You are on page 1of 6

Acid Base Balance

pH Inverse logarithm of the H concentration If the H+ are high in number, the pH is low (acidic). If the H+ are low in number, the pH is high (alkaline). pH The pH scale ranges from 0 to 14: 0 is very acidic, 14 is very alkaline. Each number represents a factor of 10. If a solution moves from a pH of 6 to a pH of 5, the H+ have increased 10 times. pH Acids are formed as end products of protein, carbohydrate, and fat metabolism To maintain the bodys normal pH (7.35-7.45) the H+ must be neutralized or excreted The bones, lungs, and kidneys are the major organs involved in the regulation of acid and base balance Henderson Hasselbach Prove that C02 is an acid..... H+CO2 H2CO3H + HCO3+

Compensation Correction pH Body acids exist in two forms

Volatile

H2CO3 (can be eliminated as CO2 gas)

Nonvolatile Sulfuric, phosphoric, and other organic acids

Eliminated by the renal tubules with the regulation of HCO3 Buffering Systems A buffer is a chemical that can bind excessive H+ or OH without a significant change in pH A buffering pair consists of a weak acid and its conjugate base The most important plasma buffering systems are the carbonic acidbicarbonate system and hemoglobin Carbonic AcidBicarbonate Pair Operates in the lung and the kidney The greater the partial pressure of carbon dioxide, the more carbonic acid is formed

At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1 Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained

Carbonic AcidBicarbonate Pair If the amount of bicarbonate decreases, the pH decreases, causing a state of acidosis The pH can be returned to normal if the amount of carbonic acid also decreases This type of pH adjustment is referred to as compensation Carbonic AcidBicarbonate Pair The respiratory system compensates by increasing or decreasing ventilation The renal system corrects by producing acidic or alkaline urine Other Buffering Systems Protein buffering Proteins have negative charges, so they can serve as buffers for H+ Renal buffering Secretion of H+ in the urine and reabsorption of HCO3 Cellular ion exchange Exchange of K+ for H+ in acidosis and alkalosis Acid-Base Imbalances Normal arterial blood pH

7.35 to 7.45

Obtained by arterial blood gas (ABG) sampling Acidosis Systemic increase in H+ concentration Alkalosis Systemic decrease in H+ concentration Acidosis and Alkalosis Four categories of acid-base imbalances Respiratory acidosiselevation of pCO2 as a result of ventilation depression Respiratory alkalosisdepression of pCO2 as a result of alveolar hyperventilation Acidosis and Alkalosis Four categories of acid-base imbalances Metabolic acidosisdepression of HCO3 or an increase in noncarbonic acids Metabolic alkalosiselevation of HCO3 usually caused by an excessive loss of metabolic acids Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis How Do We Figure Out What We Have? Try to simplify it as much as possible but recognize that many times there may be one or more problems CONCEPT:

Calculated pH Measured pH

Normal Values pH-7.35-45 PCO2-40-50 P02-80-100 HCO3-22-26

Get into the habit of looking at the pH and the CO2 first Acid Base Rule #1 Rule I states that an acute change in Pc02 of 10 torr is associated with an increase or decrease in pH of 0.08 U. Rule II states that for every 0.0 I-V change in pH not caused by a change in Pc02, there is a 2/3 mEql change in the base. How Does This Work?? Example 1 pH=7.32 PC02=50 Acidotic or Alkalotic? Apply Rule 1- Ph 10t=0.08 units Calculated pH-(7.40-0.08)=7.32 Measured pH=7.32......therefore we have an acute respiratory acidosis!! What if the Measured and Calculated pH are different? Ph=7.26

PCO2-50 Now calculate using Rule 1 Calculated pH-7.32 Measured pH-however is 7.26 (0.06 u change) Rule II-0.0 I-U change in pH not caused by a change in Pc02, there is a 2/3 mEql change in the base. 0.06 x 2/3=4meq/L deficit in base thus mixed Respiratory and Metabolic Acidosis!!!

What if the Measured and Calculated pH are different?

Ph=7.26 PCO2-50 Now calculate using Rule 1 Calculated pH-7.32 Measured pH-however is 7.26 (0.06 u change) Rule II-0.0 I-U change in pH not caused by a change in Pc02, there is a 2/3 mEql change in the base. 0.06 x 2/3=4meq/L deficit in base thus mixed Respiratory and Metabolic Acidosis!!! Disorders Acute Respiratory Acute Obstructive Airway Disorders Croup Epiglottitis Foreign body

Asthma Bronchiolitis Chronic Obstructive Airway Disorders Bronchopulmonary dysplasia Cystic fibrosis Pulmonary Restrictive Disorders Pneumonia Aspiration Adult respiratory distress syndrome Pulmonary edema Interstitial lung disease Pleural effusion Pneumothorax rain tumor Circu latory crises Cardiac arrest Severe pulmonary edema Massive pulmonary embolism B Flail chest Kyphoscoliosis Pierre Robin syndrome Neuromuscular Disorders Muscular dystrophy Multiple sclerosis Spinal muscular atrophy Guillain-Barre syndrome Brainstem injury or tumor Botulism Spinal cord injury or tumor Myasthenia gravis Diaphragmatic paralysis Pickwickian syndrome Poliomyelitis Central Nervous System Depressants Narcotics General anesthesia Sedatives Cerebral trauma or infection Iatrogenic Causes Inadequate mechanical ventilation Hyperalimentation with high carbohydrate content Sorbent regenerative hemodialysis Anion Gap An abnormal anion gap occurs as a result of an increased level of an abnormal unmeasured anion Examples: DKAketones, salicylate poisoning, lactic acidosisincreased lactic acid, renal failure, etc. As these abnormal anions accumulate, the measured anions have to decrease to maintain electroneutrality

Anion Gap Used cautiously to distinguish different types of metabolic acidosis By rule, the concentration of anions () should equal the concentration of cations (+). Not all normal anions are routinely measured. Increase Anion Gap Cardiovascular collapse Diabetic ketoacidosis Lactic acidosis (tissue hypoxia) Starvation Drugs/toxins (methanol, ethanol, salicylate, fructose, sorbitol, cyanide, carbon monoxide, paraldehyde) Organic acid metabolism (pyruvate) Hepatic failure Renal failure Congenital enzymatic defects Glucose 6-phosphate deficiency Fructose l,6-diphosphatase deficiency Pyruvate carboxylase deficiency Methylmalonic aciduria MUDPALES MUDPALES -acronym, which details the main causes for anion gap metabolic acidosis (Methanol, Uremia Diabetic ketoacidosis, Paraldehyde, Alcohol, Lactic acidosis, Ethylene glycol, Salicylate toxicity Rule III So far-We have not looked at HCO3Rule III states the following: Total body bicarbonate deficit = Base deficit (mEqlL) x Patient's weight (kg) x 0.3 (HCO}- is located primarily in ECF, which is equal to 30% of body weight; thus total base deficit can be determined by multiplying base deficit by body weight by 0.3 e.g. 10 kg child PH=7.26 Calculated pH=7.32-XX=0.08 U difference PCO2=50 therefore there is 6meq base deficit 6Meq/l x 10kg x0.3=18 (help correct by giving deficit) -can also use 1mEq/kg as a rough estimate to correct) Anion Gap

Normal anion gap = Na+ + K+ = Cl + HCO3 + 10 to 12 mEq/L (other miscellaneous anions [the ones we dont measure]phosphates, sulfates, organic acids, etc.) Normal Anion Gap Diarrhea Intake of chloride-containing compounds (HCI, NH4 Cl,

CaCI2' MgC12 , arginine HCI, cholestyramine) Hyperalimentation Pancreatic, small bowel. or biliary tubes or fistulas Ureterosigmoidostomy, ileal conduit Carbonic anhydrase inhibitors (acetazolamide) Extracellular fluid volume expansion Mineralocorticoid deficiency (adrenal disorders) Renal tubular acidosis Early uremic acidosis Disorders Metabolic Alkalosis Vomiting Gastrointestinal suctioning CI--wasting diarrhea CI--deficient formula Diuretics Hypokalemia Hypocalcemia Hypochloremia Exogenous alkali intake: HC03-, citrate, lactate, acetate Excessive steroid use Renal failure Extracellular fluid volume depletion Cystic fibrosis Excess mineralocorticoid Hyperaldosteronism, Cushing's syndrome. adrenogenital syndrome Laxative, licorice abuse Excessive tobacco chewing Bartter's syndrome Why A/B Balance????? 0xy Hgb Diss Curve When this system is active, the exchange demonstrates why erythrocytes tend to give up oxygen more rapidly when PCO2 is elevated (as in respiratory acidosis), resulting in a shift to the right of the oxyhemoglobin dissociation curve. Erythrocytes hold on to oxygen when PC02 is decreased (as in respiratory alkalosis), resulting in a shift to the left in the oxyhemoglobin dissociation curve This is termed the Bohr effect. What to Do!!! Recognize the problem!!!!

Remember body is trying to get back to homeostasis THINK!!!!!!-Moralism=if you see hyperventilation-its not hyperventilation syndrome Use acronyms Slow assistance in correction

You might also like