ARTERIAL BLOOD GASES

DR. ABDULAZIZ AL SHAER CONSULTANT INTENSIVIST 21/2/2010

Indications

 Oxygenation  Ventilation  Acid-base disorders

Normal Arterial Blood Gases

pH PaCO 2 PaO 2 SaO 2 HCO 3 Base excess CaO 2 7.35 – 7.45

35-45 mmHg 70 – 100mmHg 93 – 98% 22 – 26 mEq/L -2.0 to 2.0 mEq/L 16 – 22ml O 2 /dl

Use of Venous VS. Arterial pH

As compared with arterial blood gases: pH ↓ 0.03 – 0.04

PaCO 2 HCO 3 ↑ 7 - 8 mmHg ↓ 2 mEq/L

Technical Considerations

 PaO 2 , PaCO 2 , and pH are directly measured with standard   Oxygen saturation is calculated from standard O dissociation curves.

2 Bicarbonate concentration is calculated using the Henderson-Hasselbalch equation: [HCO 3 -] pH = pKa + log --------------- 0.03 [PaCO 2 ] pKa is the negative logarithm of the dissociation constant of carbonic acid Simplified equation: [PaCO 2 ] [H] = 24 x ---------- [HCO 3 -]

Technical considerations

 Leukocytosis and thrombocytosis accelerate the decline of PaO 2 and pH and elevation of PaCO 2 within a stored sample  Significant increases in PaCO more than 20 minutes 2 and decreases in pH occur when samples are stored at room temperature for

Technical considerations

      Increased dead space in the syringe lowers PaCO 2 .

Air bubble falsely increases PaO 2 .

PaCO 2 and PaO 2 may diffuse out of plastic Heparin and liquid solutions cause spuriously low PaCO 2 .

Dry (sodium or lithium) heparin in ABG kits may interfere with electrolyte measurement and, when concentrated, may lower pH.

Timing of ABG collection relative to ventilator changes should permit equilibration of alveolar and arterial PO 2 .

Oxygenation

 PAO 2 = PIO 2 PIO 2 – 1.25 (PaCO 2 ) = FIO 2 (PB – 47 mmHg)  P(A-a)O 2 = PAO 2 – PaO 2  CaO 2 = (Hgb x 1.34 x SaO 2 )+(0.003 x PaO 2 )  V

D

O 2 = CaO 2 x CO

Oxygenation

    PAO 2 remains constant with age, but PaO 2 decreases with age.

PaO 2 (corrected for age): 100 mmHg – 0.3 x age Normal P(A-a)O mmHg breathing room air (it increases with age).

2 ranges from 5 to 25 A higher than normal P(A-a)O 2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.

Causes of Hypoxemia

NON-RESPIRATORY Cardiac right-to-left shunt Decreased PIO 2 Low mixed venous oxygen content P(A-a)O 2 Increased Normal Increased RESPIRATORY Pulmonary right-to-left shunt Ventilation-perfusion imbalance Diffusion barrier Hypoventilation (increased PaCO 2 ) P(A-a)O 2 Increased Increased Increased Normal

O2 delivery

  V

D

O 2 CaO 2 = CaO 2 x CO = (Hgb x 1.34 x SaO 2 )=(0.003 x PaO 2 ) – O 2 saturation and not PaO 2 is the parameter of oxygenation that contributes most to O 2 delivery.

– The relationship between PaO curve.

2 and SaO 2 is demonstrated by the oxygen-hemoglobin dissociation

Oxygen-Hemoglobin dissociation curve

Left shift Decreased temp Decreased 2-3 DPG Decreased (H+) CO Right shift Reduced affinity’s Increased temp Increased 2-3 DPG Increased (H+)

Ventilation

    The only way to assess ventilation is to check PaCO2 through ABGs.

V A =K x V CO2 /P A CO 2 – V – K is 0.863 to covert V mmHg – V CO2 is CO 2 – P A A is alveolar ventilation CO 2 production CO2 is the alveolar CO 2 and V pressure and in 2 .

A units from V A = 0.863 x V CO2 /PaCO 2 PaCO 2 = 0.863 x V CO2 /V A

Ventilation

   V A = f x (Vt – V

D

) The only physiologic reason for elevated PaCO 2 is inadequate alveolar ventilation (V A ) for the amount of the body’s CO 2 production (VCO 2 ).

Since alveolar ventilation (V A ) equals minute ventilation (V E ) minus dead space ventilation (V

D

), hypercapnia can arise from insufficient V E , increased V

D

, or a combination of both.

Ventilation

  Examples of inadquate V E : – Sedatives – Respiratory muscle paralysis, weakness, CIM, MS, low Mg/Phos – Neuropathy: GBS, CIPN – Central hypoventilation Examples of increased V

D

: – Chronic obstructive pulmonary disease – Severe restrictive lung disease

Acid-base interpretation

Simplified Henderson-Hasselbalch equation: [PaCO 2 ] [H] = 24 x ---------- [HCO 3 -] [H] is normally is 40nEq/L which gives a pH of 7.40

  Acidemia: blood pH < 7.35

Alkalemia: blood pH > 7.45

pH

7.00

7.10

7.30

7.40

7.52

7.70

8.00

[H + ] in nEq/L

100 80 50 40 30 20 10

Approach to Acid-Base Disorders

Do numbers make sense?

  Consider the clinical setting!

Is the patient acidemic or alkalemic?

    Is the primary process metabolic or respiratory?

If metabolic acidosis, gap or non-gap?

Is compensation appropriate?

Is more than one disorder present?

Simple Acid-Base Disorders

Disorder pH H + Primary Disorder Compensatory Response Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis ↓ ↑ ↓ ↑ ↑ ↓ ↑ ↓ ↓ HCO 3 ↑ HCO 3 ↑ pCO 2 ↓ pCO 2 ↓ pCO 2 ↑ pCO 2 ↑ HCO 3 ↓ HCO 3 -

Acute Respiratory Acidosis

  pH will decrease by 0.08 for each 10 mmHg increase is PaCO 2 .

Compensation by retaining HCO 3 - by the kidney.

 HCO 3 - will decrease by 1 for each 10mmHg increase in PaCO 2 .

Chronic Respiratory Acidosis

  pH will decrease by 0.03 for each 10 mmHg increase is PaCO 2 .

Compensation by retaining HCO 3 - by the kidney.

 HCO 3 - will decrease by 4 for each 10 mmHg increase in PaCO 2 .

Acute Respiratory Alkalosis

  pH will increase by 0.08 for each 10 mmHg increase is PaCO 2 .

Compensation by dumping HCO 3 - by the kidney.

 HCO 3 - will increase by 2 for each 10 mmHg decrease in PaCO 2 .

Chronic Respiratory Alkalosis

  pH will increase by 0.03 for each 10 mmHg fall is PaCO 2 .

Compensation by dumping HCO 3 - by the kidney.

 HCO 3 - will rise by 5 for each 10 mmHg fall in PaCO 2 .

Expected changes in pH and HCO

3

- for a 10 mmHg change in PaCO

2

Acute Resp Acidosis Chronic

pH ↓ by 0.08 HCO 3 ↑ by 1 pH ↓ by 0.03 HCO 3 ↑ by 3 - 4

Resp Alkalosis

pH ↑ by 0.08 HCO 3 ↓ by 2 pH ↑ by 0.03 HCO 3 ↓ by 5

Metabolic Acidosis

    Primary disorder is low HCO 3 Compensation by decreasing PaCO 2 Expected PaCO 2 : (1.5 x HCO 3 -)+8 ± 2 There are two types – Increased anion gap – Normal anion gap

Metabolic Acidosis: Elevated Anion Gap

AG = Na + - (Cl + HCO 3 -) = 12 ± 2

Anion Gap in Hypoalbuminemia

  The true anion gap is underestimated in hypoalbuminemia; AG must be adjusted.

Formulas for adjusted AG: – For every 1.0 fall in albumin, increased AG by 2.5

– Consider the patient’s “normal” AG to be (2 x alb) + (0.5 x phosphate) – Adjusted AG = Observed AG + (2.5 x [normal alb – adjusted alb]

Causes AG Acidosis

 Ketoacidosis  Lactic acidosis  Intoxications  Renal failure  Rhabdomyolysis

Ketosis

 Diabetes  Starvation  Alcoholic  Isopropyl alcohol * *Ketosis with normal AG and HCO 3

 Type A:

Lactic Acidosis

Hypoxic Lactate: pyruvate > 10:1  Type B: Glycolytic Lactate: pyruvate = 10:1

Intoxications Causing High AG Acidosis

 Aspirin  Methanol  Ethylene Glycol  Paraldehyde

The Delta/Delta: Δ AG/Δ HCO

3  Rationale: For each unit INCREASE in AG (  “Normal” values: – AG = 12 – HCO 3 = 24

Use of the Delta/Delta: Examples

AG (12)

 18 ↑ (6)  18 ↑ (6)  18 ↑ (6)

HCO 3

18 ↓ (6) 22 ↓ (2) 12 ↓ (12)

Diagnosis

Appropriate: pure AG acidosis HCO 3 has ↓ less than predicted, so HCO 3 is too high; mixed AG acidosis AND met alk HCO 3 has ↓ more than predicted, so HCO 3 is too low; mixed AG AND non-AG acidosis

Osmolar Gap

 Measured serum osmolality > Calculated serum osmolality by > 10 mOsm  Calculated osmolality: – 2[Na] + BUN/2.8 + glucose/18 ethanol/4.6

– BUN, glucose and ethanol are converted from mg/dl to mmol/L – If using mmol/L: 2[Na] + BUN + glucose + ethanol

Causes of High Osmolar Gap

     Isotonic hyponatremia Hyperlipidemia Hyperproteinemia Mannitol Glycine infusion Chronic renal failure Ingestions: Ethanol, isopropyl alcohol, ethylene glycol, mannitol Contrast media

Relationship between AG and Osmolar Gap

 Ethylene glycol  Methanol  Renal failure  Isopropyl alcohol  Ethanol  Lipids, proteins

AG

+ + + -

Osm gap

+ + + + + +

Approach to Metabolic Acidosis

Osmolar Gap Normal Uremia Lactate Ketoacids Salicylate High Increased Ethylene glycol Methanolol Normal Anion Gap GI Fluid Loss?

Yes No Diarrhea Illeostomy Enteric fistula Urine pH >5.5

<5.5

Distal RTA (Type 1) Low Serum K High Proximal RTA (Type 2) Type 4 RTA

Metabolic Alkalosis

   Etiology: Requires both generation of metabolic alkalosis (loss of H tract or kidneys) and maintenance of alkalosis (impairment in renal excretion) + through GI HCO 3 Causes of metabolic alkalosis – Loss of Hydrogen – Retention of bivarbonate – Contraction alkalosis Maintenance factors: Decrease in GFR, increase in HCO 3 reabsorption

Use of Spot Urine Cl and K

Urine Chloride > 20 mEq/L Very Low (< 10mEq/L) Vomiting, NG suction Postdiuretic, posthypercapneic Villous adenoma, congenital chloridorrhea, post- alkali Low (< 20mEq/L) Urine Potassium 30 mEq/L Laxative abuse Other profound K depletion Diuretic phase of diuretic Rx, Barter’s, Gitelman’s, primary aldo, Cushings, Liddle’s, secondary aldosteronism

Treatment of Metabolic Alkalosis

 Remove offending culprits.

 Chloride (saline) responsive alkalosis: Replete volume with NaCl.

 Chloride non-responsive (saline resistant) alkalosis Acetazolamide (CA inhibitor) Hydrochloric acid infusion Correct hypokalemia if present

Case studies

Q.1

22 male known D.M. developed sever upper respiratory infection

 Na 128 K 5.9 Cl 94  Hco3 6 Pco2 = 15 Po2=102  PH =7.19  Glucose = 324

 1A R the data internally consistent?

yes it is internally consistent Pco2= [H]* [HCO3] /24 Pco2=61*6/24 Pco2=15  1B Is the patient acidemic or alkalemic?

< 7.4 so acidemic  1C Is the primary disorder respiratory?

Pco2 is not elevated so this metabolic

Q 1 cont.

  1D The patient has MA ,is this hyperchloremic or high anion gap MA ?

AG = Na-Cl-HCO3 = 28 ( normal 10-12) so high AG MA 1F Is the compensation for the MA is appropriate?

Expected Pco2 =1.5*HCO3 +8 -+ 2 so expected 17 -+ 2

so simple compensated MA

 1E Is there another ( M alk) acid base disturbance present ? What is the delta anion gap Delta AG=measured AG-normal AG=28-10=18 Adding the delta gap to the measured HCO3 give the predicted starting HCO3 ( before the anion gap acidosis).

Here, 18+6=24 ,normal preacidosis level of HCO3.

so NO underlying met alkalosis

Q 1 cont.

1G what a re the causes of an increase AG DKA , alcoholic ketoacidosis, and lactic acidosis Drugs and toxin methanol and ethylene glycol

Most likely her is DKA

Q.2 47 female CRF admitted with sever alcoholic intoxication, she is somnolent and febrile, RR 10 /min   

Na = 134 K=6.1 Cl= 112 HCO3=10 Pco2 =30 Po2=52 PH=7.10 Creatnine =3.7 BUN=62

 2A R the data internally consistent?

 the data are internally consistent Pco2=[H]*[HCO3]/24 Pco2=70*10/24 Pco2=29

 2B Is the patient acidemic or alkalemic?

PH< 7.4 ,so the patient is acidemic  2C Is the primary disorder respiratory?

This MA as the Pco2 is not elevated

 2D the pt has MA is this hyperchlormic or a high anion gap type MA ?

 AG 134-112-10=12 so the patient has normal AG or hyperchlormic MA

 2E Is the compensation for the MA appropriate?

Expected Pco2=1.5*HCO3+8 +- 2 for this degree of acidemia Expected Pco2 = 1.5*10+8+- 2= 23 +- 2 The measured Pco2 is that is

acidosis.

30 which is higher than what is expected with adequate compensation. therefore, this is mixed acid base disturbance ,

combined metabolic and respiratory

Even though the Pco2 is low it is not low enough

  2F What could it cause this acid-base disorder ?

This MA is may be related to the patient underlying CRF .The respiratory acidosis may be related to the alcoholic intoxication with reduction in respiratory drive ( R.R. is only 10 b/min). Alternatively, and less likely, the patient may have respiratory failure for another reason ( e.g. acute lung injury)  Double acid-base disorder: Metabolic and respiratory acidosis

Q.3

A 32 man with history of chronic alcohol use is brought to the emergency center after 3 days of nausea, vomiting and abdominal pain.4 hrs ago he took, something to help with pain. He is awake and alert, and PE is unremarkable:   

Na=132 K=3.9 Cl=82 HCO3= 4 Pco2= 10 Po2 110 PH=7.25 Glucose = 68 BUN = 14 Blood alcohol=106 Urinanalysis : no protein or ketones, positive for Crystals

 3A Are the data internally consistent ?

The data are internally consistent Pco2=55*4/24  Pco2=29 3B Is the patient acidmic or alkalemic?

Acidmic

 3C Is the primary disorder respiratory?

This is MA as the Pco2 is not elevated  3D The patient has MA is this hyperchlormic or high AG type MA ?

AG= 132-82-4= 46 so high AG metabolic acidosis

3E Is there another ( metabolic alkalosis) acid base disturbance present? What is the delta gap?

Delta AG 46-10=36 the potential fate of this anion is to become bicarbonate. HCO3 level before acid base disturbance was 36+4=40 .therfore, there is an underling metabolic alkalosis as well  3F Is the compensation for the metabolic acidosis appropriate?

Expected Pco2 1.5*4+8+-2=14+-2 As the measured Pco2 is 10 the compensation is close enough to say that it is appropriate.

3.G What are the potential causes of the increase in AG ?

In the absence of ketones ,the diagnosis of diabetic ketoacidosis or alcoholic ketoacidosis is not likely.IN the other hand the patient has taken something's in association with an anion gap MA and crystals in the urine. whereas methanol ingestion give metabolic acidosis, they do not yield crystaluria.On the other hand, this is consistent with ethylene glycol ingestion.

3.H

How one make the diagnosis of the ethylene glycol ingestion ?

 the presence of an osmolal gap would suggest that the patient ingested a compound with a small molecular weight. Ethylene glycol level are essential, but will take time to obtain. The demonstration of crystals in the urine,especialy calcium oxalate crystals ,would be highly suggestive of ethylene glycol.

 What are the possible causes of the metabolic alkalosis ?

The vomiting, presumably due to ulcer, gastritis, or pancreatic diseases, lead to alkalosis.

So this double acid-base disorder: MA secondary to ethylene glycol ingestion and Metabolic Alkalosis due to vomiting.

Q.4

male with mild CHF and COPD is admitted to hospital with recurrent pneumonia. required intubation for 2 days .after extubation he been treated with ceftrixone and enalopril. 5 days later,when he is awake,alert and ambulating, the following lab abnormalities were observed :    Na=129 K=3.2 Cl=81 HCO3=38 Pco2 =48 Po2 =68 on 1 l/min PH=7.51 Glucose= 108 BUN=21 Creatnine=1.8

 4.A

Are the data internally consistent ?

Internally consistent Paco2=29*38/24=46 ( pretty close)  4.B

Is the patient acdmic or alkalemic?

PH > 7.4 so alkalemic.

 4.C

Is the primary disorder respiratory? Metabolic alkalosis since the Pco2 is not low

 4.D

Is the compensation appropriate ?

Expected Pco2=0.7*HCO3+ 21+-1.5

= 0.7*38+21+-1.5= 48+-1.5

 Pco2 is 48 so change in Pco2 is appropriate, and the hypoventilation due to Metabolic alkalosis so this is simple compensated metabolic alkalosis.

4.E

What are the various type of metabolic alkalosis ?

Metabolic alkalosis is divided to chloride responsive and resistant Urine CL=46,Urine Na 51, and Urinary K =75 so as the urinary Cl is high, this is indicative of a chloride resistant metabolic alkalosis

  4.F

What are the causes of a chloride resistant metabolic alkalosis ?

This not common chloride responsive M Alkalosis are generally caused by gastric or renal loss of chloride. C resistant met alkalosis occur in the presence of mineral corticoid or glucocortcoid excess stats. These include primary aldosteronism or Cushing's syndrome. CS is caused by either increase in ACTH from central or peripheral source or an adrenal glucocorticoid producing adenoma. Measuring the ACTH level would distinguish ACTH-dependent versus ACTH independent Cushing's Syndrome  .

 4.G

What is the most likely cause of the chloride resistant metabolic alkalosis at this patient?

Chloride-resistant metabolic alkalosis in the setting of recurrent pneumonia is likely mediated by lung cancer with post obstructive pneumonia. Lung cancers are not infrequent producers of ACTH and ectopic ACTH syndrome.

SO Compensated, Chloride-resistant metabolic alkalosis

Q.5

46 male with COPD came to ER with increasing SOB ,CXR reveals RLL infiltrate.

 Na =140 K=4.1 Cl=98  HCO3= 30 Pco2 66 Po2 38  PH= 7.28

 5.A

Is the data internally consistent ?

The data are internally consistent Pco2=52*30/24=65   5.B

Is the patient acdmic or alkalemic ?

PH < 7.4 so the patient is acidemic  5.C

Is the primary disorder respiratory ?

This is respiratory acidosis as the Pco2 is high

 5.D

What type of respiratory acidosis is this ??

RA cab be acute or chronic. There are nomograms for changes in PH in acute versus chronic respiratory acidosis. In acute RA ,the [HCO3]=[(Pco2-40)/10]+24,or 27.In chronic RA [HCO3]=[Pco2 40)/3]+24 so [(66-40)/3]+24 or 33 .in this case ,the HCO3=30,midway suggesting an acute and chronic process.

5.E What are the causes of the acute and chronic respiratory acidosis ?

Most likely is COPD with acute pneumonia.

so this Respiratory acidosis, acute on chronic

Q.6

47 years women with history of being drinking with nausea ,vomiting and fever .

 Na=140 K=2.9 Cl = 96  HCO3 = 19 Pco2 = 49 Po2 =45  PH= 7.15 Glucose= 96  Urinalysis: 4 + ketones 

CXR… LUL,RML,RLL infiltrates

6.A

Is the data internally consistent .

The data is internally consistent Pco2=65*18/24=49  6.B

Is the patient acidmic or alkalemic?

The patient is acidemic  6.C

Is the primary disorder respiratory?

There is primary respiratory acidosis, but it magnitude is insufficient to cause this degree of acidemia( all else being equal, raising the Pco2 to 49 should lower the PH to 7.33). Thus, there must be another basis for part of the acidosis(ie,metabolic acidosis). This must be double acid-base disturbance, in other words, a metabolic and a respiratory acidosis

 6.D

Patient has MA so is it hyperchloremic or high AG MA?

AG 140-96-18=26 High anion gap type acidosis  6.E

What are the causes of high AG MA??

Most likely diagnosis in this patient is alcoholic ketoacidosi as the patient has 4+ ketones in her urine.An alternative possibility would be diabetic ketoacidosis, but this unlikely in view of the normal blood glucose level of 96.

 6.F

What about the compensation ?

In MA ,the Pco2 should decrease . Because the Pco2 is increased, there is no compensation. As Discussed above, this a double acidosis.

6.G

What is the most likely explanation for the patients clinical syndrome ?

Most likely this patient is chronic alcoholic with nausea and vomiting( resulting in a metabolic alkalosis: did you notice the delta gap [14]+the [HCO3]= 32 ?) who discontinued her alcohol intake and developed alcoholic ketoacidosis ( MA) and also developed pneumonia resulting in respiratory acidosis .

Q.7

62 male admitted to ICU with SOB. Number of empty bottles had been found in his apartment, including furosemid,enalapril,potassium chloride,asprin. XCR reveals pulmonary edema ?

 Na=140 K= 2.8 Cl=108  HCO3 =10  Pco2 =16  Po2 = 106  PH= 7.42

7.A Is the data internally consistent ?

The data are internally consistent Pco2=38*10/24=16 7.B

Is the patient acidmic or alkalemic?

Neither. The PH is normal, but this dose not exclude underlying acid-base disorder 7.C

Is the primary disorder respiratory?

For any primary acid base disorder, one cannot fully return PH to normal. The finding of normal PH implies 2 primary disorders. There must be a primary respiratory alkalosis( Pco2=16) but also a primary metabolic acidosis ( because the PH is normal)

 7.D

The patient has MA so is it hyperchlormic or high AG MA ?

AG = 22 so this high AG MA  7.E

Is there metabolic alkalosis present as well ? What is the delta gap?

The delta AG 22-10=12. when one adds 12 to the measured bicarbonate of 10 to equal 22,this indicates that there is no underlying metabolic acidosis.

 7. F What is the most likely cause of this acid-base disturbance ?

This patient appears to have ingested salicylates. The finding of

mixed acid –base

disturbance of a respiratory alkalosis and metabolic acidosis is very suggestive of this disturbance. In particular, this acid-base disturbance in the setting of pulmonary edema is highly suggestive of

salicylate intoxication.

Q.8

28 women is admitted with unexplained delirium and acidosis s after cleaning her motorcycle with solvents .

 Na= 139 K=1.7 Cl= 115  HCO3 = 12 Pco2= 28 Po2= 92  PH=7.24 BUN= 7 Creatnine=1.3



Urinalysis PH=6.5



SG = 1.020



No cells or casts

 8.A

Is the data internally consistent ?

The data internally consistent, Pco2=56*12/24=28  8.B

Is the patient acidmic or alkalemic?

Acidemic  8.C

Is the primary disorder respiratory ?

This is MA as the Pco2 is not elevated

 8.D

The patient has MA so is it hyperchlormic or high AG MA?

As AG is 12 this hyperchloremic MA. This is an important finding because one of the possible causes of the acidosis would be methanol ingestion. Methanol is a solvent often used to clean machine engines. In contrast to the finding of this patient, however, methanol ingestion would be expected to cause a high AG MA..So Methanol can be excluded based on this acid base abnormality.

 8.E what are the causes of the hyperchlormic MA ?

 Gastrointestinal loss of Na in excess of chloride, as is typical in diarrhea  Inorganic acid ingestion such as ammonium chloride  Renal tubular acidosis ( RTAs)

8 .F How one distinguish between these possibilities ?

The

urine PH

is the most helpful test to distinguish various causes of hyperchlormic metabolic acidosis. In the setting of systemic acidosis, a healthy kidney is able to acidify the urine so the urine PH is low ( <5.5).

Ingestion of inorganic acid

or

diarrhea-induced

acidosis dose not interfere with kidney function and is associated with urine PH < 5.5.

In contrast, in some types of RTA ( egg, distal RTA or type 1 RTA) the urine cannot be acidified normally. This result in an inappropriately high ( > 5.5) urinary PH despite systemic acidosis.

 This patient has a urine Therefore,

PH of 6.5

the degree of systemic acidosis. , a value clearly inappropriately high for 

the patient has distal RTA

8.G

What are the potential causes of the distal renal tubular acidosis in this women ??

Other than Methanol ,

toluene

solvent in cleaning solutions.

is often used as This patient inadvertently absorbed ( through the skin) toluene from the solvent and developed a distal RTA.

So Hyperchlormic metabolic acidosis secondary to toluene intoxication.

Case 1

 A 30 y/o man with DM presents with a week of polyuria, polydipsia, fever to 102, nausea, and abdominal pain. He is orthostatic on admission.

130 l 94 l 75 l 906 6.1 l 6 l 2.3

pH 7.14

pCO 2 pO 2 18 102

130 l 94 l 75 l 906 7.14/18/102 6.1 l 6 l 2.3

Case 1 cont

      Anticipate the disorder DKA (with anion gap acidosis) Acidemic or alkalemic?

Metabolic or respiratory?

pH = acidemic; must be metabolic low HCO 3 , low pCO 2 ) If metabolic acidosis: gap or non-gap?

AG = 30; + anion gap metabolic acidosis Is compensation appropriate?

PaCO 2 should = last 2 digits of pH [18] or (1.5 x HCO 3 ) + 8 [17] Mixed disorder?

AG = 30 (-18); HCO 3 = 6 (-18); thus simple AG met acidosis

Case 2

 A 30 y/o man with DM presents with a week of polyuria, polydipsia, fever to 102 and vomiting for four days.

135 l 89 l 50 l 1181 6.1 l 10 l 2.3

pH 7.26

pCO 2 pO 2 23 88

135 l 89 l 50 l 1181 7.26/23/88

Case 2 cont

      Anticipate the disorder DKA (AG acidosis); met alk from vomiting Acidemic or alkalemic?

Metabolic or respiratory? pH = acidemic; must be metabolic low HCO 3 , low pCO 2 ) If metabolic acidosis: gap or non-gap?

AG = 36; + anion gap metabolic acidosis Is compensation appropriate?

pCO 2 should = last 2 digits of pH [26] or (1.5 x HCO 3 ) + 8 [23] Mixed disorder?

AG = 36 (-24); HCO 3 = 10 (-14); HCO 3 is too high; mixed AG

Case 7

 A 55 y/o woman with a history of a CVA presents to clinic complaining of shortness of breath 140 l 100 l 30 l 115 3.9 l 30 l 1.5

pH 7.36

pCO 2 pO 2 38 91

140 l 100 l 30 l 115 7.36/38/91

Case 7 cont

    Anticipate the disorder Resp alk due to CNS disorder or acute pulmonary process Acidemic or alkalemic?

pH = acidemic Metabolic or respiratory? If metabolic acidosis: AG?

HCO 3 on?

is high (not metabolic acidosis); pCO 2 is < 40 (not respiratory acidosis); AG is normal (10), so what’s going

140 l 100 l 30 l 115 7.36/38/91

Case 7 cont

 LAB ERROR!

By Henderson-Hasselbach H + = 24 x pCO 2 /HCO 3 pH should be 7.50

= 24 x (38/30) = 30

Case 8

 You are in the ER, and are aware that the lab has been having intermittent problems with the chemistry auto analyzer. A 30 y/o diabetic man, well known to you from pervious visits, comes in with severe nausea and vomiting. His blood alcohol level is very high. The ER attending advises you to check his labs and send him home if they are OK 140 l 84 l 28 l 160 3.0 l 24 l 1.3

pH 7.40

pCO 2 pO 2 40 88

140 l 84 l 28 l 160 7.40/40/88 3.0 l 24 l 1.3

Case 8 cont

     Anticipate the disorder Vomiting - > met alk; if unconscious, resp acidosis Acidemic or alkalemic?

Metabolic or respiratory? pH, PCO2 and HCO2 are all normal  no apparent disorder Lab error? Check H-H equations.

H + = 24 x pCO 2 /HCO 3 = 24 x (40/24) = 40 pH should be 7.40

Do you send him home?

AG = 32; + anion gap acidosis AG = 32 (-20); HCO = 24 ( 0); so HCO have a superimposed metabolic alkalosis. Thus, mixed AG acidosis and metabolic alkalosis 3 is too high; must

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