FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES
Acid - Base balance is primarily concerned with two ions: Hydrogen (H+) Bicarbonate (HCO3- )
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
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 acidii) Renal or gastrointestinal wasting of bicarbonateiii) 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 ACIDOSISCATOTID 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
Normal Anion Gap: (HYPER CHLORAEMIC)Increased GIT Losses of HCO3: Diarrhea Anion exchange resins (cholestyramine) Ingestion of CaCl2; MgCl2, Fistulae (pancreatic; biliary; small bowel) UreterosigmoidostomyIncreased 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 therapyDiabetic 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/IVSalicylate-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 edn2)Barash Clinical anesthesia 4th edn.3)Clinical Anesthesiology,Morgan 4th edn.4) Harrisons Principles of Internal Medicine 18th edn.