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ACID BASE BALANCE Paula Ruedebusch, ARNP, DNP ACID-BASE BALANCE Acid-base balance is carefully regulated to maintain a normal PH via multiple mechanisms ACID BASE IMBALANCES Rare – WHY? Secondary ABG needed Co-exist Life-threatening IS PH IMPORTANT? Yes!! pH <6.9 or >7.7: generally incompatible with life pH determines shape and thus function of many biological molecules, particularly proteins Enzymes & ion channels are examples of protein molecules sensitive to pH (modifies structural bonds, changing shape and function) WHERE DOES H+ COME FROM? Intake (PO, IV, IM, NG, NJ) Food: fatty acids, amino acids Drugs : e.g., aspirin, toxins, paraldehyde, ethylene glycol, methanol, formaldehyde, others ) CO2 production: CO2 is not an acid but it combines with water to form carbonic acid which then dissociates into H+ and HCO3- Metabolic acids: Citric acid cycle intermediates (aerobic metabolism) Lactic acid (anaerobic metabolism) Ketoacids--produced when some fats are incompletely metabolized. Other organic acid production. 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 (CONT’D) 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 (CONT’D) Acids are formed as end products of protein, carbohydrate, and fat metabolism To maintain the body’s 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 ORGANIC ACID PRODUCTION Many metabolic intermediates are organic acids (fatty acids, amino acids, citric acid cycle components, lactic acid produced by anaerobic metabolism) Pyruvic acid pyruvate + H+ Lactic acid lactate + H+ Metabolic organic acid production can get out of control, producing an immense acid load Anerobic metabolism produces lactic acid leading to lactic acidosis (seen in perfusion & oxygenation problems) Ketoacids from incomplete fat metabolism (diabetes mellitus, starvation, alcoholism) ANAEROBIC METABOLISM Sugar can be burned without oxygen – anaerobically Far more energy is released from burning energy aerobically Glycolysis is anaerobic, and is carried out in the cytosol ANAEROBIC METABOLISM ACID ELIMINATION Renal elimination in urine Respiratory elimination of CO2 (ventilation) Emesis/gastric suction (Buffers keep pH from changing much despite an acid load) WHERE DOES BASE COME FROM? Some foods contain base—not many. Some fruits, vegetables (broccoli, artichoke, leek, eggplant, others); they contain an anion that binds H+ Some drugs contain base (bicarbonate; antacids) HOW IS BASE ELIMINATED? There is not normally much base consumption so most of acid-base balance involves eliminating acid Loss of intestinal or colonic fluid results in loss of base Urine can be slightly basic (up to pH 8.0) PH 1. 2. 3. MAINTENANCE How is pH maintained in a narrow range in the face of great acid intake and production? Buffers: immediately blunts pH change Ventilation: rapid response; eliminates 75% of acid Renal regulation: slow—takes days BUFFERING SYSTEMS A buffer is a chemical that can bind excessive H+ or OH– without a significant change in pH Buffers moderate pH change: If you add H+ to a buffer solution, pH will change less than one would predict based on the amount of added H+. This is because the buffer has bound up the H+ Similarly, buffers blunt the effect of added base. PHYSIOLOGIC BUFFERS In In In plasma: HCO3- (goes to H2CO3 then CO2 and H20) Protein (goes to H+protein compound) interstitial fluid: HCO3- intracellular fluid: Hemoglobin Protein Phosphate CARBONIC ACID-BICARBONATE 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 ACID–BICARBONATE PAIR (CONT’D) 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 ACID–BICARBONATE PAIR (CONT’D) The respiratory system compensates by increasing ventilation to expire carbon dioxide or by decreasing ventilation to retain carbon dioxide The renal system compensates by producing acidic or alkaline urine COMPENSATION ACID-BASE IMBALANCES Normal arterial blood pH Acidosis 7.35 to 7.45 Obtained by arterial blood gas (ABG) sampling Systemic increase in H+ concentration or decrease in bicarbonate Alkalosis Systemic decrease in H+ concentration or increase in bicarbonate ABG NORMS Lab Normal Range pH 7.35 – 7.45 PaO2 80-100 PaCO2 35-45 HCO3 22-26 ACIDOSIS AND ALKALOSIS Four categories of acid-base imbalances: Respiratory acidosis—elevation of pCO2 as a result of ventilation depression Respiratory alkalosis—depression of pCO2 as a result of alveolar hyperventilation Metabolic acidosis—depression of HCO3– or an increase in noncarbonic acids Metabolic alkalosis—elevation of HCO3– usually caused by an excessive loss of metabolic acids RESPIRATORY ACIDOSIS RESPIRATORY ACIDOSIS: THE PROBLEM Definition: Alveolar hypoventilation causes CO2 retention; PaCO2 increases Causes: suppression of medullary respiratory centers by drugs (narcotics, sedation, alcohol) trauma (increased intracranial pressure); problems with the breathing muscles (paralysis, anesthesia, weakness) or fatigue; Thoracic deformities, obesity Lung problems (COPD, pneumonia, trauma) RESPIRATORY ACIDOSIS: SIGNS, SYMPTOMS ABG: acid pH, elevated PaCO2 and HCO3 Observe respiratory symptoms (slow or shallow or absent breathing) Chronic problem: metabolic compensation moves toward higher HCO3- & higher pH RESPIRATORY ACIDOSIS: THE COMPENSATION Increase renal H+ loss and HCO3- retention RESPIRATORY ACIDOSIS: CLINICAL MANAGEMENT Acute problems: increase ventilation (reverse respiratory suppression, provide mechanical ventilation, relieve chest wall restriction, restore muscle function) Chronic problems: Support compensation; do not try to remedy the high HCO3- level; use caution in administering oxygen; support ventilation RESPIRATORY ALKALOSIS: DEFINITION & ETIOLOGY Definition: Alveolar hyperventilation causes excess CO2 elimination; PaCO2 falls Causes: Iatrogenic (i.e., caused by care provider: overventilation with mechanical ventilator—can be accidental or deliberate) Hypoxemia (induces increased ventilation) Trauma to medullary respiratory centers Anxiety, pain Spontaneous RESPIRATORY ALKALOSIS - CAUSES RESPIRATORY ALKALOSIS: SIGNS, SYMPTOMS alkalotic pH, low PaCO2, low HCO3 Chronic problem: renal compensation lowers HCO3-; partially corrects pH Observe respiratory symptoms (hyperventilation) Irritability Paresthesia, cramps, tetany, carpopedal spasm, Chvostek’s sign, Trousseau’s sign, cardiac arrhythmias ABG: CHOVSTEK’S SIGN TROUSSEAU’S SIGN CHOVSTEK AND TROUSSEAU VIDEO https://www.youtube.com/watch?v=kvmwsTU0InQ RESPIRATORY ALKALOSIS: COMPENSATION Increase renal H+ retention This takes several days RESPIRATORY ALKALOSIS: CLINICAL MANAGEMENT Fix acute problems: correct hypoxemia, reduce rate &/or volume of ventilation, relieve anxiety, relieve pain, etc If anxiety related, consider having the patient breathe with a paper bag over his face—this causes him to re-breathe some of his exhaled CO2 and can raise the PaCO2 Support compensation if needed RESPIRATORY ALKALOSIS CASE Patient is a 40 y/o female with chronic asthma; she now has acute pneumonia (lung infection) ABG: pH: 7.6; PaCO2: 24; HCO3- 22mEq/l; hypoxemia S/Sx: hands & feet are twitching; reflexes are abnormally brisk; positive Chvostek sign; positive Trousseau’s sign Dx: acute respiratory alkalosis; no compensation Rx: administer additional inspired O2 to improve PaO2, eliminating hypoxic drive to overventilate ETIOLOGY OF METABOLIC ACIDOSIS Excess GI HCO3- loss (diarrhea, loss of pancreatic fluid) Excess renal HCO3- loss (some types of renal failure) Drugs/toxins: amphotericin B, acetozolamide, others MORE CAUSES OF METABOLIC ACIDOSIS Lactic acidosis Ketoacidosis Drugs/toxins: salicylate, ethylene glycol, paraldehyde Rhabdomyolysis METABOLIC ACIDOSIS: SIGNS, SYMPTOMS ABG: acid pH, low HCO3-, low or normal PaCO2 Observe respiratory symptoms (deep/rapid respirations) Headache, lethargy, progresses to coma Anorexia, nausea, vomiting, diarrhea Cardiac arrhythmias METABOLIC ACIDOSIS: THE COMPENSATION Respiratory: reduce PaCO2 by breathing quickly and deeply METABOLIC ACIDOSIS: CLINICAL MANAGEMENT Fix acute problems: improve perfusion, reverse hyperglycemia, etc. Support compensation: do not try to remedy the low PaCO2; observe patient closely for signs of fatigue—this could slow ventilation and result in a combination of metabolic acidosis & respiratory acidosis If severe, (pH<7.1), administer sodium bicarbonate intravenously (IV) METABOLIC ACIDOSIS CASE Patient is 30 y/o previously healthy man, now hemorrhaging Hypotensive; tachycardic Inadequate tissue perfusion, thus anaerobic metabolism ABGs: pH: 7.3; PaCO2: 30; HCO3-: 14mEq/l Dx: metabolic acidosis; respiratory compensation Rx: Correct problem (stop bleeding, correct hypotension by administering saline/blood products); support compensation (i.e., allow him to continue rapid breathing) METABOLIC ALKALOSIS: DEFINITION & ETIOLOGY Definition: Primary increase in plasma [HCO3-] Causes: Loss of H+ (gastric loss, renal loss) Gain of HCO3 Contraction alkalosis METABOLIC ALKALOSIS: SIGNS, SYMPTOMS alkalotic pH, high HCO3-; high PaCO2 Observe respiratory symptoms (hyperventilation) Irritability Paresthesia, cramps, tetany, carpopedal spasm Hypokalemia & acidic urine if hypovolemic ABG: METABOLIC ALKALOSIS: CLINICAL MANAGEMENT Correct problem Support compensation if needed Compensation = Slowed ventilation: increased PaCO2 METABOLIC ALKALOSIS CASE 25 y/o male; 4 day hx of vomiting; C/O exhaustion; tachycardic, orthostatic hypotension; hypopneic; brisk reflexes; Labs: hypokalemia, hypochloremia; acidic urine ABG: pH: 7.5; PaCO2: 48; HCO3-: 36mEq/l Dx: metabolic alkalosis, respiratory compensation; this is “contraction alkalosis” or hypokalemic, hypochloremic metabolic alkalosis, caused by loss of GI fluids & sustained by hypovolemia Rx: control vomiting; correct saline (extracellular fluid) deficit; then administer K+; do not try to increase ventilation VENTILATION CAN IMPROVE ACID BASE BALANCE Ventilation can eliminate metabolically produced acid (eliminate CO2 thus eliminate acid). This is the normal way to eliminate 75% of the acid load. Ventilation can eliminate excess acid when it is produced by metabolism or gained. e.g., from aspirin poisoning. This is called respiratory compensation for a metabolic acidosis. Ventilation can retain acid when the body is too alkalotic. This is called respiratory compensation for a metabolic alkalosis. VENTILATION CAN WORSEN ACID BASE BALANCE Decreased ventilation: raises PaCO2; results in higher H+ levels; called respiratory acidosis Increased ventilation: lowers PaCO2; results in lower H+ levels; called respiratory alkalosis VENTILATION High PaCO2 and low PaO2 both stimulate ventilation When PaCO2 rises, this stimulates ventilation; the patient breathes faster/deeper; this lowers PaCO2 (“blows it off”) When PaCO2 is lower than normal, this can inhibit drive to breathe The greater the respiratory rate/depth, the lower will be the patient’s PaCO2 The lower the respiratory rate/depth, the higher will be the patient’s PaCO2 RENAL Kidney normally eliminates about 25% of the acid load Filtration: H+ & HCO3- are filtered Reabsortion & secretion mechanisms: REMEMBER… CLEAR YOUR HEAD AND GET READY! ABGS! ABGS! ABGS! STEPS FOR ABG ANALYSIS 1. 2. 3. 4. 5. What is the pH? Acidoticor Alkalotic? What is the primary disorder present? Is there appropriate compensation? Is the compensation acute or chronic? What is the differential for the clinical processes? NORMAL ABG VALUES Lab Normal Range pH 7.35 – 7.45 PaO2 80-100 PaCO2 35-45 HCO3 22-26 STEP 1: Look at the pH: is the blood acidic or alkalemic? EXAMPLES : pH: 7.31 pH: 7.48 pH: 7.43 STEP 2: WHAT IS THE PRIMARY DISORDER? What disorder is present? pH PaCO2 or HCO3 Respiratory Acidosis Metabolic Acidosis pH low PaCO2 high pH low HCO3 low Respiratory Alkalosis pH high PaCO2 low Metabolic Alkalosis pH high HCO3 high ROME ROME ROME STEP 3-4: COMPENSATED VS. UNCOMPENSATED Compensated: pH is anywhere inside the normal ranges (Anything between 7.35 to 7.45) Uncompensated: pH is anywhere outside the normal ranges - greater than 7.45 or less than 7.35, and the value (CO2 or HCO3) that does not match the pH will still be in the normal range. Partially compensated: pH is anywhere outside the normal ranges, and the value that does not match the pH will be outside its normal range, indicating the body is attempting to get the pH back to normal. For example, if the pH (7.20) and CO2 (50) are acidotic, the HCO3 should be on the alkalotic side (27). TEST YOURSELF! 2. An arterial blood gas value of PaCO2 = 47, pH = 7.30, Bicarbonate = 24 indicates: A. B. C. D. Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis ABG PRACTICE! pH: 7.40 N PaCO2: 37 N HCO3: 23 N ABG PRACTICE pH: 7.23 PaCO2: 50 HCO3: 22 N = Uncompensated respiratory acidosis ABG PRACTICE pH: 7.36 PaCO2: 50 HCO3: 29 N = Compensated respiratory acidosis ABG PRACTICE pH: 7.50 PaCO2: 18 HCO3: 24 N = Uncompensated respiratory alkalosis ABG PRACTICE pH: 7.50 PaCO2: 42 N HCO3: 33 = Uncompensated metabolic alkalosis REAL-LIFE IMPORTANCE QUESTIONS?