abgs and acid-base
DESCRIPTION
Deborah Cappell, MD. ABGs and Acid-Base. ABG. The ABG contains pH, PCO2, PO2 as analyzed by three electrodes at 37C The presence of air bubbles can falsely can alter PO2 and PCO2 closer to RA. Ice keeps the gases from escaping from the solution. - PowerPoint PPT PresentationTRANSCRIPT
ABGs and Acid-Base
Deborah Cappell, MD
ABG
The ABG contains pH, PCO2, PO2 as analyzed by three electrodes at 37CThe presence of air bubbles can falsely can alter PO2 and PCO2 closer to RA. Ice keeps the gases from escaping from the solution.Leukocyte larceny can cause a false decrement in PO2 due to WBC consumption of oxygen.
ABG question #1A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx c/w chronic bronchitis. His SpO2 via pulse oximeter is 95%. However, an ABG via co-oximeter reveals PCO2 54, PO2 65, SpO2 86%. According to a standard Hgb dissociation curve the SpO2 should be >90%. Which explains the discrepancy btwn his PO2 and SpO2?A. He has significant leukocytosisB. He has carboxyhemoglobinemiaC. He has respiratory alkalosisD. He has 2,3,-diphosphoglycerate deficiencyE. He is hypothermic
ABG question #1A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx c/w chronic bronchitis. His SpO2 via pulse oximeter is 95%. However, an ABG via co-oximeter reveals PCO2 54, PO2 65, SpO2 86%. According to a standard Hgb dissociation curve the SpO2 should be >90%. Which explains the discrepancy btwn his PO2 and SpO2?A. He has significant leukocytosisB. He has carboxyhemoglobinemiaC. He has respiratory alkalosisD. He has 2,3,-diphosphoglycerate deficiencyE. He is hypothermic
Explanation of ABG question 1
Pulse oxymeter does not distinguish oxygenated Hgb from carboxy or met hemoglobin.However, the co-oximeter can differentiate hgb, carboxy-hgb and met-hgb. The carboxy-hgb was 10.7% in this pt likely from smoking.Hence using only standard oximetery in the setting of smoke inhalation can give a false sense of security. An ABG by co-oximetry to r/o carboxy-hgb is necessary.
Explanation of ABG question 1Leukocyte larceny will falsely reduce PO2 and SpO2. Resp Alkalosis will shift the Hgb dissociation curve to the left and give a higher SpO2 for the same PO2.2,3 diphosphoglycerate deficiency shifts the Hgb dissociation curve to the left as well.
Only the measured SpO2 would be less than then PO2 not the calculated SpO2 less than PO2.
As the temperature decreases, pH increases.When blood flows to the cool periphery the pH increases as PCO2 and H+ falls, so SpO2 rises with cooling and the PO2 decreases.
QuestionA 23 yo male admitted to ICU with resp failure from diffuse PNA. PMH IVDU and HIV. He is Rx with IV Bactrim and prednisone for presumptive PCP. His initial PaO2 was 55.Within 24 hours he is intubated for hypoxemic resp failure. Initial post-intubation ABG on 100% was 7.45/32/82 94%. CXR diffuse infiltrates. The following day on 70% his ABG is 7.45/30/121 SpO2 of 97%. He is bronched and the BAL is positive for PCP.On day 5 he is on 40% and a weaning trial is begun.
QuestionAfter 60 min of CPAP with PS of 5 and 40% oxygen his ABG is 7.43/35/90 SPO2 77%.What is the most appropriate next step in this patient's management?
A. Repeat the ABGB. Extubate to nonrebreatherC. Administer amyl nitrate by inhalation then sodium thiosulfate IVD. Switch the patients Abx from Bactrim to pentamidine and administer IV methylene blue
QuestionAfter 60 min of CPAP with PS of 5 and 40% oxygen his ABG is 7.43/35/90 SPO2 77%.What is the most appropriate next step in this patient's management?
A. Repeat the ABGB. Extubate to nonrebreatherC. Administer amyl nitrate by inhalation then sodium thiosulfate IVD. Switch the patients Abx from Bactrim to pentamidine and administer IV methylene blue
Answer Explained
This pt has clinically improved, however his SpO2 has declined despite an adequate PaO2. A recognized complication of sulfonomides is methemoglobinemia. (Then Hgb cannot bind oxygen because of oxidation of fe.)
[Also can happen with nitrites, nitrates, phenacetin, aniline dyes, and lidocaine]
Rx methylene blue IV by reducing the Fe.
SEEK
A 33 yo female with p/w lower abdominal pain for 1 day, assoc with nausea and decreased appetite. PE VS anl, abd soft with lower abd diffuse tenderness and the patient vomited twice during the exam. Pelvic showed b/l adnexal tenderness. WBC 19K, with 90% PMN. She received Metronidazole, Cipro, Morphine and metoclopramide and was sent for CT abd/pelvis.
SEEK
2 hours later she had acute onset SOB and feeling of impending doom. She was cyanotic despite 100% Oxygen by NRB. HR 132, BP 160/100, RR 28, SpO2 85% and the ABG 7.36/35/240. Naloxone was given but cyanosis and dyspnea continued, and she became lethargic. What is the best Rx for the disorder that caused the acute decompensation?
SEEK
What is the best Rx for the disorder that caused the acute decompensation?
A. High dose corticosteroidsB. Broad spectrum AbxC. SurgeryD. Sodium nitrite and sodium thiosulfateE. Methylene Blue
SEEK
What is the best Rx for the disorder that caused the acute decompensation?
A. High dose corticosteroidsB. Broad spectrum AbxC. SurgeryD. Sodium nitrite and sodium thiosulfateE. Methylene Blue
SEEK
The pt has methemoglobinemia due to administration of metoclopramide and Rx with Methylene blue will reduce the seum ferric iron. Metoclopramide is an oxidizing agent which can convert ferrous (++) iron in hgb to the ferric form (+++). When given in excessive doses or to pt with enzyme deficiencies to convert methgb to hgb toxic levels may develop. MetHgb has a higher Oxygen affinity and reduces blood oxygen content shifting the curve to the left. Cyanosis develops at 15%, sx at 30% and Change in MS at 50%. Level >70% are usually fatal.
SEEK
Many drugs are oxidants and cause this: chloroquine, dapsone, local anesthetics (benzocaine, nitrates (nitroglycerin, nitroprusside, NO), and sulfonamides. High levels of MetHgb turn blood brown and does not turn red when exposed to air. SpO2 is inaccurate. The SpO2 not correlating with abg is a clue that co-oximetry is needed.
SEEK
Rx for MetHgb >30% with methylene blue which is a cofactor for NADP-metHb reductase and increases that enzymes capacity to reduce ferric iron. Dose is 1-2 mg/kg over >5 minutes. Higher doses may increase MetHgb levels in doses >15mg/kg and in pt with G6PD.This pt has PID and abx are useful.Sodium nitrite and sodium thiosulfate are used as antidotes to cyanide poisoning and work by increasing metHgb levels to facilitate transport of cyanide as cyanomethemoglobin from mitochondrial cytochromes to hepatocytes.
ABG
Interpreting an ABG requires first an appreciation for the alveolar gas equation.Alveolar-arterial oxygen gradient:Aa= PAO2- PaO2 FIO2(P
B-P
H20)-Pa
CO2/R -Pa
O2
Where FIO2 = 0.21 PB=760 PH2O = 47A normal Aa gradient is dependent on age, body position, and nutritional status.
(It is increased with age, obesity, fasting, supine position, heavy exercise and fasting)
ABG
An increased Aa gradient can be caused by A. HypoventilationB. HyperventilationC. Pulmonary embolusD. A and CE. B and C
ABG
An increased Aa gradient can be caused by A. HypoventilationB. HyperventilationC. Pulmonary embolusD. A and CE. B and C
Hypoventilation will increase PCO2 and decrease PaO2 proportionally. Hyperventilation will decrease PCO2 and increase PaO2 proportionally.VQ mismatch will increase the Alveolar-arterial gradient.
C. Pulmonary embolus
Question Acid-Base
In a hemodynamically stable pt on RA with nl BP and CXR which of the following arterial and venous ABG come from the same pt?(pH/PCO2/PHCO3 arterial;venous)A. 7.4/40/24 ; 7.4/40/24B. 7.25/23/10 ; 7.29/20/9C. 7.3/55/28 ; 7.2/65/33D. 7.39/44/23 ; 7.35/50/24 E. 7.4/24/24 ; 7.37/30/26
Question Acid-Base
In a hemodynamically stable pt on RA with nl BP and CXR which of the following arterial and venous ABG come from the same pt?(pH/PCO2/PHCO3 arterial;venous)A. 7.4/40/24 ; 7.4/40/24B. 7.25/23/10 ; 7.29/20/9C. 7.3/55/28 ; 7.2/65/33D. 7.39/44/23 ; 7.35/50/24 E. 7.4/24/24 ; 7.37/30/26
Answer, explained
7.39/44/23 and 7.35/50/24The mean difference btwn arterial and venous pH was 0.036, PCO
2 6, HCO3 1.5
Venous pH should be lower and PCO2 higher than arterial. Bicarb is slightly higher in venous than arterial blood.If only a trend is what is being followed, eg in DKA, venous blood gases are likely adequate.
Answer, explained
(Option A has same values for venous and arterial, option B the direction of change art to venous is backward, option C the magnitude of change is too great, option E makes no physiologic sense.)
SEEK
A pregnant asthmatic is in the ER. She is 22 yo with asthma since early child with rare medication use until her pregnancy. She is 34 weeks pregnant and this is her 1st pregnancy. In her 2nd trimester she was seen in her OB’s office and was Rx with IV corticosteroids and then started on inhaled corticosteroids and a long-acting beta agonist. She did well until the last 2 days when DOE progressed to dyspnea at rest and over the prior evening used her rescue beta agonist many times.
SEEK
On PE she is in moderate distress, using accessory muscles to breath while sitting upright. She can speak only 2-3 words at a time and there is insp and exp wheezing with decreased air movement. ABG on RA is 7.36/38/78. In this patient the most likely acute acid-base disturbance is:
A. Metabolic AlkalosisB. Metabolic AcidosisC. Respiratory AcidosisD. Respiratoy AlkalosisE. No acute acid-base disturbance
SEEK
On PE she is in moderate distress, using accessory muscles to breath while sitting upright. She can speak only 2-3 words at a time and there is insp and exp wheezing with decreased air movement. ABG on RA is 7.36/38/78. In this patient the most likely acute acid-base disturbance is:
A. Metabolic AlkalosisB. Metabolic AcidosisC. Respiratory AcidosisD. Respiratory AlkalosisE. No acute acid-base disturbance
SEEK explained
This ABG is signaling ventilatory failure from acute asthma. There are changes in pregnancy which must be taken into account. During pg oxygen consumption rises to 40-100% above baseline. This is due to fetal/placental needs and increased CO and work of breathing. Increased oxygen consumption is associated with a 30-50% increase in CO2 production by the 3rd trimester requiring an increase in minute ventilation that starts in the 1st trimester and peaks at 20-40% above baseline at term.
SEEK explained
Alveolar ventilation is increased above the level needed to eliminate the increased CO2 production and hence PCO2 falls to 27-32 mm Hg in most of pregnancy. The augmented ventilation is attributed to respiratory stimulation from increased progesterone and results in a 30-35% increased in TV while RR remains the same/slightly increased. Renal compensation results in a pH of 7.4-7.45 and bicarb 18-21.
SEEK explained
The patient has an increased Aa gradient likely related to VQ mismatch from asthma. The pregnancy with the acute respiratory distress make the sequence of chronic resp alkalosis from pregnancy, with renal compensation by chronic metabolic acidosis, now complicated by acute respiratory acidosis. This example underscores the clinical context importance in interpreting abg.
How to approach an Acid-Base
Disorder
Primary Problem
pH Compensation
Met Acidosis
Decreased bicarb
Decreased Decreased PaCO2
Met Alkalosis
Increased bicarb
Increased Increased PaCo2
Resp Acidosis
Increased PaCO2
Decreased Increased Bicarb
Resp Alkalosis
Decreased PaCO2
Increased Decreased Bicarb
Acid Base1.Determine if acidemia (pH<7.36) or alkalemia is present (pH>7.44). In mixed disorders the pH will be normal but the bicarb/pCO2/AG will be abnl.2. Is the primary disturbance met or resp? Does the change in PCO2 account for the direction of pH change?3. Is there appropriate compensation for the primary disturbance? (see table ahead)4. Is the AG elevated? If so is there a Δgap? If so is there an additional non-gap acidosis or a metabolic alkalosis?
Appropriate Compensation
Met acidosis:PCO2 = 1.5XHCO3 +8 ±2
Met AlkalosisPCO2 = 0.7XHCO3 +21 ±1.5(If bicarb >40 PCO2=0.75xHCO3)+19 ±7.5)
Resp AcidosisAcute HCO3 = [(PCO2-40)/10] +24Chronic HCO3 = [(PCO2-40)/3]+24
Resp Alkalosis Acute HCO3 = [(40-PCO2)/5]+24Chronic HCO3=[(40-PCO2)/2]+24
SEEKA 60 yo female is admitted with 2 day of cough
productive of purulent sputum. She has a history of severe COPD on home 2L Oxygen NC. On admission the HR is 120, BP 140/95, RR 28. Labs reveal Na 135, K 3.5, Cl 92, Bicarb 33. ABG on RA is 7.2/80/45. What is the acid-base disorder?
A. Inconsistent and uninterpretable dataB. Acute respiratory acidosisC. Chronic respiratory acidosisD. Acute on chronic respiratory acidosisE. Acute respiratory acidosis with anion gap
metabolic acidosis
SEEKA 60 yo female is admitted with 2 day of cought
productive of purulent sputum. She has a history of severe COPD on home 2L Oxygen NC. On admission the HR is 120, BP 140/95, RR 28. Labs reveal Na 135, K 3.5, Cl 92, Bicarb 33. ABG on RA is 7.2/80/45. What is the acid-base disorder?
A. Inconsistent and uninterpretable dataB. Acute respiratory acidosisC. Chronic respiratory acidosisD. Acute on chronic respiratory acidosisE. Acute respiratory acidosis with anion gap
metabolic acidosis
SEEK
The first step is to check the internal consistency with the Henderson-Hasselback equation. The [H+] = 24xPaCO2/[HCO3] or each change in pH of 0.01 represents a 1meq decreased in [H+] so that at a pH of 7.2 the [H+] is around 62. 62does not=24X80/33=58.
SEEKRespiratory acidosis is when pH is less the 7.4 and CO2 is increased.
In acute resp acidosis the Ph declines 0.08 for each 10 rise in CO2. So if the baseline CO2 was 40, the CO2 of 80 should decrease pH by 0.32 to 7.08.In chronic resp acidosis the pH decline 0.03 for each 10 increase in CO2. A patient with chronic resp acidosis with CO2 of 80 would have a pH of 7.28. Rather a combination of acute respiratory acidosis superimposed on chronic resp acidosis with baseline CO2 of 60 is more consistent with these values.
SEEK
Finally any acid base problem should include anion gap calculation. The ag in the case is 10 and normal is 12+/- 4 so this pt does not have an AG met acidosis.
Respiratory Acidosis
Ineffective alveolar respiration or increased CO2 productionEtiologies include: airway obstruction, resp center depression, neuromuscular d/o, pulm d/o, high carb diet
Respiratory Alkalosis
HyperventilationEtiologies:Hypoxemic drive (eg altitude, shunt), acute/chronic pulm dz, vent over-breathing, stimulation of resp center (eg pain, psychogenic, pregnancy)
Metabolic Alkalosis
Etiologies:Cl depletion (hypovolemic)
Ucl <20Saline responsive
Cl expanded (Hypervolemic)Ucl >20 Saline resistant
Etiologies of metabolic alkalosis
Hypovolemic/Cl depletedGI loss: vomit, gastric suction, Cl rich diarrhea, villous adenomaRenal loss of HDiureticPost-hypercapniaHigh dose carbenicillin
Etiologies of metabolic alkalosis
Hypervolemic/Cl expandedRenal H loss: primary hyperaldo, primary hypercortisolism, adrenocorticotropic hormone xs.Pharm xs steroidsRenal A. stenosis with RV HTNRenin secreting tumorHypokalemiaBicarb overdose
Pharm Milk-alkali syndromeMassive blood transfusion
Metabolic Acidosis
An increase in acid accumulation or decreased extracellular bicarb.Compensate with increased ventilation and decreased PaCo2 and increased renal H excretion.During prolonged acidosis the last two digits of pH =PaCO2 as long as pH>7.1 down to PaCO2 of 10.PaCo2 = 1.5xHCO3 +8 ± 2Or ;Δ PaCO2 = 1.2 X Δ bicarb
Δ
Etiologies of Metabolic Acidosis
Increase in endogenous acid production (ketoacidosis), exogenous acid input (poisons), xs bicarb loss (diarrhea) or decreased renal excretion of endogenous acid (chronic renal failure).Divided into anion gap and non-anion gap acidosis.
Δ
Etiologies of Metabolic Acidosis
AG = Na -(Cl+HCO3) = 10 ±4AG increases with decreased unmeasured cations or increased unmeasured anions.
(Unmeasured anions: proteins, phosphate, sulfates and organic acids vs unmeasured cations K,Ca, Mg)
Hypoalbuminemia will decrease the normal AG to 4-5. For every 1 decrease in Alb a decrease of 2.5-3 in AG is expected. Similarly parproteinemia will decrease the normal anion gap.
Δ
Etiologies of Metabolic Acidosis
Increased anion gap:Methanol UremiaDiabetic ketoacidosisParaldehydeINH/IronLactic acidosis (including metformin)Ethylene glycol, EtOHSalicylates, starvation ketosis(others: CO, CN, Sulfur, theophylline, toluene)
Δ
Etiologies of Metabolic Acidosis
Normal anion gap:Bicarb loss (kidney/gut)
diarrheaurinary diversionfistulas/drain from bile/small bowel etcRTA
Acid addition (with Cl- as the anion)HclNH4ClArginine HCLLysine HCLCaCl2/MgCL2 (oral)sulfur
Δ
The DELTA GAPIf there is an abnormal AG you can look for triple disorders by checking for the delta gapIn an uncomplicated AG met acidosis for every 1 increase in AG the HCO3 should decrease by 1. If this is not the case there is likely a mixed d/o.Δgap=(AG-12) – (24-HCO3)The normal Δgap should be zero ± 6.A positive delta gap indicates either simultaneous metabolic alkalosis (eg vomitting) or resp acidosis.A negative delta gap indicates then a concomitant normal AG hyperchloremic acidosis (eg diarrhea) or chronic resp alkalosis is present.
Acid Base1.Determine if acidemia (pH<7.36) or alkalemia is present (pH>7.44). In mixed disorders the pH will be normal but the bicarb/pCO2/AG will be abnl.2. Is the primary disturbance met or resp? Does the change in PCO2 account for the direction of pH change?3. Is there appropriate compensation for the primary disturbance?4. Is the AG elevated? If so is there a Δgap? If so is there an additional non-gap acidosis or a metabolic alkalosis?
Question38 yo male with chronic renal failure p/w weakness, anorexia and nausea to ER. He has recently had increased n/v but had refused HD. PE: bibasilar crackles, regular cardiac rhythm, and 2+ edema. Labs: Na 135, K 5.2 Cl 80 HCO3 24, BUN 100 Cr 12. ABG: pH7.4 pCO2 37 HCO3 22.Which best describes the acid-base statusA. No acid-base abnormalityB. Met acidosis and respiratory alkalosisC. Metabolic acidosis and metabolic alkalosisD. Respiratory acidosis and respiratory alkalosis
Question38 yo male with chronic renal failure p/w weakness, anorexia and nausea to ER. He has recently had increased n/v but had refused HD. PE: bibasilar crackles, regular cardiac rhythm, and 2+ edema. Labs: Na 135, K 5.2 Cl 80 HCO3 24, BUN 100 Cr 12. ABG: pH7.4 pCO2 37 HCO3 22.Which best describes the acid-base statusA. No acid-base abnormalityB. Met acidosis and respiratory alkalosisC. Metabolic acidosis and metabolic alkalosisD. Respiratory acidosis and respiratory alkalosis
Answer ExplainedRecognize a large AG with normal bicarb may indicate a mixed metabolic acidosis and metabolic alkalosis.Would expect AG acidosis from renal failure. His AG is 31. His bicarb should therefore be 5. [For each increase in AG from 12 bicarb should decrease by the same 19]Due to the n/v he also has a metabolic alkalosis which increased his bicarb back to 24 with decreased Cl.No evidence of resp alkalosis since the PCO2 is nl. Very rare if ever to see mixed resp alk and acidosis.
Question
A 52 yo f with advanced pulm sarcoid on prednisone 30 qd for 2 yrs. Pt is admitted with 2 days of fever, flank pain, dysuria and vomiting for 6 hours. On admit HR 120 BP 80/60 RR 28. UA is loaded with WBC and gram stain is loaded with gram negative bacilli. ABG on RA: 7.44/24/68. Na 135, K 3.5, Cl 86, HCO3 16. What is the acid-base disorder?
Question
A. Inconsistent and un-interpretable dataB. Chronic resp alkalosisC. Acute and chronic resp alkalosisD. Resp Alkalosis and anion gap metabolic acidosisE. Resp Alkalosis, anion gap metabolic acidosis, and metabolic alkalosis.
Question
A. Inconsistent and un-interpretable dataB. Chronic resp alkalosisC. Acute and chronic resp alkalosisD. Resp Alkalosis and anion gap metabolic acidosisE. Resp Alkalosis, anion gap metabolic acidosis, and metabolic alkalosis.
Answer explainedPH is greater than 7.4 (alkalemia) and PaCO2 is reduced so the primary abnormality is respiratory alkalosis. (This is likely related to pain she is hyperventilating)Is there a metabolic component? The AG is 135-(86+16)=33. Normal AG is 8-16. So there is an AG acidosis. If the bicarb is not increased for each increase in AG there is a mixed d/o. The delta gap = (AG-12) – (24-bicarb)=
(33-12)-(24-16)= 13. (normal is zero +/- 6)A positive delta gap implies simultaneous resp acidosis or metabolic alkalosis. Here chronic met alkalosis likely related to chronic steroid use and vomiting.
MKSAP Question
A 75 yo female is BIBEMS after ingesting 50 tabs of enteric coated asa. She has chronic OA and DM type 2. She has refractory arthritis and periph neuropathy. On PE T 100, HR 135 RR 28 BP 105/65.
Which of the following labs is most consistent with her presentation?
Na K Cl CO2
BUN Cr Glu
A 147 2.9 105 18 35 1.5 355
B 140 4.5 105 28 35 1.5 355
C 140 3.3 105 28 10 0.7 45
D 121 4.3 105 18 35 1.5 655
E 130 5.3 110 18 35 2.5 655
Which of the following labs is most consistent with her presentation?
Na K Cl CO2
BUN Cr Glu
A 147 2.9 105 18 35 1.5 355
B 140 4.5 105 28 35 1.5 355
C 140 3.3 105 28 10 0.7 45
D 121 4.3 105 18 35 1.5 655
E 130 5.3 110 18 35 2.5 655
MKSAP explained
Mixed anion gap metabolic acidosis with resp alkalosis and volume depletion characteristic of salicylism.Early salicylate OD: central hypervent with resp alk then renal compensationLater metabolic acidosis due to uncoupled oxidative phophorylation and ketosis.Progressively salicylates enter cns causing change in Mental status and tinnitis. Volume loss can be worse by renal and vomit losses causing increased BUN/Cr.Stress can cause hyperglycemia.
MKSAP explained
So the answer is mild hypernatremia due to renal free water loss, AG acidosis with low bicarb, and volume depletion with elevated BUN/Cr, with mild hyperglycemia.B: normal AG, mild dehydration and hyperglycemia eg vomiting.C: mild hypokalemia and hypoglycemia without volume depletion eg hypoglycemic episodeD: AG with hyperglycemia and hyponatremia likely with DKA and hyperkalemiaE Hyperkalemia, hyperchloremia, low bicarb and normal AG eg RTA.
QuestionA 20 yo college student is BIB fraternity brothers to the ER because he is unarousable. No PMH until the party the previous night.BP 120/70 HR 118 RR 32 Sclera anicteric, pupils 8 mm and poorly responsive. Fundoscopy reveals sl blurring of the disk margins b/l with decreased retinal sheen. PE otherwise unresponsive and unremarkable.Na 142, K 4.3 Cl 98 HCO3 10 Glu 108, BUN 14 Osm (measured 348) 7.22/24/108. Blood alcohol level is 45. UA is unremarkable. What is the etiology of his metabolic acidosis?
Question cont
A. Methanol ingestionB. Toluene toxicityC. Ethylene Glycol ingestionD. Ethanol intoxicationE. Isopropanol ingestion
Question cont
A. Methanol ingestionB. Toluene toxicityC. Ethylene Glycol ingestionD. Ethanol intoxicationE. Isopropanol ingestion
Answer explainedThis pt has a high AG and elevated osmolal gap. This suggests either methanol or ethylene glycol intoxication. Optic nerve dysfunction on exam makes methanol most likely.The osmolal gap is calc osmolality -osm measure2XNa + Glu/18 + BUN/2.8- measured295-358. or a gap of 63 ( part of which is explained by EtOH (EtOH/4.6 = 45/4.6 = 10)High AG met acidosis is usually methanol/ethylene glycol.
Answer explainedMethanol causes optic n injury with blurred disc, retinal edema (increased sheen), loss of pupilary light reflex. Rx with EtOh or fomepizole to decrease formation of formaldehye.Ethylene Glycol also causes increased AG and osmolal gap met acidosis. It is associated with oxalate crytaluria and not optic n injury.Ethanol with ketolactic acidosis would not explain the optic findings.Isopropanolol is met to acetone and causes osmolal gap without AG acidosisToluene (glue-sniffing) intoxication is not associated with osmolal gap only AG acidosis.
Causes of an osmolal gap >10
Anion gap metabolic acidosis
Ethylene glycol
Methanol
Formaldehyde
ESRD without HD
Paraldehyde
Alcoholic ketoacidosis
No metabolic acidosis
Isopropyl alcohol
Diethyl ether
Mannitol
Osm gap = Osm(measured)- Nax2 + Glu/18 + BUN/2.8 + EtOH/4.6
Acid Base: Take Home Message1.Determine if acidemia (pH<7.36) or alkalemia is present (pH>7.44). In mixed disorders the pH will be normal but the bicarb/pCO2/AG will be abnl.2. Is the primary disturbance met or resp? Does the change in PCO2 account for the direction of pH change?3. Is there appropriate compensation for the primary disturbance?4. Is the AG elevated? If so is there a Δgap? If so, is there an additional non-gap acidosis or a metabolic alkalosis?