Blood gases.pdf

Nephrology L6: Blood gases interpretation  Nephrology Blood gases 1. History taking and physical examination. 2. Assess accuracy of data (validity). 3. Identify the primary disturbance. a. Check arterial pH → acidosis or alkalosis b. HCO3-...

Nephrology L6: Blood gases interpretation  Nephrology Blood gases 1. History taking and physical examination. 2. Assess accuracy of data (validity). 3. Identify the primary disturbance. a. Check arterial pH → acidosis or alkalosis b. HCO3- & pCO2 analysis → primary disorder. 4. Compensatory responses. 5. Calculate AG. 6. Corrected AG 7. Osmolar gap 8. Formulate acid-base diagnosis. 1- History taking and physical examination. ❖ Metabolic alkalosis ❖ Metabolic acidosis ❖ Respiratory alkalosis ❖ Respiratory acidosis 2- Assess accuracy of data (validity). ❖ = 24 (PaCO2)/ [HCO3-] ❖ = 6.1 + log (HCO3 / 0.03 PaCO2) ❖ = 7.634 + log (HCO3 / PaCO2)  40 (35 – 45)  7.40 (7.35 – 7.45)  40 (35 – 45)  24 (22 – 26) pg. 1  Nephrology 3- Identify the primary disturbance 1.Arterial pH < 7.4 > 7.4 2.Look at PCO2, HCO3 pg. 2  Nephrology 4- Compensatory responses.  PCO2    HCO3 Δ PCO2 = 1.2 Δ HCO3  HCO3    PCO2 Acute: Δ HCO3 = 0.1 Δ PCO2 Chronic: Δ HCO3 = 0.4 Δ PCO2  PCO2    HCO3 Δ PCO2 = 0.6 Δ HCO3  HCO3    PCO2 Acute: Δ HCO3 = 0.2 Δ PCO2 Chronic: Δ HCO3 = 0.4 Δ PCO2 ❖ Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2) ❖ Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5) ❖ 2ry compensatory response is appropriate in direction and magnitude to the 1ry effect ❖ If the actual pCO2 or [HCO3-] is different from the predicted values  You must suspect a 2nd acid-base disorder.  The [HCO3] will  by 1 mmol/I for every 10 mmHg  in pCO2 above 40 mmHg.  Expected [HCO3] = 24 + { (Actual pCO2 - 40) / 10 }  The [HCO3] will  by 4 mmol/I for every 10 mmHg  in pCO2 above 40mmHg.  Expected [HCO3] = 24 + 4 { (Actual pCO2 - 40) / 10}  The [HCO3] will  by 2 mmol/I for every 10 mmHg  in pCO2 below 40 mmHg.  Expected [HCO3] = 24 - 2 { ( 40 - Actual pCO2) / 10 }  The [HCO3] will  by 5 mmol/I for every 10 mmHg  in pCO2 below 40 mmHg.  Expected [HCO3] = 24 - 5 { 40 - Actual pCO2 ) / 10 } (range: +/- 2) pg. 3  Nephrology 5- Calculate AG. (MA) ❖ Anions and Cations in Serum (Values in mEq/L) 15 140 2 4.5 24 1.5 5 5 1 104 Actually there is no gap. Anion Gap = Measured Cations - Measured Anion AG = unmeasured Anions - unmeasured cations pg. 4  Nephrology ❖ When an acid (HA) is added to serum, the H+ is buffered by HCO3− while the remaining anion (A) results in an anion gap. ❖ In simple AG-MA when HCO3− goes down by 1 mEq/l (due to buffering of one H+), the anion gap increases by 1 mEq/l due to the addition of (A). However, if (A) is excreted with Na+ in the urine leaving Cl- behind, NAG-MA ensues. ❖ In NAG-MA, the decline is HCO3− is accompanied by an equal rise in Cl-, therefore, the anion gap remains unchanged. ❖ In AG-MA, the decline in HCO3− is due to excess H+ which is accompanied by an unmeasured anion. (e.g., lactate) ❖ The gap reflects unmeasured anions, mostly the negative charge on albumin. ❖ The gap is used to differentiate metabolic acidosis caused by loss of HCO3- (normal gap) from acidosis caused by organic acids like ketoacids, lactic acid, or toxins like ethylene glycol, or methanol (high gap) pg. 5  Nephrology ❖ The mnemonic to remember AG is GOLD 1. GIT HCO3 loss MARK:  diarrhea  Glycols (ethylene and propylene glycols)  external fistulas  Oxoproline (pyroglutamic acid) 2. Renal HCO- loss:  L-lactate  proximal RIA  D-lactate  distal RTA  Methanol  Hyperkalemic RIA  Aspirin 3. Miscellaneous  Renal failure  NH4CI ingestion  ketoacidosis  Sulfer ingestion 6- Corrected AG ❖ AG corrected = AG + 2.5 (4- serum albumin) 7- Osmolal gap (in high AG) ❖ Osmolal gap (measured - calc) should be ≤ 10  Calculate Osm = 2 [Na+] + glucose/18 + BUN/2.8  High osmolar gap > 10 indicate presence of toxic substance as: (MUD PILES) methanol, ethylene glycol and Salicylate ❖ standard bicarbonate is the bicarbonate concentration under standard conditions of 40 mmHg pCO2, temperature of 37 degrees Celsius and saturated with oxygen. ❖ The actual bicarbonate is the concentration of bicarbonate in the blood. ❖ In acid-base measurements, the bicarbonate concentration is not measured but is calculated from the pH and the pCO2 using the Henderson-Hasselbach equation. ❖ The pH is the natural logarithm of the hydrogen ion concentration. ❖ The pCO2 is the partial pressure of carbon dioxide. ❖ The Henderson-Hasselbach equation is pH = pK + log [bicarbonate] / [carbon dioxide]. pg. 6  Nephrology ❖ To convert from kPas to mmHg multiply by 7.5 ❖ Difference of AB-SB can reflect the respiratory affection on serum HCO3-. ❖ AB > SB ❖ AB < SB ❖ AB = SB < Normal ❖ AB = SB > Normal F ❖ is the total of buffer negative ion of blood. ❖ HCO3. ❖ plasma proteins. ❖ Hemoglobin. ❖ HPO42- (phosphate). ❖ 45-55 mmol/L mean: 50 mmol/L ❖ decreas BB ❖ increase BB ❖ The base excess is defined as the difference between the patient’s HCO3- after correction to a pH of 7.4 by a change in the PCO2 and the normal HCO3- at pH 7.4. It can be used in the following manner to interpret changes in the HCO3- levels.  If the base excess is between – 2 and + 2 then the observed changes in bicarbonate are due to movement based on the equation above and there is No metabolic acidosis or alkalosis.  If the base excess is less than – 2, then there is a metabolic acidosis, which may be the compensatory process. Another term for this is a base deficit.  If the base excess is greater than + 2, then there is a metabolic alkalosis, which may be the compensatory process. pg. 7 Nephrology ❖ Acute kidney injury (AKI) ❖ Chronic kidney disease (CKD) stages 4-5 ❖ L-Lactic acidosis ❖ Alcoholic ketoacidosis ❖ D-Lactic acidosis ❖ Starvation ketoacidosis ❖ Diabetic ketoacidosis ❖ Methanol ❖ Salicylates ❖ Ethylene glycol ❖ 5-Oxoproline (pyroglutamic ❖ Propylene glycol acid) ❖ Isopropyl alcohol ❖ Paraldehyde pg. 8  Nephrology 1- CKD ❖ Consequence of MA in CKD  Bone resorption.  Hypotension and systemic inflammation.  increase Muscle protein catabolism.  increase progression of CKD.  Aggravate 2ry hyperparathyroidism. ❖ KIDGO guideline: in patient with CKD and MA, alkali therapy usually NaHCO3 be used to maintain serum HCO3 within normal range. ❖ Alkali therapy usually consists of NaHCO3 or sodium citrate in dose of 0.5 to 1 meqL/kg/day. ❖ Citrate is preferred than bicarbonate as not produce bloating but should avoided in patient taking aluminum containing antacid as it increases absorption of aluminum. 2- Lactic Acidosis ❖ when O2 delivery to cell is inadequate ❖ when cell process can not use O2 Anearobic metabolism of glucose → pyruvate → lactate Hypotension  O, delivery,  glycolysis,  ATP,  pyruvate production →  lactic acid production Tissue hypoxia  Respiratory alkalosis stimulation of glycolysis and lactate production, tissue hypoxia, B-adrenergic stimulation, and lactate production  Carbon monoxide binds more rapidly to Hb than O2, → less delivery to tissues & hypoxia, inhibition of electron transport system,  ATP,  anaerobic glycolysis pg. 9  Nephrology ❖  Lactate metabolism,  pyruvate dehydrogenase complex (PDC) activity, respiratory alkalosis, and hypoglycemia may precipitate lactate production ❖ Presence of microvascular disease and atherosclerosis compromising circulation, drug use such as metformin,  PDC activity ❖ Stimulation of lactate production by alkalinization due to HCO3. dialysate baths containing lactate ❖ Lymphomas, leukemias, and carcinomas (breast, lung, colon, pancreas), production of lactate by tumor cells via  anaerobic glycolysis,  cytokine production, hypoxia- inducible factor ❖  Anaerobic glycolysis ❖ Inhibits PDC activity, thereby limiting glucose metabolism to glycolysis only ❖ Increased muscle activity, compromised blood flow, and tissue hypoxia ❖ Inhibits lactate uptake by the liver,  epinephrine release causing increased production of pyruvate ❖ Promotes lactate production from glucose in the small intestine,  NADH/NAD* ratio, inhibits gluconeogenesis from lactate, inhibition of mitochondrial respiration, patients with renal, hepatic, and cardiac failure are at risk ❖ Impairs gluconeogenesis from lactate to glucose, depletes NAD+ favoring lactate accumulation ❖ Toxic products of methanol (formaldehyde, formic acid) inhibit oxidative phosphorylation & ATP synthesis ❖  NADH/NAD ratio during metabolism of ethylene glycol via alcohol dehydrogenase ❖ If plasma lactate concentration > 4 mmol/l even in absence of overt acidemia (Normal level 0.5 to 1.5 mmol/l) pg. 10  Nephrology ❖ used in sever acidemia PH < 7.1 & serum HCO3 < 6 MEq/L as it may cause hemodynamic instability. ❖ increase the PCO2. ❖ accelerate production of lactate ❖ lower ionized Ca ❖ expand ECF volume and Hypernatremia ❖ 1-2 MEq/kg as IV bolus in adequate ventilated patients ❖ repeat the dose after 30-60 MIN if PH still < 7.1. 3- D-lactate ❖ In humans, d-lactate is produced by subjects with intestinal bypass surgery for obesity or intestinal resection or patients with chronic pancreatic insufficiency. ❖ Some patients on prolonged antibiotics may develop d-lactic acidosis due to overgrowth of G+ve anaerobes such as d-lactate-producing bacteria (lactobacilli). ❖ episodes of neurologic manifestations (confusion, slurred speech, ataxia, memory loss, irritability and encephalopathy, ❖ normal l-lactate levels. ❖ Low carbohydrate or starch diet, oral vancomycin, or metronidazole. 4- Ketoacidosis ❖ Arises when glucose is not available to cell (glucose problem) due to: A- Insulin lack (diabetic KA). B- Glucose depletion (starvation KA). C- Cell dysfunction (alcoholic KA). pg. 11 Nephrology ❖ Hyperglycemia: blood glucose > 200mg/dl ❖ Metabolic acidosis ❖ Ketosis: ketones in blood or urine ❖ BOHB > 3mmol/l is consistent with DKA 1. IV fluid 2. IV insulin 3. Role of NaHCO3 ❖ Indication  If ph < 7 in whom decreased cardiac contractility and VD impair tissue perfusion.  If life threatening hyperkalemia. ❖ Dose:  100 meq of sodium bicarbonate in 400 ml sterile water with 20 meq of KCL if serum K < 5.3 mEq/L over two hours.  PH and HCO3 monitored every 2 hours and can repeat dose until PH rise over 7. ❖ cachexia ❖ degree of acidosis is mild (HCO3- is not less than 18 mEq/L) ❖ Resumption of food intake corrects ketoacidosis. ❖ recent stopping ingestion of ethanol, hypoglycemia, and contracted ECF (usually due to vomiting) ❖ ethanol itself, starvation, insulin deficiency, excess glucagon & catecholamines. ❖ fluid replacement with D5W & normal saline, thiamine & correction of electrolytes. pg. 12 Nephrology 5- Acidosis Due to Toxins Acetoacetic acid, B- ❖ Commonly seen in alcoholic intoxication, low hydroxybutyric acid mortality ❖ Blindness and mortality high, if not recognized and Formic acid treated early Glycolic acid, oxalic ❖ Acute kidney injury, ↓ cardiac contractility, acid mortality high, if not treated early ❖ Hospital-acquired lactic acidosis, minimal clinical Lactic acid manifestations Acetone ❖ No acidosis, acetone breath, low mortality ❖ Respiratory alkalosis and metabolic acidosis in Salicylic acid adults, metabolic acidosis in children the first step in the metabolism of all toxic alcohols is catalyzed by the enzyme alcohol dehydrogenase (ADH) ❖ Diarrhea ❖ external fistulas ❖ proximal RIA ❖ Hyperkalemic RIA ❖ distal RTA ❖ NH4CI ingestion ❖ Sulfer ingestion Impaired distal Decreased proximal HCO3 Aldosterone def. acidification of urine reabsorption or resistance Variable > 5.5 if HCO3 > reabsorbed > 5.5 threshold and < 5.5 if below < 5.5 May be < 10 meq/L Above 12 meq/L Above 17 meq/L Usually reduced rarely Normal or reduced worsen by alkali Elevated elevated pg. 13  Nephrology < 3% > 15-20% < 3% Response to NaHCO3 or Measurement of Response to NaHCO3 ammonium chloride plasma aldosterone 1-3 meq/kg/d 10-15 meq/kg/d 1-3 meq/kg/d Nephrocalcinosis & renal Rickets in children stones; Osteomalacia and Osteomalacia in None uncommon adults; calculi is rare. 1. Correct any underlying disorder (control diarrhea, etc). 2. Treatment with bicarbonate should be reserved for severe metabolic gap acidosis: If the pH < 7.20  Target:  PH more than 7.2  HCO3 more than 16 ❖ HCO3- deficit = deficit/L (desired serum HCO3 - measured HCO3-) X 0.5 X body weight (volume of distribution for HCO 3-) ❖ To avoid hypernatremia and hyperosmolality, 3 ampoules (50-mL ampules of 8.4% NaHCO3 (50 mEq each) are added to 1 L of 5% dextrose in water. OR add loop diuretic if not dehydrated over 2-4 hour and reassess PH,HCO3 ❖ Maximum rate of administration: 1 Meq/kg/hour ❖ Consider administration of calcium gluconate separately to prevent fall in ionized Ca2+ after alkali administration to improve cardiac function pg. 14  Nephrology ❖ A 1ry ↑ in serum [HCO3-] ❖ consequence of loss of H+ from the body or gain in HCO3- ❖ In its pure form, it manifests as alkalemia (pH > 7.40) ❖ Compensatory mechanism → alveolar hypoventilation with ↑ (PaCO2) → ↓Δ pH that would otherwise occur ❖ Δ PaCO2 = 0.5-0.7 X Δ plasma [HCO3-] ❖ That respond to chloride administration (NaCl/KCl). ❖ Common. ❖ Usually caused by:  vomiting and diuretics.  Post hypercapnia.  Cl loss in villous adenoma. ❖ 1ry hyperaldosteronism ❖ Bartter syndrome ❖ 11B-HSD2 -Genetic, licorice, chewing tobacco, ❖ Gitelman syndrome carbenoxolone ❖ Severe potassium depletion ❖ CAH -11-Hydroxylase or 17-hydroxylase deficiency ❖ Current use of thiazides and loop ❖ Current use of diuretics in hypertension diuretics ❖ Cushing syndrome ❖ Hypomagnesemia ❖ Exogenous mineralocorticoids or glucocorticoids ❖ Liddle syndrome ❖ Reno vascular hypertension ❖ Exogenous alkali administration –NaHCO3, ❖ Hypercalcemia metabolism of lactic acid or ketoacids ❖ Refeeding syndrome ❖ Milk alkali syndrome ❖ Massive blood transfusion pg. 15 Nephrology ❖ intravenous infusion of isotonic sodium chloride solution ❖ use potassium chloride to correct the hypokalemia ❖ use potassium chloride to correct the alkalosis ❖ carbonic anhydrase inhibitor or a potassium-sparing diuretic ❖ Depends on underlying cause  Primary hyperaldosteronism: aldosterone antagonist spironolactone or with other potassium-sparing diuretics  Cushing syndrome: Potassium-sparing diuretics until surgical therapy  Licorice ingestion: Discontinuation of licorice  Bartter syndrome and Gitelman syndrome: potassium supplementation, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs, or ACE inhibitors  Liddle syndrome: amiloride or triamterene but not with spironolactone. pg. 16  Nephrology Case -1 ❖ A 60-year-old man is admitted for a 2-week history of cyclic fever, weight loss of 10 lb, nausea, vomiting, and night sweats. He is not on any medications, and he has not seen a physician in years. Physical examination is normal except for a blood pressure of 100/40 mmHg and a pulse rate of 102 beats per minute. There is no lymphadenopathy. He weighs 74 kg. Pertinent laboratory results are as follows: ❖ high AG metabolic acidosis with appropriate respiratory response Based on the osmolal gap of 14, do you suspect any alcohol intoxication? ❖ Answer No. There are no clinical manifestations that are attributable to toxic alcohol ingestion with such a high AG. The osmolal gap of 14 can be attributable to causes other than alcohols. What other pertinent laboratory tests you order at this time? ❖ Serum lactate and ketones are the appropriate laboratory tests at this time. Serum lactate levels were 14 mmol/L, and ketones were positive. Thus, there are 20 (ΔAG 20; observed AG − normal AG: 30−10 = 20) excess anions in this patient. Of the 20 excess anions, lactate accounts for 14, and the remaining anions are possibly from ketoacids (due to starvation) and sulfate and phosphate from renal failure. pg. 17  Nephrology Case -2 ❖ A 34-year-old man, brought to the emergency department by his friend, complains of weakness, fatigue, poor appetite, and dizziness for 2 weeks. He has not seen any physician for 5 years. Other than daily cocaine use, he has no significant medical history. He is not on any prescription medications. Physical examination reveals orthostatic blood pressure and pulse changes. Except for anal condyloma acumunata, the remaining examination is unremarkable. Rapid HIV test is positive. ❖ Laboratory values on admission are: ❖ Question 1 What is the acid–base disorder? Hyperkalemic hyperchloremic (non-AG) metabolic acidosis with appropriate respiratory compensation ❖ Question 2 Which one of the following is the correct diagnosis? (A) Proximal RTA (type II) (B) Distal RTA (type I) (C) Incomplete RTA (type III) (D) Type IV RTA with hypoaldosteronism (E) Hyperkalemic RTA with a defect in voltage gradient ❖ The answer is D Serum and urine chemistry and orthostatic changes suggest Addison disease, which causes type IV RTA. Hypoaldosteronism due to adrenal gland destruction by viruses (HIV, CMV) and bacteria (mycobacterium tuberculosis) or fungal agents has been described. Patients with type IV RTA due to aldosterone deficiency can acidify their urine. Proximal RTA is unlikely because of hyponatremia and hyperkalemia. Note that the patients with proximal RTA can acidify their urine at this level of serum [HCO3−], as all of this HCO3 − can be reabsorbed and generate an acid urine. Patients with incomplete RTA cannot acidify their urine even after an acid load. Also, hyperkalemic distal RTA patients with a defect in voltage gradient cannot acidify their urine. Therefore, options A, B, C, and E are incorrect. pg. 18  Nephrology Case -3 ❖ A 19-year-old thin female student is brought to the emergency department by her friends for altered mental status, euphoria, and dizziness after a rave party. She has no history of drug abuse and is not on any medications. Physical examination is normal except for a blood pressure of 90/60 mmHg with pulse rate of 102 beats/min. Laboratory results on admission and 18 h later are ❖ Characterize the acid–base disorder on admission and 18 h later.  On admission, she has a high AG metabolic acidosis with appropriate respiratory compensation, and 18 h later, the acid–base disorder is hypokalemic hyperchloremic metabolic acidosis, and respiratory compensation is appropriate. ❖ Question 2 Which one of the following agents causes these types of acid–basedisorders? (A) Topiramate (B) Ifosfamide (C) Toluene (D) Cisplatin (E) Tenofovir ❖ Toluene is initially metabolized to hippurate, which causes a high AG metabolic acidosis. Subsequently, hippurate is rapidly excreted in the urine with volume expansion, and the AG disappears. The typical acid–base disorder is hyperchloremic metabolic acidosis with severe hypokalemia. Hypokalemia is related to more distal delivery of Na+ with hippurate, leaving Cl− behind. Some of the patients are unable to acidify their urine due to impaired H+ secretion. All other drugs cause proximal RTA with adequate urinary acidification once serum [HCO3−] is below18mEq/L. pg. 19  Nephrology Case -4 ❖ A 42-year-old man is admitted because of dizziness and weakness. His blood pressure is 120/80 mmHg with a pulse rate of 90 beats/min (sitting) and 100/64 mmHg with a pulse rate of 110 beats/min (standing). He is not on any medications but admits to vomiting. Admitting electrolyte and ABG values ❖ Question 1 Analyze the acid–base disturbance (use steps that are necessary).  Step 1 Check the validity of pH.  According to the Henderson equation, the [H+] is 26, which corresponds to a pH of 7.53. Therefore, the reported pH is correct.  Step 2 Identify the primary disorder.  the primary acid–base disturbance is metabolic alkalosis.  Step 3 Calculate the AG.  The AG is 13, which is normal (calculate AG in all primary acid–base disorders so that the hidden metabolic acidosis is not missed).  Step 4 Identify the cause of the primary disorder.  The cause for metabolic alkalosis is vomiting.  Step 5 Calculate the expected compensation.  The respiratory compensation is appropriate , suggesting that this acid–base disturbance is a simple metabolic alkalosis. pg. 20  Nephrology Case -5 ❖ A 50 years old man is admitted to the ICU with anterior wall myocardial infarction. Six hours later, he develops shortness of breath. Physical examination and chest X-ray are consistent with pulmonary edema. Electrolytes and ABG values: ❖ Question / Which one of the following BEST characterizes the acid-base disturbance? a) Metabolic acidosis and respiratory alkalosis b) Metabolic alkalosis and metabolic acidosis c) Respiratory acidosis and metabolic acidosis d) Respiratory alkalosis and metabolic alkalosis e) None of the above  The answer is E The acid-base disorder should be analyzed systematically. Once the labs are available, the next step is to check whether the pH is correct or not. One must use the Henderson equation to obtain the [H* and then the pH.  The Henderson equation is: pg. 21  Case -6 ❖ A 17-year-old female student is admitted for confusion and acute kidney injury. She is able to give some history that she had a fight with her boyfriend 2 days ago, and she drank some liquid that was in their garage. She has no other significant medical or illicit drug history. In the ED, her vital signs are stable. Other than altered mental status and confusion, her physical examination is normal. She weighs 60 kg. ❖ Laboratory results are as follows: ❖ Characterize the acid–base disorder?  High AG metabolic acidosis with respiratory alkalosis. ❖ What is her osmolal gap?  Osmolal gap is the difference between measured serum osmolality and calculated serum osmolality. Therefore, her osmolal gap is 16 (312–296 = 16 mOsm), which is high. ❖ What is your diagnosis of this acid–base disorder?  The presence of calcium oxalate crystals (envelope-like) in the urine sediment is the clue for her acid–base disturbance, which is ethylene glycol ingestion. One of the final products of ethylene glycol is oxalic acid, which is excreted as oxalate. ❖ What is your initial management?  Antidote for ethylene glycol is fomepizole. The initial dose is 15 mg/kg followed by 10 mg/kg every 12h for 4 doses. Continue fomepizole, if ethylene glycol levels are not below 20 mg/dL. At the same time, hydration with D5W and three ampules (150 mEq) of NaHCO 3 to run at 120 mL/h to improve volume status should be started. ❖ Is dialysis needed in this patient?  Yes, if no improvement in renal function and metabolic acidosis following adequate hydration and administration of fomepizole and NaHCO3. pg. 22