its relationship to undissociated acids and anion content.

or pH which is -log H activity

Hasselbalch (1916)
complicated Henderson's simple equation by adopting Sorensen's pH notation. Henderson-Hasselbalch Equation:
pH = pK + log ( [HCO3-]) [CO2]

Astrup and Siggaard-Andersen (1958) introduced Base Excess to measure the metabolic component of acid-base disturbances. This brilliant concept allows us to predict the treatment required to correct metabolic disturbances. Metabolic acidosis is described as a "negative" base excess. How much easier to have print reports like: "There is a metabolic acidosis of 10 mEq/L"; or "There is a metabolic alkalosis of 5 mEq/L".

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 to return E.C.F. to normal (mEq/L) Calculated Bicarbonate Dose : 0.3 x Wt x BE Treatable Volume :Treatable Volume = 30% of Body Weight

Balance" and Status"

The terms "balance" and "status" should be distinguished. Balance is generally used to describe the relationships between inputs and outputs or turn over of substances. Status or level are terms used to describe the instantaneous activity or concentration of a substance

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)

pH
7.4

CO2 Respiratory Component (acid)

HCO3-

Metabolic Component (base)

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

Buffers

Chemical substance that minimizes the pH change in a solution 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

Respiratory Regulation of Acid-Base Balance

PaCO2

PCO2 is the partial pressure of carbon dioxide. The normal value in arterial blood is 40 mmHg (or 5.33 kPa). The mixed venous PCO2 is approximately 46 mmHg (6.13 kPa)

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

The end-exhaled value is usually very similar. Under anesthesia, the end exhaled value is often lower than arterial value,

(ETCO2) PACO2 - PaCO2 = 5 mmHg

Kidney Regulation of Acid-Base Balance

Why is it important for the body to maintain a normal pH?

To optimize enzyme activity. To allow hemoglobin to release O2 to the tissues. To improve myocardial contractility. To allow for acceptable reaction rates for intracellular reactions

Incidence

Acidosis may occur as a "normal" part of a surgical procedure. For example, reperfusion after bypass will normally result in transient acidosis. Post successful CPR Also, keep in mind that as a tourniquet comes off.

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

.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 7.45 and a HCO3 greater than 26.

Mixed acid-base disorders


Two or more simple acid-base disorders coexist

Metabolic Acidosis + Respiratory Acidosis


Metabolic Acidosis + Respiratory Alkalosis


pH usually very low Pa CO2 too high HCO3- too low

pH may be near normal Pa CO2 too low HCO3- too low

Metabolic Alkalosis + Respiratory Alkalosis

Metabolic Alkalosis + Respiratory Acidosis

pH usually very high Pa CO2 too low HCO3- too high

pH may be near normal Pa CO2 too high HCO3- too high

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 of lipophilic, uncharged base, to cross the blood-brain barrier (Shulman et al 1984)

Anesthesia related Respiratory acidosis .

1- Hypoventilation

is of primary concern as a cause related 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 shallow respirations) Opiods

2- Increased CO2 production

Increased CO2 production


Hyperthermia (MH, acute bacteremia) High dose catecholamine (inotropic)

Increased glucose load


(hyperalimentation )

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).

Effect of Metabolic Acidosis on Body Functions

Increased serum potassium. This occurs as hydrogen ions enter the cell to compensate for excess hydrogen in the extracellular space. Hydrogen ions are exchanged for potassium ions and hyperkalemia results. Decreases in CNS activity. Decreased myocardial activity, myocardial depression. Dysrrhythmias. Decreased vascular tone resulting in decreases in blood pressure. Increased CNS blood flow. Decreased O2 binding to hemoglobin causing a right shift in the oxyhemoglobin dissociation curve.

Anion Gap (AG)

AG is a measure of the relative abundance of unmeasured anions. Used to evaluate patients with metabolic acidosis. AG= [Na+]- {[Cl-] + [HCO3-]} 140- {(104 +24) } = 12.

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)

Normal AG metabolic acidosis is caused by the loss of HCO3- 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 renal failure.

High AG metabolic acidosis is due to the accumulation of [H+] plus an unmeasured anion in the ECF. ====Most likely caused by organic acid

accumulation or renal failure with impaired [H+] excretion.

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 dissociation curve. Dysrythmias. Increased airway resistance. Decreased CNS blood flow. .

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

Metabolic Alkalosis : Causes include

Excessive loss of hydrogen ions (vomiting, GI suction). Chloride and potassium loss (diuretics). Hypovolemia. Hyperaldosteronism. Steroid administration.

Hypovolemia

This is one of the first factors that should be considered in the intraoperative and postoperative patient that develops metabolic alkalosis.

Lack of Hemoglobin buffer system. 29%

Stepwise approach to diagnosing acid-base disorders


Is the patient Acidemic or Alkalemic Identify the primary Acidbase disorder by evaluating 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)

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 maintaining cardiovascular stability.

The dose calculated

The dose calculated will be sufficient to return the metabolic disturbance to about zero. This complete dose is very rarely recommended.
A typical dose of bicarbonate might be 1 mEq per kilogram of body weight followed by repeat blood gas analysis As described above, it is customary to either give a small standard dose and reevaluate; or give about half the calculated dose.

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)

There are several reasons for the partial correction

1. Bicarbonate is, initially, injected into the plasma volume, about 3 liters, instead of into the calculated treatable space, 21 liters. 2. When bicarbonate is added to acid it ,the majority of the bicarbonate is converted to carbon dioxide and has to be eliminated. 3. The carbon dioxide which is produced enters the cells freely, unlike the bicarbonate ions which have been administered.

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.

Treating Metabolic Alkalosis

As with metabolic acidosis, ideal treatment is the correction of the underlying abnormality.
A common transient cause is iatrogenic; correction of acute metabolic acidosis with sodium bicarbonate leaves a residual metabolic alkalosis.

hydration, and renal function should gradually correct this.

Contraction Alkalosis "Further from Neutral"

Dehydration concentrates the body's electrolytes. As the extracellular fluid (pH = 7.4) is on the alkaline side of neutral (pH = 6.8), the relative alkaline mixture of electrolytes is concentrated and shifts the pH to more alkaline value.
Rehydration, e.g., with oral fluids or intravenous Ringer's lactate or acetate restores the normal electrolyte concentration and, pH.

This "strong ion difference" is commonly abbreviated "SID"). the relationship between SID and [H ]+as well as[ OH,]-

Dilutional Acidosis "Further from Neutral"

The reverse of contraction alkalosis. Diluting the normal slightly alkaline mixture of extracellular electrolytes, also dilutes the alkalinity.
This moves the pH closer to neutral at body temperature (6.8)

Conclusion
Identify the main disorder: Disorder
pH respiratory alkalosis respiratory acidosis metabolic alkalosis PaCO2 (mmHg) HCO3 (mEq/L)

metabolic acidosis

> 7.40 < 40 < 7.40 > 40 > 7.40 < 7.40

> 24 < 24

ALGORITHM FOR ACIDBASE 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.

Determine the anion gap (AG, normal = 12). If the 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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