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MODERATOR: PROF.DINESH.K
Why pH 7.35-7.45 is
necessary ?
 FOR OPTIMAL FUNCTIONING
 OF CELLULAR ENZYMES &
 METABOLIC PROCESSES
   Acid - Base balance is primarily
    concerned with two ions:
     Hydrogen (H+)
     Bicarbonate (HCO3- )
Metbolic acidosis and alkalosis
   6.1 = the pKa of carbonic acid
   0.03 is the solubility coefficient in blood of
    carbon dioxide (CO2)
   pH is the dependent variable while the
    bicarbonate concentration [HCO3-] and Paco2 are
    independent variables;
   Systemic arterial pH is maintained between 7.35
    and 7.45
    extracellular and intracellular chemical buffering
    mechanism
   Respiratory
   renal regulatory mechanisms.
Chemical Buffers: (First
  system within minutes)
 Bicarbonate-buffer-
  system
 Phosphate buffer-system

 Protein-buffer-system
   BICARBONATE BUFFER
    H++ HCO3ˉ == H2O+ CO2 ( pK 6.1 )
   NON-BICARBONATE BUFFERS
    1.   ALBUMIN ( PK 6.5)
    2.   Hb
    3.   phosphate[H2PO4ˉ == H+ + HPO4ˉˉ ( pK6.8)]
    4.   Bone
   Chemoreceptors in the
    medulla of brain sense pH
    changes and vary the rate
    and depth of breathing to
    compensate for pH
    changes.
   The lungs combine CO2
    with water to form
    carbonic acid. carbonic
    acid leads to a  in pH.
The kidneys regulate
   plasma [HCO3–] through
   three main processes:
(1) reabsorption of filtered
   HCO3–,
(2) formation of titratable
   acid, and
 (3) excretion of NH4+ in
   the urine
 Renal   compensation begins 12-24 hr
  after, hyperventilation starts.

 It
   takes 3-4 days to complete appropriate
  metabolic compensation.
  Metabolic acidosis can be defined as primary
   decrease in [HCO3]
i) Consumption of HCO3 by a strong nonvolatile
   acid
ii) Renal or gastrointestinal wasting of bicarbonate
iii) Rapid dilution of ECF compartment with a
   bicarbonate free fluid.
   Cardiovascular
     Impairment of cardiac contractility
     Arteriolar dilatation, venoconstriction, and
      centralization of blood volume
     Increased pulmonary vascular resistance
     Reduction in cardiac output, arterial blood pressure,
      and hepatic and renal blood flow
     Sensitization to reentrant arrhythmias and reduction
      in threshold of ventricular fibrillation
     Attenuation of cardiovascular responsiveness to
      catecholamines
   Respiratory
     Hyperventilation-Kussmaul breathing is the very deep
      and labored breathing
     Decreased strength of respiratory muscles and
      promotion of muscle fatigue
LUNG
                       ACIDOSIS


CATOTID BODY           MEDULLA            C.T ZONE



                        LUNG


                O2 SENSITIVE K+CHANNEL


 HYPERPNOEA    VASOCONSTRICTION/PPHN     TACHYPNOEA
   Metabolic
     Increased metabolic demands
     Insulin resistance
     Inhibition of anaerobic glycolysis
     Reduction in ATP synthesis
     Hyperkalemia
     Increased protein degradation
   Cerebral
     Inhibition of metabolism and cell-volume
      regulation
     Headache
     Lethargy
     Confusion
     and coma
HYPOXIA                                  ACIDOSIS

                ATP dependent K+
                CHANNEL


       CEREBRAL VASODILATION—ICP Incr.




HEADACHE            LETHARGY             CONFUSION
Most commonly defined as the difference between
  major measured cations and major measured
  anions.
 Anion Gap = [Na+] - ([Cl-] + [HCO3-])

 Normal range: 10-12mmol/L
Increase Anion Gap Acidosis:
 Methanol
 Uraemia
 Diabetic ketoacidosis
 Salicylate poisoning
 Lactic ketoacidosis
 Ethylene glycol
 Ethanol overdose
 Paraldehyde
Normal Anion Gap: (HYPER CHLORAEMIC)
Increased GIT Losses of HCO3:
 Diarrhea
 Anion exchange resins (cholestyramine)
 Ingestion of CaCl2; MgCl2,
 Fistulae (pancreatic; biliary; small bowel)
 Ureterosigmoidostomy
Increased renal losses of HCO3:
 Renal tubular acidosis
 Carbonic anhydrase inhibitors
 Hypoaldosteronism
 Dilutional
  Large amount of bicarbonate free fluids
 Total parentral nutrition.

 Increased intake of chloride-containing acids :

  · Ammonium chloride
  · Lysine hydrochloride
  · Arginine hydrochloride
    Is acidosis being caused by measured or
    unmeasured anions (i.e., chloride)? Look at blood
    chemistry
    Calculate anion gap( normal 10-12mmol/L)
    If gap is normal, there is too much chloride
    present, owing to excessive administration, excess
    loss of sodium (diarrhea, ileostomy), or renal
    tubular acidosis
    If gap is wide (>16), there are other unmeasured
    anions present, causing acidosis
   Check serum lactate—if >2, probably lactic
    acidosis
    If high lactate is explained by circulatory
    insufficiency (shock, hypovolemia, oliguria,
    under-resuscitation, anemia, carbon monoxide
    poisoning, seizures), then ―type A‖ lactic acidosis
   If not think about ―type B (rare)‖ causes—
    biguanides, fructose, sorbitol, nitroprusside,
    ethylene glycol, cancer, liver disease
    Look at creatinine and urine output
    If patient is in acute renal failure, these may be
    renal acids.
      Look at blood glucose and urinary ketones
   If patient is hyperglycemic and ketotic, this is
    diabetic ketoacidosis
    If patient is ketotic (unmeasured anion) and
    normoglycemic, this is either alcoholic (check
    blood alcohol) or starvation ketosis
    Check for presence of chronic alcohol abuse—
    high mean corpuscular volume, increased γ-
    glutamyl transferase on liver panel
If all of these tests are negative, think of intoxication
 Send toxicology laboratory tests (particularly
  salicylates) and serum osmolality, and calculate
  osmolality using the formula: 2(Na + K) +
  Glucose/18 + BUN/2.8
 Look for unmeasured source of osmoles: if gap
  between measured and calculated serum osmolality
  >12, think of alcohol, particularly ethylene glycol,
  isopropyl alcohol, and methanol
General measures
 Any respiratory component of acidemia should be
  corrected.
 A PaCO2 in the low 30s may be desirable to partially
  return pH to normal.
 If arterial pH remains below 7.20; alkali therapy
  usually in the form of NaHCO3(usually a 7.5%
  solution) may be necessary. The amount of NaHCO3
  given is decided emperically as a fixed dose
  (1mEq/kg) or is derived from the base excess and the
  calculated bicarbonate space
    (NaHCO3 = 30% x Body wt x base deficit)
 Half of the calculated deficit should be administered
  within the first 3–4 hours to avoid overcorrection.
 Large amounts of HCO3– may have deleterious

   effects.
  - hypernatremia
  - hyperosmolality
  - volume overload
   - worsening of intracellular acidosis.
Specific therapy
Diabetic ketoacidosis:
 replacement of existing fluid deficit(as a result of
  hyperglycemic osmotic diuresis)
 Insulin

 Potassium,phosphate and magnesium
In alcoholic ketoacidosis,
 Thiamine should be given with glucose to avoid
  Wernicke encephalopathy DOSE – 10-25 mg IM/IV
Salicylate-Induced Acidosis:
 Vigorous gastric lavage with isotonic saline (not
  NaHCO3)
 Alkalinization of urine with NaHCO3 to a pH >7.5
  increases elimination of salicylate.
   Ethanol infusions (an iv loading dose; 8-10ml/kg
    of a 10% ethanol in D5 solution over 30 min with
    the concomitant administration of a continous
    infusion at 0.15 ml/kg/hr to achieve a blood
    ethanol level of 100-130mg/dL) are indicated
    following methanol/ehtylene glycol intoxication.
Ethylene Glycol—Induced Acidosis:
   saline or osmotic diuresis,
   thiamine and pyridoxine supplements.
  Fomepizole-alcohol dehydrogenase
  inhibitor(15mg/kg).
   Ethanol
   Hemodialysis
   Preoperative assessment should emphasize volume
    status and renal function.
   Acidemia can potentiate the depressant effects of
    most sedatives and anaesthetic agents on the CNS and
    circulatory systems.
    As most OPIOIDS are weak bases; acidosis can
    increase the fraction of the drug in the nonionized
    form and facilitate penetration of opiod into the brain.
    Increased sedation and depression of airway reflexes
    may predispose to pulmonary aspiration.
   Circulatory depressant effects of both volatile and
    intravenous anaesthetics can be exaggerated.
   Any agent that rapidly depresses sympathetic tone can
    potentially allow unopposed circulatory depression in
    the setting of acidosis.
   Halothane is more arrythmogenic in the presence of
    acidosis.
   Succinylcholine avoided in acidotic patient with
    hyperkalaemia to prevent further increase in K+.
Metabolic alkalosis
 Manifested by an elevated arterial pH

 Increase in the serum [HCO3–]

 Increase in Paco2 as a result of compensatory
  alveolar hypoventilation.It is often accompanied
  by hypochloremia and hypokalemia.
   Metabolic alkalosis occurs as a result of net gain
    of [HCO3–] or loss of nonvolatile acid (usually
    HCl by vomiting) from the extracellular fluid.
   metabolic alkalosis represents a failure of the
    kidneys to eliminate HCO3– in the usual manner.
   The kidneys will retain, rather than excrete, the
    excess alkali and maintain the alkalosis if (1)
    volume deficiency, chloride deficiency, and K+
    deficiency exist in combination with a reduced
    GFR, which augments distal tubule H+ secretion.
    (2) hypokalemia exists because of autonomous
    hyperaldosteronism.
 Alkalosis increases affinity of Hb for O2
 and shifts the ODC to the left,making it
 more difficult for Hb to give up O2 to
 tissues.
 Movement of H+ out of the cells in
 exchange of extracellar K+ into cells,can
 produce hypokalaemia.
 Alkalosisincreases 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.
   Mental confusion
   Obtundation
   Predisposition to seizures
   Paresthesia, muscular cramping, tetany,
    aggravation of arrhythmias, and hypoxemia in
    chronic obstructive pulmonary disease.
   Related electrolyte abnormalities include
    hypokalemia and hypophosphatemia.
   Primary treatment is correcting the underlying
    stimulus for HCO3– generation.
   [H+] loss by the stomach or kidneys can be
    mitigated by the use of proton pump inhibitors or
    the discontinuation of diuretics.
   Isotonic saline-reverse the alkalosis if ECFV
    contraction is present.
   Acetazolamide-a carbonic anhydrase
    inhibitor,accelerate renal loss of HCO3 which is
    usually effective in patients with adequate renal
    function.
   Dilute hydrochloric acid (0.1 N HCl) is also
    effective but can cause hemolysis, and must be
    delivered centrally and slowly.
   Hemodialysis against a dialysate low in [HCO3–]
    and high in [Cl–] can be effective when renal
    function is impaired
   Combination of alkalemia and hypokalemia can
    precipitate severe atrial and ventricular
    dysrhythmia.
   Potentiation of non-depolarizing neuromuscular
    blockade is reported with alkalemia but more
    directly related to concomitant hypokalemia.
1)Miller’s Anesthesia 7th edn
2)Barash Clinical anesthesia 4th edn.
3)Clinical Anesthesiology,Morgan 4th edn.
4) Harrison's Principles of Internal Medicine 18th
  edn.
Metbolic acidosis and alkalosis

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Metbolic acidosis and alkalosis

  • 2. Why pH 7.35-7.45 is necessary ?
  • 3.  FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES
  • 4. Acid - Base balance is primarily concerned with two ions: Hydrogen (H+) Bicarbonate (HCO3- )
  • 6. 6.1 = the pKa of carbonic acid  0.03 is the solubility coefficient in blood of carbon dioxide (CO2)  pH is the dependent variable while the bicarbonate concentration [HCO3-] and Paco2 are independent variables;
  • 7. Systemic arterial pH is maintained between 7.35 and 7.45  extracellular and intracellular chemical buffering mechanism  Respiratory  renal regulatory mechanisms.
  • 8. Chemical Buffers: (First system within minutes)  Bicarbonate-buffer- system  Phosphate buffer-system  Protein-buffer-system
  • 9. BICARBONATE BUFFER H++ HCO3ˉ == H2O+ CO2 ( pK 6.1 )  NON-BICARBONATE BUFFERS 1. ALBUMIN ( PK 6.5) 2. Hb 3. phosphate[H2PO4ˉ == H+ + HPO4ˉˉ ( pK6.8)] 4. Bone
  • 10. Chemoreceptors in the medulla of brain sense pH changes and vary the rate and depth of breathing to compensate for pH changes.  The lungs combine CO2 with water to form carbonic acid. carbonic acid leads to a  in pH.
  • 11. The kidneys regulate plasma [HCO3–] through three main processes: (1) reabsorption of filtered HCO3–, (2) formation of titratable acid, and (3) excretion of NH4+ in the urine
  • 12.  Renal compensation begins 12-24 hr after, hyperventilation starts.  It takes 3-4 days to complete appropriate metabolic compensation.
  • 13.  Metabolic acidosis can be defined as primary decrease in [HCO3] i) Consumption of HCO3 by a strong nonvolatile acid ii) Renal or gastrointestinal wasting of bicarbonate iii) Rapid dilution of ECF compartment with a bicarbonate free fluid.
  • 14. Cardiovascular  Impairment of cardiac contractility  Arteriolar dilatation, venoconstriction, and centralization of blood volume  Increased pulmonary vascular resistance  Reduction in cardiac output, arterial blood pressure, and hepatic and renal blood flow  Sensitization to reentrant arrhythmias and reduction in threshold of ventricular fibrillation  Attenuation of cardiovascular responsiveness to catecholamines
  • 15. Respiratory  Hyperventilation-Kussmaul breathing is the very deep and labored breathing  Decreased strength of respiratory muscles and promotion of muscle fatigue
  • 16. LUNG ACIDOSIS CATOTID BODY MEDULLA C.T ZONE LUNG O2 SENSITIVE K+CHANNEL HYPERPNOEA VASOCONSTRICTION/PPHN TACHYPNOEA
  • 17. Metabolic  Increased metabolic demands  Insulin resistance  Inhibition of anaerobic glycolysis  Reduction in ATP synthesis  Hyperkalemia  Increased protein degradation
  • 18. Cerebral  Inhibition of metabolism and cell-volume regulation  Headache  Lethargy  Confusion  and coma
  • 19. HYPOXIA ACIDOSIS ATP dependent K+ CHANNEL CEREBRAL VASODILATION—ICP Incr. HEADACHE LETHARGY CONFUSION
  • 20. Most commonly defined as the difference between major measured cations and major measured anions.  Anion Gap = [Na+] - ([Cl-] + [HCO3-])  Normal range: 10-12mmol/L
  • 21. Increase Anion Gap Acidosis:  Methanol  Uraemia  Diabetic ketoacidosis  Salicylate poisoning  Lactic ketoacidosis  Ethylene glycol  Ethanol overdose  Paraldehyde
  • 22. Normal Anion Gap: (HYPER CHLORAEMIC) Increased GIT Losses of HCO3:  Diarrhea  Anion exchange resins (cholestyramine)  Ingestion of CaCl2; MgCl2,  Fistulae (pancreatic; biliary; small bowel)  Ureterosigmoidostomy Increased renal losses of HCO3:  Renal tubular acidosis  Carbonic anhydrase inhibitors  Hypoaldosteronism
  • 23.  Dilutional Large amount of bicarbonate free fluids  Total parentral nutrition.  Increased intake of chloride-containing acids : · Ammonium chloride · Lysine hydrochloride · Arginine hydrochloride
  • 24. Is acidosis being caused by measured or unmeasured anions (i.e., chloride)? Look at blood chemistry  Calculate anion gap( normal 10-12mmol/L)  If gap is normal, there is too much chloride present, owing to excessive administration, excess loss of sodium (diarrhea, ileostomy), or renal tubular acidosis
  • 25. If gap is wide (>16), there are other unmeasured anions present, causing acidosis  Check serum lactate—if >2, probably lactic acidosis  If high lactate is explained by circulatory insufficiency (shock, hypovolemia, oliguria, under-resuscitation, anemia, carbon monoxide poisoning, seizures), then ―type A‖ lactic acidosis  If not think about ―type B (rare)‖ causes— biguanides, fructose, sorbitol, nitroprusside, ethylene glycol, cancer, liver disease
  • 26. Look at creatinine and urine output  If patient is in acute renal failure, these may be renal acids. Look at blood glucose and urinary ketones  If patient is hyperglycemic and ketotic, this is diabetic ketoacidosis  If patient is ketotic (unmeasured anion) and normoglycemic, this is either alcoholic (check blood alcohol) or starvation ketosis  Check for presence of chronic alcohol abuse— high mean corpuscular volume, increased γ- glutamyl transferase on liver panel
  • 27. If all of these tests are negative, think of intoxication  Send toxicology laboratory tests (particularly salicylates) and serum osmolality, and calculate osmolality using the formula: 2(Na + K) + Glucose/18 + BUN/2.8  Look for unmeasured source of osmoles: if gap between measured and calculated serum osmolality >12, think of alcohol, particularly ethylene glycol, isopropyl alcohol, and methanol
  • 28. General measures  Any respiratory component of acidemia should be corrected.  A PaCO2 in the low 30s may be desirable to partially return pH to normal.  If arterial pH remains below 7.20; alkali therapy usually in the form of NaHCO3(usually a 7.5% solution) may be necessary. The amount of NaHCO3 given is decided emperically as a fixed dose (1mEq/kg) or is derived from the base excess and the calculated bicarbonate space (NaHCO3 = 30% x Body wt x base deficit)
  • 29.  Half of the calculated deficit should be administered within the first 3–4 hours to avoid overcorrection.  Large amounts of HCO3– may have deleterious effects. - hypernatremia - hyperosmolality - volume overload - worsening of intracellular acidosis.
  • 30. Specific therapy Diabetic ketoacidosis:  replacement of existing fluid deficit(as a result of hyperglycemic osmotic diuresis)  Insulin  Potassium,phosphate and magnesium
  • 31. In alcoholic ketoacidosis,  Thiamine should be given with glucose to avoid Wernicke encephalopathy DOSE – 10-25 mg IM/IV Salicylate-Induced Acidosis:  Vigorous gastric lavage with isotonic saline (not NaHCO3)  Alkalinization of urine with NaHCO3 to a pH >7.5 increases elimination of salicylate.
  • 32. Ethanol infusions (an iv loading dose; 8-10ml/kg of a 10% ethanol in D5 solution over 30 min with the concomitant administration of a continous infusion at 0.15 ml/kg/hr to achieve a blood ethanol level of 100-130mg/dL) are indicated following methanol/ehtylene glycol intoxication.
  • 33. Ethylene Glycol—Induced Acidosis: saline or osmotic diuresis, thiamine and pyridoxine supplements. Fomepizole-alcohol dehydrogenase inhibitor(15mg/kg). Ethanol Hemodialysis
  • 34. Preoperative assessment should emphasize volume status and renal function.  Acidemia can potentiate the depressant effects of most sedatives and anaesthetic agents on the CNS and circulatory systems.  As most OPIOIDS are weak bases; acidosis can increase the fraction of the drug in the nonionized form and facilitate penetration of opiod into the brain.  Increased sedation and depression of airway reflexes may predispose to pulmonary aspiration.
  • 35. Circulatory depressant effects of both volatile and intravenous anaesthetics can be exaggerated.  Any agent that rapidly depresses sympathetic tone can potentially allow unopposed circulatory depression in the setting of acidosis.  Halothane is more arrythmogenic in the presence of acidosis.  Succinylcholine avoided in acidotic patient with hyperkalaemia to prevent further increase in K+.
  • 36. Metabolic alkalosis  Manifested by an elevated arterial pH  Increase in the serum [HCO3–]  Increase in Paco2 as a result of compensatory alveolar hypoventilation.It is often accompanied by hypochloremia and hypokalemia.
  • 37. Metabolic alkalosis occurs as a result of net gain of [HCO3–] or loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid.  metabolic alkalosis represents a failure of the kidneys to eliminate HCO3– in the usual manner.
  • 38. The kidneys will retain, rather than excrete, the excess alkali and maintain the alkalosis if (1) volume deficiency, chloride deficiency, and K+ deficiency exist in combination with a reduced GFR, which augments distal tubule H+ secretion. (2) hypokalemia exists because of autonomous hyperaldosteronism.
  • 39.  Alkalosis increases affinity of Hb for O2 and shifts the ODC to the left,making it more difficult for Hb to give up O2 to tissues.  Movement of H+ out of the cells in exchange of extracellar K+ into cells,can produce hypokalaemia.
  • 40.  Alkalosisincreases 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.
  • 41. Mental confusion  Obtundation  Predisposition to seizures  Paresthesia, muscular cramping, tetany, aggravation of arrhythmias, and hypoxemia in chronic obstructive pulmonary disease.  Related electrolyte abnormalities include hypokalemia and hypophosphatemia.
  • 42. Primary treatment is correcting the underlying stimulus for HCO3– generation.  [H+] loss by the stomach or kidneys can be mitigated by the use of proton pump inhibitors or the discontinuation of diuretics.  Isotonic saline-reverse the alkalosis if ECFV contraction is present.
  • 43. Acetazolamide-a carbonic anhydrase inhibitor,accelerate renal loss of HCO3 which is usually effective in patients with adequate renal function.  Dilute hydrochloric acid (0.1 N HCl) is also effective but can cause hemolysis, and must be delivered centrally and slowly.  Hemodialysis against a dialysate low in [HCO3–] and high in [Cl–] can be effective when renal function is impaired
  • 44. Combination of alkalemia and hypokalemia can precipitate severe atrial and ventricular dysrhythmia.  Potentiation of non-depolarizing neuromuscular blockade is reported with alkalemia but more directly related to concomitant hypokalemia.
  • 45. 1)Miller’s Anesthesia 7th edn 2)Barash Clinical anesthesia 4th edn. 3)Clinical Anesthesiology,Morgan 4th edn. 4) Harrison's Principles of Internal Medicine 18th edn.