simlpe and practical approach to acid base disturbance



systematic approach to interpretation of acid base ststus.

1. Examine arterial pH: Is acidemia or alkalemia present?

2. Examine PaCO₂: Is the change in PaCO₂ consistent with a respiratory component?

3. If the change in PaCO₂ does not explain the change in arterial pH, does the change in [HCO₃^–] indicate a metabolic component?

4. Make a tentative diagnosis (see Tables below).

5. Compare the change in [HCO₃^–] with the change in PaCO₂. Does a compensatory response exist? Because arterial pH is related to the ratio of PaCO₂ to [HCO₃^–], both pulmonary and renal compensatory mechanisms are always such that PaCO₂ and [HCO₃^–] change in the same direction. A change in opposite directions implies a mixed acid–base disorder.

6. If the compensatory response is more or less than expected, by definition a mixed acid–base disorder exists.

7. Calculate the plasma anion gap in the case of metabolic acidosis.

8. Measure urinary chloride concentration in the case of metabolic alkalosis.

 




Compensatory Mechanisms

         Physiological responses to changes in [H⁺] are characterized by three phases: (1) immediate chemical buffering, (2) respiratory compensation (whenever possible), and (3) a slower but more effective renal compensatory response that may nearly normalize arterial pH even if the pathological process is still present.

immediate chemical buffur

bicarbonate buffur

hemoglobin buffur

intracellular proteins

phosphate and ammonia

the bicarbonate buffer consists of H₂CO₃ and HCO₃^–, CO₂ tension (PCO₂) may be substituted for H₂CO₃, because:

the Henderson–Hasselbalch equation for bicarbonate can be written as follows:

It should be emphasized that the bicarbonate buffer is effective against metabolic but not respiratory acid–base disturbances.

Pulmonary Compensation

         Changes in alveolar ventilation responsible for pulmonary compensation of PaCO₂ are mediated by chemoreceptors within the brain stem in response to changes in cerebrospinal spinal fluid pH.

Pulmonary Compensation during Metabolic Acidosis

         Decreases in arterial blood pH stimulate medullary respiratory centers. The resulting increase in alveolar ventilation lowers PaCO₂ and tends to restore arterial pH toward normal.

Pulmonary Compensation during Metabolic Alkalosis

Increases in arterial blood pH depress respiratory centers. The resulting alveolar hypoventilation tends to elevate PaCO₂ and restore arterial pH toward normal.  Hypoxemia, as a result of progressive hypoventilation, eventually activates oxygen-sensitive chemoreceptors; the latter stimulates ventilation and limits the compensatory pulmonary response. 



Renal Compensation

•  control the amount of HCO₃^– reabsorbed from filtered tubular fluid
• form new HCO₃^–
•  eliminate H⁺ in the form of titratable acids and ammonium ions

Renal Compensation during Acidosis

The renal response to acidemia is 3-fold:

 (1) increased reabsorption of the filtered HCO₃^–

 (2) increased excretion of titratable acids

 (3) increased production of ammonia.

Renal Compensation during Alkalosis

exceretion of large amount of HCO3.

Metabolic alkalosis is commonly associated with increased mineralocorticoid activity even in the absence of sodium and chloride depletion.

Base Excess

         Base excess is the amount of acid or base that must be added for blood pH to return to 7.40 and PaCO₂ to return to 40 mm Hg at full O₂ saturation and 37°C.

Acidosis

Physiological Effects of Acidemia

·         Direct myocardial and smooth muscle depression reduces cardiac contractility and peripheral vascular resistance, resulting in progressive hypotension.

·         Progressive hyperkalemia as a result of the movement of K⁺ out of cells in exchange for extracellular H⁺ is also potentially lethal. Plasma [K⁺] increases approximately 0.6 mEq/L for each 0.10 decrease in pH.

·         Central nervous system depression is more prominent with respiratory acidosis than with metabolic acidosis.

Respiratory Acidosis

         Respiratory acidosis is defined as a primary increase in PaCO₂ leading to an increase in [H⁺] and a decrease in arterial pH.

Causes of Respiratory Acidosis.

Alveolar hypoventilation 

·         Central nervous system depression

·         Neuromuscular disorders

·         Chest wall abnormalities

·         Pleural abnormalities

·         Airway obstruction

·         Parenchymal lung disease

·         Ventilator malfunction

Increased CO₂ production 

·         Large caloric loads

·         Malignant hyperthermia

·         Intensive shivering

·         Prolonged seizure activity

·         Thyroid storm

·         Extensive thermal injury (burns)

Acute Respiratory Acidosis

         The compensatory response to acute (6–12 h) elevations in PaCO₂ is limited. As a result, plasma [HCO₃^–] increases only about 1 mEq/L for each 10 mm Hg increase in PaCO₂ above 40 mm Hg.

Chronic Respiratory Acidosis

"Full" renal compensation characterizes chronic respiratory acidosis. plasma [HCO₃^–] increases approximately 4 mEq/L for each 10 mm Hg increase in PaCO₂ above 40 mm Hg.

Treatment of Respiratory Acidosis

·         Measures aimed at reducing CO₂ production are useful only in specific instances (eg, dantrolene for malignant hyperthermia, muscle paralysis for tetanus, antithyroid medication for thyroid storm, and reduced caloric intake).

·         Temporizing measures aimed at improving alveolar ventilation include bronchodilation, reversal of narcosis, administration of a respiratory stimulant (doxapram), or improving lung compliance (dieresis

·         Intravenous NaHCO₃ is rarely necessary unless pH is < 7.10 and HCO₃^– is < 15 mEq/L.

         Patients with a baseline chronic respiratory acidosis require special consideration. When such patients develop acute ventilatory failure, the goal of therapy should be to return PaCO₂ to the patient's "normal" baseline.

Metabolic Acidosis

         Metabolic acidosis is defined as a primary decrease in [HCO₃^–]. Pathological processes can initiate metabolic acidosis by one of three mechanisms: (1) consumption of HCO₃^– by a strong nonvolatile acid, (2) renal or gastrointestinal wasting of bicarbonate, or (3) rapid dilution of the extracellular fluid compartment with a bicarbonate-free fluid.

         A fall in plasma [HCO₃^–] without a proportionate reduction in PaCO₂ decreases arterial pH.

Causes of Metabolic Acidosis.

Increased anion gap 

  Increased production of endogenous nonvolatile acids

·         Renal failure

·         Ketoacidosis

·         Diabetic

·         Starvation

·         Lactic acidosis

·         Mixed

·         Nonketotic hyperosmolar coma

·         Alcoholic

·         Inborn errors of metabolism

·         Ingestion of toxin:

o    Salicylate

o    Methanol

o    Ethylene glycol

o    Paraldehyde

o    Toluene

o    Sulfur

·         Rhabdomyolysis

Normal anion gap (hyperchloremic) 

  Increased gastrointestinal losses of HCO₃^–
 

·         Diarrhea

·         Anion exchange resins (cholestyramine)

·         Ingestion of CaCl₂, MgCl₂
 

·         Fistulas (pancreatic, biliary, or small bowel)

·         Ureterosigmoidostomy or obstructed ileal loop

  Increased renal losses of HCO₃^–
 

·         Renal tubular acidosis

·         Carbonic anhydrase inhibitors

·         Hypoaldosteronism

  Dilutional

·         Large amount of bicarbonate-free fluids

·         Total parenteral nutrition (Cl^– salts of amino acids)
 

  Increased intake of chloride-containing acids

·         Ammonium chloride

·         Lysine hydrochloride

·         Arginine hydrochloride

The Anion Gap

         The anion gap in plasma is most commonly defined as the difference between the major measured cations and the major measured anions:

Anion Gap = Na – ( Cl + HCO3 )

Anion Gap = 140 - _104 + 24) =12 mEq/L

Normal range 7-14 mEq/L

High Anion Gap Metabolic Acidosis

        

1.    Failure to Excrete Endogenous Nonvolatile Acids

Endogenously produced organic acids are normally eliminated by the kidneys in urine. Glomerular filtration rates below 20 mL/min (renal failure) typically result in progressive metabolic acidosis from the accumulation of these acids.

2.    Increased Endogenous Nonvolatile Acid Production

Severe tissue hypoxia following hypoxemia, hypoperfusion (ischemia), or inability to utilize oxygen (cyanide poisoning) can result in lactic acidosis.

3.    Ingestion of Exogenous Nonvolatile Acids

         Ingestion of large amounts of salicylates frequently results in metabolic acidosis.

Normal Anion Gap Metabolic Acidosis

         Metabolic acidosis associated with a normal anion gap is typically characterized by hyperchloremia. Plasma [Cl^–] increases to take the place of the HCO₃^– ions that are lost. Hyperchloremic metabolic acidosis most commonly results from abnormal gastrointestinal or renal losses of HCO₃^–.

        

Treatment of Metabolic Acidosis

          Alkali therapy in the form of NaHCO₃  is given if PH is below 7.20. the dose is decided empirically as a fixed dose (1 mEq/kg) or is derived from the base excess and the calculated bicarbonate space.

         Specific therapy for the underlying condition.

Bicarbonate Space

         The bicarbonate space is defined as the volume to which HCO₃^– will distribute when it is given intravenously. Although this theoretically should equal the extracellular fluid space (approximately 25% of body weight), in reality it ranges anywhere between 25% and 60% of body weight depending on the severity and duration of the acidosis.

In practice, only 50% of the calculated dose (105 mEq) is usually given, after which another blood gas is measured.

Anesthetic Considerations in Patients with Acidosis

·         Acidemia can potentiate the depressant effects of most sedatives and anesthetic agents on the central nervous and circulatory systems. Increased sedation and depression of airway reflexes may predispose to pulmonary aspiration.

·         Halothane is more arrhythmogenic in the presence of acidosis.

·         Succinylcholine should generally be avoided in acidotic patients with hyperkalemia to prevent further increases in plasma [K⁺].

·         Respiratory—but not metabolic—acidosis augments nondepolarizing neuromuscular blockade and may prevent its antagonism by reversal agents.

Alkalosis

Physiological Effects of Alkalosis

·         Alkalosis increases the affinity of hemoglobin for oxygen and shifts the oxygen dissociation curve to the left, making it more difficult for hemoglobin to give up oxygen to tissues.

·         Movement of H⁺ out of cells in exchange for the movement of extracellular K⁺ into cells can produce hypokalemia.

·         Alkalosis increases the number of anionic binding sites for Ca²⁺ on plasma proteins and can therefore decrease ionized plasma [Ca²⁺], leading to circulatory depression and neuromuscular irritability.

·         Respiratory alkalosis reduces cerebral blood flow, increases systemic vascular resistance, and may precipitate coronary vasospasm.

·         In the lungs, respiratory alkalosis increases bronchial smooth muscle tone (bronchoconstriction) but decreases pulmonary vascular resistance.

Respiratory Alkalosis

Respiratory alkalosis is defined as a primary decrease in PaCO₂.

Causes of Respiratory Alkalosis.

Central stimulation 

·         Pain

·         Anxiety

·         Ischemia

·         Stroke

·         Tumor

·         Infection

·         Fever

·         Drug-induced

·         Salicylates

·         Progesterone (pregnancy)

·         Analeptics (doxapram)

Peripheral stimulation 

·         Hypoxemia

·         High altitude

·         Pulmonary disease

·         Congestive heart failure

·         Noncardiogenic pulmonary edema

·         Asthma

·         Pulmonary embolism

·         Severe anemia

Unknown mechanism 

  Sepsis

  Metabolic encephalopathies

Iatrogenic 

  Ventilator-induced

Treatment of Respiratory Alkalosis

         Correction of the underlying process is the only treatment for respiratory alkalosis. For severe alkalemia (arterial pH > 7.60), intravenous hydrochloric acid, arginine chloride, or ammonium chloride may be indicated.

Metabolic Alkalosis

         Metabolic alkalosis is defined as a primary increase in plasma [HCO₃^–]. Most cases of metabolic alkalosis can be divided into (1) those associated with NaCl deficiency and extracellular fluid depletion, often described as chloride sensitive, and (2) those associated with enhanced mineralocorticoid activity, commonly referred to as chloride resistant.

 Causes of Metabolic Alkalosis.

Chloride-sensitive 

  Gastrointestinal

·         Vomiting

·         Gastric drainage

  Renal

·         Diuretics

·         Posthypercapnic

·         Low chloride intake

  Sweat

    Cystic fibrosis

Chloride-resistant 

·         Increased mineralocorticoid activity

·         Primary hyperaldosteronism

·         Edematous disorders (secondary hyperaldosteronism)

·         Cushing's syndrome

·         Licorice ingestion

·         Bartter's syndrome

·         Severe hypokalemia

Miscellaneous 

  Massive blood transfusion

  Acetate-containing colloid solutions

  Alkaline administration with renal insufficiency

Treatment of Metabolic Alkalosis

·         Correction of metabolic alkalosis is never complete until the underlying disorder is treated.

·         The treatment of choice for chloride-sensitive metabolic alkalosis is administration of intravenous saline (NaCl) and potassium (KCl).

·         Alkalosis associated with primary increases in mineralocorticoid activity readily responds to aldosterone antagonists (spironolactone).

·         When arterial blood pH is greater than 7.60, treatment with intravenous hydrochloric acid (0.1 mol/L), ammonium chloride (0.1 mol/L), arginine hydrochloride, or hemodialysis should be considered.

Anesthetic Considerations in Patients with Alkalemia

·         Respiratory alkalosis appears to prolong the duration of opioid-induced respiratory depression.

·         Cerebral ischemia can occur from marked reduction in cerebral blood flow during respiratory alkalosis, particularly during hypotension.

·         The combination of alkalemia and hypokalemia can precipitate severe atrial and ventricular arrhythmias.

·         Potentiation of nondepolarizing neuromuscular blockade is reported with alkalemia but may be more directly related to concomitant hypokalemia.