AcidBase Disorders Clinical Applications J B Handler M
Acid-Base Disorders: Clinical Applications J. B. Handler, M. D. Physician Assistant Program University of New England 1
Abbreviations n n n ABG- arterial blood gas SIADH- syndrome of inappropriate ADH- anti-diuretic hormone Cr- creatinine AVP- arginine vasopressin N- nausea HA- headache OSM- osmolality DI- diabetes insipidus ACEI- angiotensin converting enzyme inhibitor HTN- hypertension HF- heart failure n n n n Nl- normal K- potassium Mg- magnesium AMI- acute myocardial infarction S 04 - sulfate Ca- calcium Nl- normal DKA- diabetic ketoacidosis Resp- respiratory EF- ejection fraction MR- mitral regurgitation DM- diabetes mellitus RRR- regular rate and rhythm 2
Acid-Base Disorders n n n n Bicarbonate buffer system CO 2 (dissolved) +H 2 O H 2 CO 3 weak acid H 2 CO 3 H + HCO 3: weak base; levels regulated by kidneys and maintained for buffering (Na. HCO 3 is salt) CO 2 +H 2 O H 2 CO 3 H + HCO 3 (+ Na) p. H=7. 40, PCO 2= 40 mm. Hg, HCO 3= 22 -28 meq/L Respiratory center/lungs regulate removal of CO 2 Total venous CO 2 = dissolved CO 2 + (H 2 CO 3) +HCO 3 (90 -95% of total CO 2) Therefore, Total venous CO 2 HCO 3 3
Acid-Base Disorders n n n Normal metabolism produces 1 meq/L (80 meq/D) of non volatile (H ) acid together with volatile acid (CO 2) daily. Body fluid p. H is tightly maintained at 7. 40 (normal range 7. 38 -7. 42) by continuous removal of H by kidneys and CO 2 by lungs. Labs: Arterial p. H, PCO 2, HCO 3 (calculated from arterial blood or measured in venous blood (total CO 2. ) HCO 3 total venous CO 2 +H 2 O H 2 CO 3 H + HCO 3 4
Types of Acid-Base Disorders Respiratory and Metabolic n Primary respiratory disorders effect PCO 2. n Primary metabolic disorders effect HCO 3. n Primary disturbances are accompanied by compensatory changes that move the p. H back towards normal but do not fully compensate/correct the primary disorder. n Magnitude of compensation depends on how long the disturbance is present. n 5
Acid Base Disorders n n Respiratory Acidosis: p. H decreased, PCO 2 increased, HCO 3 increased (comp. ), acute and chronic forms. Respiratory Alkalosis: p. H increased, PCO 2 decreased, HCO 3 decreased (comp. ), acute and chronic forms. Metabolic acidosis: p. H decreased, HCO 3 decreased, PCO 2 decreased (comp. ). Metabolic alkalosis: p. H increased, HCO 3 increased, PCO 2 increased (comp. ). 6
Respiratory Acidosis n n n Primary defect is increased PCO 2 as a result of decreased alveolar ventilation. CO 2 +H 2 O H 2 CO 3 H + HCO 3 Conditions associated with decreased ventilation: severe COPD; asthmatic who tires; drug OD with suppression of ventilatory drive, neuromuscular diseases. Symptoms: somnolence, confusion (CO 2 narcosis), coma, resp. arrest. HCO 3 increases (over time), leading to compensation. 7
Expected Changes/Compensation Respiratory acidosis n Acute – the p. H decreases 0. 08 units for every 10 mm. Hg increase in PCO 2; HCO 3 0. 1 -1 m. Eq/liter per 10 mm Hg PCO 2 n Chronic - HCO 3 1. 1 -3. 5 m. Eq/liter per 10 mm. Hg PCO 2; p. H will move towards normal – HCO 3 generated by kidneys over days 8
Case 1 n Little Billy got into some of dad’s pain meds (hydrocodone). He suffers a significant depression of mental status and respiration. You see him in the ED 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained. It shows p. H = 7. 16, PCO 2 = 70 mm. Hg, HCO 3 = 24 meq/L 9
Case 1 What is the acid/base abnormality? 1. Uncompensated metabolic acidosis 2. Compensated respiratory acidosis 3. Uncompensated respiratory acidosis 4. Compensated metabolic alkalosis 10
Case 1 Uncompensated respiratory acidosis n There has not been time for metabolic compensation to occur. As the narcotic toxicity took hold, this child slowed his respirations significantly, PCO 2 built up in the blood, and an acidosis ensued. n If compensation had occurred the p. H would have been higher as a result of an increase in_____? HCO 3 11
Treatment of Resp. Acidosis Ventilatory support until the underlying disorder can be corrected. n Narcotic antagonists (if applicable) for OD: Naloxone (Narcan) IV-has short half life; may require repeated doses. n Benzodiezepine antagonists: Flumazenil given IV may reverse benzodiazepine (OD) induced respiratory depression. Short duration of action. Use with caution. n 12
Respiratory Alkalosis Primary defect is decreased PCO 2 as a result of increased alveolar ventilation. n CO 2 +H 2 O H 2 CO 3 H + HCO 3 n 13
Respiratory Alkalosis n n n Hyperventilation: anxiety, panic attacks, sepsis, CNS insult, cirrhosis, salicylates (overdose), progesterone, mechanical over ventilation, etc. Symptoms- lightheadedness, paresthesias, tetany. Treatment- Address the underlying cause; most cases of anxiety-hyperventilation syndrome are self-limited respiratory muscle fatigue. – When acute anxiety is a factor, re-breathing into a paper bag may be useful (short term fix only). 14
Expected Changes/Compensation Respiratory alkalosis n Acute – p. H increases. 08 units for every 10 mm. Hg decrease in PCO 2 ; HCO 3 0 -2 m. Eq/liter per 10 mm Hg PCO 2 n Chronic - HCO 3 2. 1 -5 m. Eq/liter per 10 mm Hg PCO 2 15
Metabolic Acidosis n n n Primary measured defect is decreased HCO 3 (combines with increased H ions to buffer) with resultant drop in p. H. CO 2 +H 2 O H 2 CO 3 H + HCO 3 Compensatory response is decreased PCO 2. Excess fixed acids (endogenous) in blood-most common acid-base disorder. Calculation of anion gap is important: Na- (HCO 3+CL) 6 -12 on newer chem. analyzers which yield higher Cl levels (normal range 98 -107 meq/L) than older analyzers. 16
Expected Compensation Metabolic acidosis: n PCO 2 1 -1. 5 (mm. Hg) per 1 m. Eq/liter HCO 3 17
Increase Anion Gap Acidosis n n p. H decreased, HCO 3 decreased, Cl normal. Examples: Lactic Acidosis (cardiogenic shock or arrest). Lactate prod. due to inadequate tissue perfusion or hypoxia. DKA-Hyperglycemia with metabolic acidosis; increased production of ß-hydroxybutyric & acetoacetic acids (ketoacids hyperketonemia). Toxins- Ethylene glycol, salicylates, methanol. Uremia (severe renal failure)- endogenous acids. p. H < 7. 25 common, with HCO 3 <16 meq/L Anion gap > 12 meq 18
Composition of Body Fluids (meq/L)
Normal Anion Gap Acidosis (NAGA) Hallmark is acidosis, decreased HCO 3 and hyperchloremia. n GI HCO 3 losses from pancreatic or small bowel contents. n – Example: massive (secretory) diarrhea with volume contraction (Na. CL and K loss as well); HCO 3 secretion in small/large intestine is accompanied by Cl generation/absorption (countertransport); volume contraction leads to NA and Cl retention in the kidney. 20
Renal Tubular Acidosis (NAGA) n Hyperchloremic metabolic acidosis without anion gap. Chloride levels are increased. – Distal RTA-deficiency in H secretion by distal nephron; cannot acidify urine; enhanced K secretion (hypokalemia). – Proximal RTA- Inability of proximal tubule to adequately reabsorb filtered HCO 3. – Hyporeninemic hypoaldosteronemic RTA: hyperchloremic acidosis with hyperkalemia. Impaired Na reabsorption, K + H secretion. n If suspected: nephrology consult 21
Metabolic Acidosis: Sx and Rx Decreased p. H leads to hyperventilation, PCO 2 results compensatory. n Additional symptoms reflect underlying disorder. n Treatment is specific for the underlying disorder. Example: Diabetic ketoacidosis (DKA) treated with insulin, electrolyte replacement and volume expansion (details in Endocrine module). n 22
Case 2 n n n JR has had intermittent vomiting and severe diarrhea for 4 days. He has been unable to keep fluids down and has not urinated in 8 hours. He has a cardiomyopathy with compensated HF. PE: P-90, BP-90/70 with postural changes. He appears lethargic and cool to touch with a prolonged capillary refill time. His arterial blood gas reveals: p. H=7. 30, PCO 2=28 mm. Hg, HCO 3=14 meq/L. Na-136 meq/L, K-3. 0 meq/L, Cl-110 meq/L 23
Case 2 What is the acid/base abnormality? 1. Uncompensated metabolic acidosis 2. Compensated respiratory alkalosis 3. Uncompensated respiratory acidosis 4. Compensated metabolic acidosis 24
Case 2 Compensated metabolic acidosis n The prolong history of fluid loss through diarrhea has caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool accompanied by generation/absorption of chloride. The body has compensated by “blowing off” the CO 2 with increased respirations. 25
Metabolic Alkalosis n n n Hallmark: High HCO 3 with increased p. H. Most common: Saline responsive metabolic alkalosis, commonly seen with extracellular volume contraction and hypokalemia. Severe vomiting or continuous NG suction: HCl and Na. Cl losses from stomach initiate the alkalosis and volume contraction. Cl loss (and total body stores) sustains the alkalosis because renal Na reabsorption from volume contraction is accompanied by HCO 3 reabsorption (most available anion with Cl depleted). See Case 1 from “Fluid and Electrolyte Disorders” 26
Metabolic Alkalosis n n n Activation of the RAA system to maintain volume results in hypokalemia ( Na/K/H exchange in distal tubule) and additional H losses. Hypokalemic, hypochloremic metabolic alkalosis with volume contraction. Entire sequence is rapidly corrected by administering 0. 9% saline* (isotonic) with supplemental KCL. The process will self perpetuate until adequate amounts of Na/K/Cl and H 2 O are available. 27 *AKA- normal saline
Expected Compensation Metabolic alkalosis n PCO 2 0. 5 -1. 0 (mm. Hg) per 1 m. Eq/liter HCO 3 28
Case 3 n n n A 27 y. o. male is brought to the ED by his girlfriend after being found obtunded at home. PE: P-100, BP-100/60, RR- 6 p. H-7. 26, PCO 2 -65 mm. Hg, PO 2 - 68 mm. Hg, HCO 3 -31 meq/L What is the primary disorder? Has there been any compensation? What is the correct treatment? 29
Case 4 n n n Following an alcoholic binge, a 54 y. o man presents to the ED with severe N & V x 3 days. He has had only water in the last 36 hrs. PE: P-110, BP- 90/70, 70 syst upright. ETOH on breath, liver enlarged. p. H-7. 52, PCO 2 -47 mm. Hg, HCO 3 -35 meq/L, Na-129 meq/L, K-2. 7 meq/L, Cl-84 meq/L. What is the primary disorder? Compensation? Explain the electrolyte abnormalities. What is the treatment plan for this man? 30
Case 5 n n n A 16 y. o with Type 1 DM is brought to the ED after collapsing at home. He is dehydrated, disoriented, hypotensive and his breath has a sweet odor. PE: Ill appearing male c/o abdominal pain. T- 99, P-120, BP- 90/60, RR- 24; skin turgor , mucous membranes dry; lungs- clear; heart- RRR, no murmurs/gallops; abd: soft, non-tender. Urine via catheter- small volume, Sp Gr, ++for glucose and ketones. O 2 sat- 97% IV started, fluids running. Labs/ABG: 31
Case 5 (cont. ) n n n p. H-7. 24, PCO 2 -25 mm. Hg, HCO 3 -10 meq/L Glucose- 700 mg/dl, Na-124 meq/L, K-5. 2 meq/L, Cl-98 meq/L, Cr-1. 0 mg/d. L, BUN 24 mg/d. L What is the primary disorder? Compensation? What are the sources for abnormal acid production (at least 2)? How do you explain the electrolyte abnormalities? Thoughts on management? 32
Case 6 A 24 y/o med student becomes extremely anxious prior to his board exams. He is brought to the ED with light-headedness, and muscle cramps. P-100, RR-25, BP 120/70; remaining exam unremarkable. n p. H-7. 52, PCO 2 -25 mm. Hg, HCO 3 -24 meq/L n What is the primary acid-base disturbance? Has there been any compensation? n What is the treatment for this patient? n 33
Case 7 n n n A hospitalized man (medical ward without monitoring) is discovered by the nursing staff unconscious with no pulse or respirations; a “code 99” is called. During the initial response, team members start an IV, and initiate CPR. The initial ABG reveals: p. H- 7. 01, PCO 2 - 65 mm. Hg, HCO 3 - 12 meq/L, PO 2 - 43 mm. Hg Explain these findings. Management? 34
Case 7 (cont) n n n He is intubated, ventilated and given 100% O 2. There is initial delay in getting the defibrillator. CPR is continued. An ABG obtained 3” later reveals: p. H- 7. 21, PCO 2 - 41 mm. Hg, HCO 3 - 13 meq/L, PO 2 - 280 mm. Hg. Rhythm: V Fib- now ready to defibrillate Explain these findings. Management? 35
Case 7 (continued) n n n Following defibrillation, he stabilizes hemodynamically. He is placed on a ventilator with TV of 900 cc, rate of 14; Fi. O 2 -. 40 ABG 1 hour later: p. H- 7. 50, PCO 2 - 26 mm. Hg , HCO 3 - 22 meq/L, PO 2160 mm. Hg How do you explain these findings? Management? 36
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