Metabolic Acid-Base Disorders
Types of metabolic acidosis Based on the anion gap
1. High anion gap (HAG) metabolic acidosis = net gain of acid 2. Normal anion gap (NAG) metabolic acidosis = loss of bicarbonate Anion gap calculation in practice: [Na+ + K+] - [Cl- + HCO3 - ] or [Na+] - [Cl- + HCO3 - ] (Normal = 10 + 2)
Causes of metabolic alkalosis from excess HCO3-
-Base/alkali intake -Gitelman -Bartter -AD hypothyroidism -EAST syndrome
Causes of metabolic alkalosis from fluid and cl- deficents
-Gastric losses (vomiting, NG suctioning) -Diuretics (loop or thiazides) -Cystic fibrosis -Post-hypercapnia -Cl- losing diarrhea -Cl- deficient milk formula
Causes of metabolic alkalosis from Hormonal disturbance (high BP)
-Renovascular disease (hyperreninemia) -Neoplasia: from -Adrenal adenoma/hyperplasia -Renin-secreting tumor -Liquorice -Endocrinopathies: from -GCS-responsive hypoaldosteronism -Cushing syndrome - 11 beta OH steroid- dehydrogenase deficiency -11 beta & 11 beta hydroxylase deficiency -Liddle syndrome (hyperaldosteronism-like state)
What are DDx of NAG / Hyperchloremic Metabolic Acidosis
-Type 1 RTA (distal) -Type 2 RTA (proximal) -Type 4 RTA -Voltage defect of Na channels -Diarrhea -Hyperkalemia
Compensation for metabolic acidosis
1. Increased ventilation (compensatory respiratory alkalosis) 2. Renal excretion of H+ (if renal function intact) 3. K+ exchanges with excess H+ in ECF ( H+ shifts into cells, K+ shifts out of cells) => hyperkalmia usually associated with metabolic acidosis (except renal tubular acidosis 1 and 2) CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 -
Case #1 A 21-year-old male with no prior health problems is brought to the ED after being involved in a traffic accident as a pedestrian. He looks pale and is lethargic. Physical examination shows HR 122/min, BP 90/58 mmHg and RR 32/min. Labs: Serum Na 138 mEq/L; K 5.1 mEq/L; Cl 110 mEq/L; ABG: pH 7.2; PaCO2 23 mmHg; HCO3 - 10 mEq/l.
1. What is the primary A-B disorder and why? • Metabolic acidosis 2. What is the type of metabolic acidosis in the above case? • 138 - (110 + 10) = 18 (high) => Dx: HAG metabolic acidosis 3. Is compensation appropriate? • Apply Winter's equation: PaCO2 = 1.5 × [HCO3−] + 8 +/-2 = 1.5 x 10 + 8 +/- 2 = 21-23 => appropriate compensation => simple HAG metabolic acidosis
Case 6 A 15-year-old girl is admitted to the ER after fainting at school after the lunch break. She confessed to her best friend that she is on a diet and used laxatives and furosemide. She likes to eat, but her friend suspects that she is causing herself to vomit after most meals. On physical examination, she is lethargic, her HR is 110/min and her BP is 106/60 mmHg. Labs: pH 7.50; PaCO2 52 mmHg; HCO3 - 32 mEq/L. After being administered a bolus of 1 L of normal saline, her ABG is as follows: pH 7.42; PaCO2 42 mmHg; HCO3 - 26 mEq/L. 1. What is the primary A-B disturbance and why? 2. What happened after administration of normal saline?
1. What is the primary A-B disturbance and why? • Metabolic alkalosis due to ECF volume contraction (vomiting, laxatives and loop diuretics) 2. What happened after administration of normal saline? • The metabolic alkalosis improved
case 4 Which of the following is the most likely cause of these findings? 1. Deficiency of ornithine transcarbamylase 2. Inability of distal nephron to secrete H+ 3. Inability of Henle's loop to reabsorb Cl4. Inability of the proximal tubule to reabsorb HCO3 - 5. Impaired transport of aquaporin-2
2. Inability of distal nephron to secrete H+
Causes of Metabolic acidosis
Accumulation of acids (lactic acid or ketones) • Loss of bicarbonate through diarrhea or renal dysfunction • Failure of kidneys to excrete H+ CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 - [H+] = 24 ×(PaCO2 / [HCO3 - ])
from case 3 Altered function of which of the following structures is the most likely cause of this patient's abnormal results? A. Proximal convoluted tubule B. Descending loop of Henle C. Ascending loop of Henle D. Distal convoluted tubule E. Collecting duct
A. Proximal convoluted tubule
Case 8 A 1-week-old male neonate presents with irritability and polyuria. His mother needs to change his diapers about 20 times per day. • Born at 36 weeks' gestation after a pregnancy complicated by polyhydramnios. He is at the 5th percentile for length and 10th percentile for weight. • Physical examination: triangular face with a prominent forehead and large, protruding ears; dry mucosae and slow skin turgor. • Laboratory studies show serum: Na+ 129 mEq/L K+ 2.8 mEq/L Cl- 90 mEq/L Ca2+ 8.0 mg/dL HCO3 - 32 mEq/L pH 7.51 The effects of this patient's condition are most similar to the long-term administration of which of the following drugs? A. Triamterene B. Bumetanide C. Hydrochlorothiazide D. Mannitol E. Tolvaptan F. Acetazolamide G. Fludrocortisone
B. Bumetanide
Case 10 • A 17-year-old boy presents with a 7- month history of fatigue, recurrent leg cramps and weakness, and increased urinary frequency. His vitals are within normal limits. • Physical examination shows dry mucous membranes. • Laboratory studies show: Serum~ Na+ 130 mEq/L K+ 2.8 mEq/L Cl- 92 mEq/L Mg2+ 1.1 mg/dL Ca2+ 10.6 mg/dL Albumin 5.2 g/dL pH 7.55 HCO3 - 45 mEq/L Urine~ Ca2+ 70 mg/24 h (N: 100- 200) Cl- 375 mEq/24h (N: 110 -250) Impaired function of which of the following structures is the most likely cause of this patient's condition? A. Collecting duct B. Ascending loop of Henle C. Distal convoluted tubule D. Descending loop of Henle E. Proximal convoluted tubule
C. Distal convoluted tubule
Metabolic alkalosis mnemonic
C.L.E.V.E.R. P.D. • Contraction (ECF) • Licorice • Endocrine • Vomiting • Excess Alkali • Reno-vascular • Post-hypercapnia • Diuretics
Metabolic acidosis
Characterized by bicarbonate deficit - Serum [HCO3 - ] < 22mEq/L • Occurs when pH < 7.35
What is the mechanism of hyperchloremic metabolic acidosis in proximal RTA
Defect in bicarbonate reabsorption in PCT => bicarbonate wasting in the urine • Isolated • In association with other defects in PCT function: impaired reabsorption of phosphate, glucose, uric acid, and/or amino acids (Fanconi syndrome) => NAG metabolic acidosis, hypokalemia hypophosphatemia, renal glucosuria (glucosuria with a normal serum glucose concentration), hypouricemia, and/or aminoaciduria. *These features are not found in distal RTA (renal tubular acidosis)
from case 2 If the patient ingested a nephrotoxic substance, which is the most likely to have caused this presentation? A. Aspirin B. Acetaminophen C. Opiates D. Methanol E. Ethylene glycol F. Ibuprofen
E. Ethylene glycol
Case 7 A 40-year-old man presents with confusion and lethargy, unable to provide any history. His temperature is 36.7oC, BP is 80/46 mmHg, pulse is 116/min, respirations are 12/min. ABG: pH 7.56, PaCO2 50 mmHg, PaO2 80 mmHg, bicarbonate 30 mEq/L. Which of the tests below is the most useful for diagnosing the possible causes of this patient's acid-base abnormality? A. Serum ketones B. Serum Na+ C. Urine glucose D. Serum osmolality E. Urine Cl-
E. Urine Cl-
Pseudo-hypoaldosteronism type 2 (Gordon syndrome)
Gain of function mutation in the Na-Cl symporter in DCT => Excess Na and H2O reabsorption => Raised BP (hypertension) => Inhibits RAAS => Decreased aldosterone => Decreased ENaC function and Na reabsorption =>Decreased ROMK function and K secretion Decreased H excretion => Hyperkalemia and metabolic acidosis Rx: Thiazides (block the Na-Cl symporter in DCT)
Case 5 A 40-year-old man with diabetic nephropathy comes to the physician because of a 4- week history of generalized weakness. His only medication is metformin. • Serum studies show: Na+ 136 mEq/L Cl- 111 mEq/L K+ 5.7 mEq/L Glucose 135 mg/dL Creatinine 1.6 mg/dL Serum pH 7.29 HCO3 - 19 mEq/L Urine pH 5.1 Which of the following is the most likely underlying cause of this patient's abnormal findings? A. Transport defect of the PCT B. Transport defect of the DCT C. Glucocorticoid excess D. Hyperthyroidism E. Hypothyroidism F. Hypoaldosteronism G. Hyperaldosteronism
F. Hypoaldosteronism
Causes of NAG metabolic acidosis
H.A.R.D.U.P.S. • Hyperalimentation • Acetazolamide • Renal tubular acidosis • Diarrhea • Uretero-pelvic shunt • Post-hypocapnia • Spironolactone
Differentiation between exogenous and endogenous anions
High osmolar gap means AG is from an exogenous anion Step 1 - Calculate serum osmolarity/osmolality based on concentration of osmotically active solutes (Na, BUN, glucose) Step 2 - Compare with osmolarity/osmolality measured by the laboratory = osmolar/osmolal gap
Type 1 RTA (distal) DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: - Impaired DCT/CD H+ secretion (acidification) Plasma HCO3: - Variable (may be <10 mEq/L) Urine pH: -Always > 5.3 Plasma K: - Low UAG: -> 20 mEq/L (positive)
Type 4 RTA DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: -Aldosterone deficiency / resistance Plasma HCO3: -Usually > 17 mEq/L Urine pH: -Variable Plasma K: -High UAG: -> 20 mEq/L (positive)
Causes of type 4 Renal tubular acidosis (RTA) Interference with aldosterone at any stage:
Hypoaldosteronism~ • Adrenal insufficiency (synthesis) • Diabetic nephropathy (hyporeninemic hypoaldosteronism). Drugs: • NSAID use • Renin inhibitors: Aliskiren • ACE-inhibitors and ARBs Aldosterone resistance~ • Pseudohypoaldosteronism Drugs: • Aldosterone receptor blockers: spironolactone, eplerenone • ENaC blockers: triamterene, amiloride, trimethoprim
Types of metabolic alkalosis based on volume status
If ECF volume low -> SALINE-RESPONSIVE metabolic alkalosis • History of fluid loss • Characterized by Cl- deficit • Responds promptly to normal saline = 0.9% NaCl If ECF volume normal/high -> SALINE RESISTANT/NON- RESPONSIVE metabolic alkalosis -> 2 types based on BP: • Normal BP: characteristic excess bicarbonate, hypokalemia • High BP: associated with hormonal disturbances / RAAS activation
Hyperkalemia DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: -Excess K Plasma HCO3: -Variable Urine pH: -< 5.3 Plasma K: -High UAG: -Variable
Diarrhea DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: -Gastrointestinal loss of HCO3 Plasma HCO3: -Variable Urine pH: -< 5.3 Plasma K: -Low UAG: -Between -20 and -50 mEq/L (negative)
Voltage defect of Na channels DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: -Reduced Na reabsorption unrelated to aldosterone Plasma HCO3: -Usually > 17 mEq/L Urine pH: -Variable Plasma K: -High UAG: -> 20 mEq/L (positive)
Type 2 RTA (proximal) DDx of NAG / Hyperchloremic Metabolic Acidosis
Primary problem: -Reduced reabsorption of HCO3 in PCT Plasma HCO3: -Usually 14-20 mEq/L Urine pH: -Usually < 5.3 Plasma K: -Low UAG: -Unreliable
What is the significance of urine anion gap (UAG)?
Principle: H+ buffered in the kidney by NH3 to form NH4 + => if more H+ secreted, have increased NH4 + excretion => combines with Cl- to form NH4Cl => in the normal kidney the more H+ excreted as NH4 +, the more Cl- is excreted as NH4Cl => UAG decreases. UAG= [Na+] + [K+] - [Cl-] • If kidney function is normal and acidosis is caused by bicarbonate loss via GI (diarrhea) => normal H+ excretion in urine => increased NH4 + excretion => increased binding of Cl- => high Cl- in urine => negative UAG (between -20 to -50 mEq/L) RTA 1 and 4 there is a defect in H+ excretion in urine => low NH4 + => low Cl- binding as NH4Cl => low Cl- in urine => positive UAG (> 20 mEq/L)
What are the possible etiologies of distal RTA?
Proton pump failure: o Sjogren's syndrome o Inherited genetic defects (infants) of the H+/K+ ATP-ase antiporter o Medullary sponge kidney o Reflux nephropathy. • Increased permeability of luminal membrane: o Amphotericin B
The concept of Anion Gap
Serum cations = "measured" (Na+) and "unmeasured" (K+, Mg+, Ca+) Serum anions = "measured" (HCO3 - and Cl- ) and "unmeasured" (SO4 - , PO4 - , anionic proteins, organic acids) Serum is electrically neutral! => Serum cations = serum anions => Measured Anions + Unmeasured Anion = Measured Cations + Unmeasured Cations Na+ + unmeasured cations = HCO3 - + Cl- + unmeasured anions => Na+ - (HCO3 - + Cl- ) = unmeasured ANIONS - unmeasured CATIONS = ANION GAP
from case 3 What further tests are necessary at this point, and why?
Serum glucose • If normal => renal glucosuria caused by a defect in the reabsorption of glucose in proximal renal tubuli (PCT) • => should also check serum phosphate, calcium, magnesium • Tests that reflect renal damage/dysfunction: serum albumin, urea, creatinine Urinalysis: • Urine pH (via pH electrode, NOT dipstick) = relative amount of H+ vs buffer (NH4, PO4) • If < 5.3 => acidification is normal • If 5.3 or higher => impaired acidification • Urine electrolytes: Na, K, Cl, phosphate • Aminoacids • Urine albumin/creatinine ratio
Case #3 A 9-year-old boy presents with a 6-month history of progressive fatigue, difficulty concentrating at school and increased urination. He is at the 15th percentile for height and weight. Physical examination shows dry mucous membranes, blue discoloration of the gums, and pale conjunctivae. Serum biochemistry results: • Na+ 134 mEq/L (↓) • K+ 3.2 mEq/L (↓) • Cl- 111 mEq/L (↑) • Bicarbonate 15 mEq/L (↓) Urine dipstick: pH 5.3; glucose 2+; protein 1+; ketones negative; RBC negative What further tests are necessary, and why?
The patient has a hyperchloremia and low bicarbonate, which indicate metabolic acidosis => need to perform a blood acid-base gas analysis (ABG/VBG) to differentiate between a primary hyperchloremic metabolic acidosis and a metabolic acidosis supposed to compensate for respiratory alkalosis. • In either case, PaCO2 would be < 35 mmHg. Most important parameter is blood pH: • If pH high (> 7.45) => primary disorder = respiratory alkalosis with compensatory metabolic acidosis • If pH low (< 7.35) => primary disorder = metabolic acidosis => must calculate the anion gap (AG)
from case 4 Patient's UAG
UAG = Na+ + K+ - Cl- = 35 + 40 -18 = 57 mEq/L = "POSITIVE" (> 20 mEq/L)
There are 2 ways of "losing" HCO3 -
a. By buffering protons (H+), when ACID is ADDED to the blood => high AG (HAG) metabolic acidosis • Think shock, DKA, ethylene glycol poisoning b. By HCO3 - LOSS due to GI or renal disturbances, such as diarrhea, renal tubular diseases etc. => normal (non)-AG (NAG) metabolic acidosis • Think diarrhea, use of loop diuretics, renal tubular acidosis Either of these 2 processes may cause metabolic acidosis, but they may also co-exist => MIXED HAG and NAG metabolic acidosis • Thus, AG not only helps us distinguish HAG versus NAG metabolic acidosis, but also helps us diagnose a mixed HAG + NAG metabolic acidosis. • AG also helps us diagnose mixed metabolic acidosis + metabolic alkalosis.
Causes of proximal RTA in children
o Inherited mutations of NHE3, NBCe1, Na+/K+ ATPase (mainly isolated) o Hereditary metabolic disorders: cystinosis, Wilson disease, tyrosinemia, Von Gierke disease (Fanconi) o Lead poisoning (as in this case - need CBC and blood smear) o Ifosfamide (alkylating agent used in cancer).
Causes of proximal RTA in adults
o Light chain-induced toxicity in monoclonal gammopathies (multiple myeloma) o Carbonic anhydrase inhibitors (acetazolamide or topiramate).
Liddle syndrome
• AD • Increased function mutation of ENaC in collecting duct *Rx: Amiloride (inhibits ENaC)
Gitelman Syndrome
• AR • Defect in Na, Cl and Mg reabsorption in DCT • Similar to Bartter but delayed, less severe and with hypomagnesemia • Similar effect: Thiazide use *Rx: Supportive
Bartter Syndrome
• AR • Loss of function mutation of Na/K/2Cl cotransporter in the thick ascending loop of Henle and inner ear; loss of ROMK function • Similar to loop diuretics -Renal outer medullary potassium channel (ROMK) -Sensorineural hearing loss (SNHL) *Rx: Indomethacin
What is the most important Dx test of metabolic alkalosis
• Classified according to urinary chloride = most important Dx test • Chloride responsive: Urine Cl- < 20 mEq/L • Chloride resistant: Urine Cl- > 20 mEq/L
NH4 + synthesis and secretion in PCT
• Glutamine = primary metabolic substrate for ammoniagenesis in PCT -> uptake = transport X both apical and basolateral membranes. • Complete metabolism of ONE glutamine => • TWO NH4 + • Secretion X apical membrane via NHE3-mediated Na+/NH4 + exchange • Less via a parallel H+ and NH4 + transport. • TWO HCO3 - • Transported X basolateral membrane via NBCe-1A. • All enzymes upregulated by acidosis!
from case 4 What are the main abnormalities in this case?
• High urine pH despite hyperchloremic (NAG) metabolic acidosis • Hypokalemia • Positive urine anion gap UAG= [Na+] + [K+] - [Cl-]
How does the high AG come about in HAG metabolic acidosis?
• If an endogenous acid (e.g., ketones in DKA) or exogenous acid (e.g., acetylsalicylic acid/aspirin) is added to the blood (AH+) => increase in the unmeasured anions A- (non-bicarbonate, non-Cl anions ) • We calculate the increase in unmeasured A- by looking at the AG: AG = unmeasured anions (A- ) - unmeasured cations = measured cations - measured anions = Na+ - (HCO3 - + Cl- ) • An added acid will cause an increase in unmeasured A- , while cations are unchanged => increase in AG will indirectly reflect the amount of added acid
from case 3 Why does the patient have hypokalemia?
• In proximal RTA bicarbonate is lost as NaHCO3 => osmotic diuresis => hypokalemia • => Steady state: low serum [HCO3 - ], hypokalemia and acidic urine
Causes of HAG metabolic acidosis
• M - Methanol => formic acid • U - Uremia - AKI, CKD with GFR <15-30 ml/min => phosphates, sulphates • D - DKA, starvation and alcoholic ketoacidosis => acetoacetate and β-hydroxybutyrate • P - Propylene glycol (additive in IV benzodiazepines) • I - Ingestions: • Ilicit drugs : cocaine / MDMA or ecstasy • Isopropyl alcohol • Iron • INH • L - Lactic acidosis => lactic acid • E - Ethylene Glycol (antifreeze) => oxalic, glycolic and glycoxylic acids • S - Salicylates
What is the mechanism of type 4 RTA?
• Main mechanism = hypoaldosteronism => impaired Na+ reabsorption => lower electronegativity across the tubular lumen => K+ secretion in principal cells and H+ secretion in a-intercalated cells => acidosis and hyperkalemia • Hyperkalemia inhibits NH4 + production in PCT because it causes intracellular alkalosis (shift of H+ outside of cells) => decrease in urine NH4 + => less buffer for a lower H+ load => low urine pH. • Decrease in renal NH4 + excretion => increase in paracellular Cl reabsorption because reduced NH4 + excretion results in reduced binding of Cl- => reduced Cl- excretion in urine => positive UAG
NH4 + reabsorption in thick ascending limb of Henle
• Primary mechanism = substitution of NH4 + for K+ -> transport by the loop diuretic sensitive, apical NKCC2 transporter (pink shade). • Cytoplasmic NH4 + dissociates into NH3 and H+ -> • NH3 transported X basolateral membrane • H+ combines with HCO3 - => H2CO3 (HCO3 - shuttling mechanism, orange shade)
Metabolic Alkalosis is characterized by
• Primary ↑ in HCO3 concentration >28 mEq/L • Compensatory ↑ in PaCO2
What are the main abnormalities that cause impaired H excretion in distal RTA?
• Proton pump defect: • Decreased activity of H+ ATP-ase on apical surface of a-intercalated cells => impaired secretion of H+ => inhibits PCT Na reabsorption => Na wasting => stimulates RAAS => hypokalemia • Decreased activity of the H+/K+ ATP-ase antiporter on apical surface of a-intercalated cells => inhibits secretion of H+ and reabsorption of K+ from the lumen of DCT => hyperchloremic metabolic acidosis + hypokalemia => urine that cannot be acidified to a pH < 5.3. • Increased permeability of the DCT luminal membrane to H+, K+, Mg2+ and bicarbonate: • Allows back-diffusion of H+ from tubular lumen into cells and leak of K+ from cells into lumen => decreased excretion of H+ and loss of K+ => acidosis and hypokalemia.
Why is urine pH < 5.3 - 5.5 in proximal RTA?
• Reduced capacity to reclaim filtered ("old") HCO3 - in PCT => HCO3 - wasting when serum [HCO3 - ] is raised above the diminished resorptive threshold => serum [HCO3 - ] = 12 - 20 mEq/L. • When the serum [HCO3 - ] is low, most of the filtered HCO3 - can be reabsorbed and distal acidification then proceeds normally => urine pH can be reduced to 5.3 or less. • Distal nephron segments have HCO3 - reabsorptive capacity but cannot replace PCT function.
metabolic alkalosis with Respiratory compensation
• The development of alkalemia is sensed by central and peripheral chemoreceptors, resulting in a reduction in the rate of ventilation and a reduction in tidal volume and thus an elevation in the PaCO2. • Difficult because hypoventilation limited by hypoxia: once respiratory center senses low PaO2, it will stimulate ventilation.
from case 2 What is the most likely diagnosis and why...
• The high osmolal gap and the envelope-shaped crystals suggest ethylene glycol poisoning. • Ethylene glycol = antifreeze or solvent -> ingested accidentally or as a suicide attempt => metabolized by alcohol dehydrogenase => generates toxic/harmful compounds: glycol aldehyde, glycolic acid, glycolate/glyoxylate, oxalic acid. • Causes acute kidney injury/AKI (due to acute tubular necrosis - ATN). • Oxalic acid precipitates with calcium in the urine => envelope-shaped Ca oxalate crystals. • Rx: inhibitor of alcohol dehydrogenase = fomepizole (4-methyl pyrazole) - most potent inhibitor and drug of choice; alternatively, ethanol.
NH4 + in the collecting duct intercalated cell
• Uptake of NH3 across the basolateral and apical membranes via transporters or diffusion => secretion in lumen, where it titrates (combines) with H+ => NH4 + • NH4 + combines with Cl => NH4Cl • H+ is excreted as NH4 + => corrects acidosis and maintains a low luminal NH3 concentration necessary for NH3 secretion!
Case #2 A 33-year-old man is brought to the Emergency Department after being found unconscious in a park next to an empty unlabeled plastic bottle. His respirations are deep and fast, at a rate of 36/min. The patient has an elevated blood pressure of 130/79 mmHg and a pulse rate of 98 beats/min his body temperature is 35.4℃, at the time of the admission. He showed signs of acute illness and presented with lethargic consciousness and restlessness. No other specific findings were found. The venous blood gas analysis results: pH 6.90, PaCO2 34 mmHg, PaO2 25 mmHg, bicarbonate 6.7 mEq/L, base excess −26.1 mEq/L. The AG is 19.7 mmol/L and the osmolal gap is 91.34 mOsm/kg H20. Envelope-shaped crystals are found in the urine sediment. After 36 h from admission, the patient develops seizures and oliguria, and is found to have the ionized Ca concentration of 8.4 mg/dL. He is stabilized and is admitted for monitoring What is the most likely acid-base disturbance based on the laboratory test results?
• VBG: pH 6.90, PaCO2 34 mmHg, PaO2 25 mmHg, bicarbonate 6.7 mEq/L, base excess −26.1 mEq/L. • AG 19.7 mmol/L > 12 • Osmolal gap 91.34 mOsm/kg H2O > 20
case 5 A 20-year-old college student is admitted to the ED for a 24-hour history of watery diarrhea. He has had 4 stools over the past 6 hours and now he feels dizzy. His vitals are normal, but his mucosae are noted to be dry, and he has slow turgor. Labs: Na 132, K 3.6, Cl 101, ABG: pH 7.3; PaCO2 37 mmHg, HCO3 - 19 mEq/L. Urine pH was <5.3. • What is the most likely A-B disturbance? • Is compensation appropriate?
• What is the most likely A-B disturbance? • AG = [Na+] - ([Cl-] + [HCO3-]) = 132 - (101+19) = 12 = NAG metabolic acidosis • Is compensation appropriate? • PaCO2 = 1.5 × [HCO3−] + 8 +/-2 = 1.5 x 19 + 8 +/- 2 = 36.5 - 38.5 => appropriate compensation
from case 3
• pH = 7.28 (< 7.35) - acidemia • Bicarbonate = 15 mEq/L (< 22 mEq/L) - deficit • PaCO2 = 30 mmHg - hypocarbia causing compensatory respiratory alkalosis • AG = Na+ - (HCO3 - + Cl- ) = 134 - (15 + 111) = 8 mEq/L Dx: NAG (hyperchloremic) metabolic acidosis partially compensated by respiratory alkalosis
