370 likes | 964 Views
. 15210430. . 3.615 1.0. . . . . ABG: 7.42/24/115. . Why do we call Normal Saline normal?. What is the Na concentration of
E N D
1. Acid & Base John R. Foringer, M.D.
Division of Renal Diseases and Hypertension
Section of Critical Care Nephrology
john.r.foringer@uth.tmc.edu
(713) 500-6868
3. Simple Acid-Base Disturbances pH = pK + log10 [HCO3]
(0.0301)(paCO2)
pH = 6. 1 + log ( metabolic component)
(respiratory component)
HCO3_ & CO2 = pH
CO2 & HCO3_ = pH
7. Normal renal processes of acid handling
12. Mixed Acid-Base Disturbances Definition
Combination of two or more of the 4 simple disturbances (primary)
Examples
Mixed respiratory-metabolic disorders
Mixed metabolic disorders
13. Compensatory Responses in Simple Acid-Base Disorders
14. What is the Base Excess? Proposed as an indicator of acid-base status that was not influenced by PaCO2
It is the sum of the concentration of buffer anions
HCO3 and hemoglobin
Problem is this only works in vitro
In vivo as the PCO2 rises the ? HCO3 is attenuated by flux into the interstitial fluid compartment
Now to overcome this: Standard Base Excess
SBE = 0.93 ([HCO3] -24.4) + 13.79 (pH -7.4)
Estimates the amount of base needed to restore the metabolic acid-base status to normal in the entire extracellular fluid compartment
16. Metabolic Acidosis
17. Why Acidosis is Bad
19. Evaluating a Low HCO3
22. Lactic Acid Type I proportional increase in lactate and pyruvate
Type II Lactate higher than pyruvate
Type A tissue hypoxia
Type B arises from malignancy, liver disease, inborn errors of metabolism, or ingestion of toxins
23. Treatment of Metabolic (Lactic) Acidosis Treatment with NaHCO3
An estimate of replacement
Dose of bicarbonate = (0.5 X BW) X (desired HCO3 current HCO3)
Goal of replacement is a pH above 7.2
24. Treatment of Lactic Acidosis Should we treat lactic acid with HCO3 ?
?PFK activity (rate limiting enzyme of glycolysis)
Acidosis ?and alkalosis ? lactate production
? CO2 production
Impairs cardiac performance
Large fluid load
27. Treatment of Lactic Acidosis Dichloroacetate
Promotes oxidation of lactate (pyruvate dehydrogenase) ?? acetyl-coenzyme A + carbon dioxide
252 patients with lactic acidosis, placebo-controlled, randomized trial of intravenous sodium dichloroacetate
Only 12 percent of the dichloroacetate-treated patients and 17 percent of the placebo patients survived to be discharged
Statistically significant but clinically unimportant changes in arterial-blood lactate concentrations and pH and fails to alter either hemodynamics or survival
28. THAM (0.3 N tromethamine) Tris-Hydroxymethyl Aminomethane
Sodium-free solution
Buffers both metabolic acids (THAM + H+ ?? THAM+)
and respiratory acids (THAM + H2CO3 ?? THAM+ + HCO3-)
[proton and CO2 scavenger]
Limits carbon dioxide generation and increases both extracellular and intracellular pH
Serious side effects
including hyperkalemia, hypoglycemia, ventilatory depression, local injury in cases of extravasation, and hepatic necrosis in neonates
Renal excretion
29. Treatment of Lactic Acidosis Carbicarb
Equimolar concentrations of sodium bicarbonate and sodium carbonate
Carbonate is a stronger base (CO32- + H+ ?? HCO3-)
Carbonate ion can react with carbonic acid, thereby consuming carbon dioxide
(CO32- + H2CO3 ?? 2HCO3-).
Increased blood and intracellular pH with little or no rise in the arterial or venous partial pressure of carbon dioxide
Risks of hypervolemia and hypertonicity
36. Disorders Responsible for Hyperchloremic Acidosis(Normal Anion Gap) Gastrointestinal Bicarbonate Loss
Diarrhea
Renal Acidification Defects
Proximal, classical distal RTA, and hyperkalemic distal RTA
Early chronic renal failure
Ingestion or administration of acid, hyperalimentation
Drugs
38. Evaluating a Low Serum HCO3 Renal Tubular Acidosis
Impaired ammonium excretion can be demonstrated by the urine net negative charge (anion gap):
urine Na + + urine K+ + urine NH4+ = urine Cl-
UNa + + UK+ - UCl- = -UNH4+
Normally: UNa + + UK+ - UCl- = -UNH4+ = < -20 in the face of acidemia
In RTAs ammonium excretion is impaired, therefore
In RTAs: UNa + + UK+ - UCl- = -UNH4+ = 0
( range +20 to 80)
40. Normal physiology of acid excretion: Proximal tubule Responsible for reabsorption of the HCO3 filtered at the glomerulus; bulk reabsorption
44. Metabolic Alkalosis
45. Metabolic alkalosis
Respiratory acidosis
Therefore, diagnosis requires a concomitant arterial pH.
46. Evaluating an Elevated Serum HCO3- Causes of Metabolic Alkalosis
Effective ECV Contraction resulting in secondary Hyperreninemic Hyperaldosteronism
Hypermineralocorticoidism resulting in ECV expansion and Hypertension.
Exogenous Alkali Loads
51. Treatment of Metabolic Alkalosis Low Urine [Cl-] (< 20 mEq/L)
0.9% NaCl
Potassium Chloride
High Urine [Cl-] (>25 mEq/L)
Cause specific (surgery, angioplasty, specific drug therapy)
53. Respiratory Acid-Base Disorders Alkalosis
Central nervous system lesions, pregnancy, endotoxemia, salicylates, hepatic failure, hypoxemia, anxiety, pain