blood gas analysis: a practical approach - wild apricot · blood gas analysis: a practical approach...

Blood Gas analysis:

a practical approach

Advanced course in General Internal Medicine

KU Leuven session, May 25 2012

Bert Bammens

Normal acid-base physiology

3 processes involved in normal acid-base balance

extra- & intracellular buffering

elimination of CO2 by lungs

reabsorption & new formation of HCO3- by kidney

extra- & intracellular buffers

Intracellular buffers

Proteins & organic phosphates buffer extracellular H+

exchanging intra-cellular Na+ en K+.



The bone as a buffer

Important contribution in case of chronic acid load.



Blood buffers

Changes in pH are buffered proportionally by different buffers.



Bicarbonate: most important extracellular buffer

• Quantitatively important

• Analysis is easy

• OPEN

STRONG buffer!




CO2(d) + H2O H+ + HCO3-

Dissociation constant: K = [H+].[HCO3-] / [CO2(d)]

Logarithmic form: pH = pK + log([HCO3-] / [CO2(d)])

OR pH = pK + log([HCO3-] / s.pCO2)




pH = pK + log([HCO3-] / s.pCO2)

pH = 6.1 + log([HCO3-] / 0.03.pCO2)

Henderson-Hasselbalch equation

at 37°C in plasma

of mammals




pH = 6.1 + log([HCO3-] / 0.03.pCO2)

OPEN

STRONG buffer!


Bicarbonate buffer is OPEN thanks to kidneys and lungs!

pH = 6.1 + log([HCO3-] / 0.03.pCO2)

elimination of CO2 by lungs

reabsorption & new formation of HCO3- by kidneys


• Net non-volatile acid production: 40 mmol/day

• Net non-volatile acid intake (food): 20 mmol/day

Net non-volatile base loss in stool: 10 mmol/day

We need to get rid of an “acid load” of 70 mmol/day

(i.e. 1 mmol/kg/day)




Moreover: reabsorption

of filtered HCO3-!


HCO3- reabsorption: 80% in proximal tubule

HCO3- + H+ H2CO3

CO2 + H2O

Carbonic anhydrases

fasten this “slow” reaction.



“new” HCO3-, titratable acid:



“new” HCO3-, NH3: synthesis & secretion in proximal tubule,

secretion & reabsorption remainder of nephron*

“Diffusion trapping”

keeps NH4+ in

tubular lumen.

*



Normal values

plasma pH 7.35-7.45

acidemia pH < 7.35

alkalemia pH > 7.45

plasma [HCO3-] 24 mmol/L

plasma pCO2 40 mmHg

Acid-base pathophysiology


ACIDEMIA: the lab result

ACIDOSIS: the physiopathological process

the lab result: ALKALEMIA

the physiopathological process: ALKALOSIS


Consider

Metabolic acidosis

Metabolic alkalosis

Respiratory acidosis (acute or chronic)

Respiratory alkalosis (acute or chronic)

Mixed acid base disorders

more than just 2 pathological conditions

when compensation is absent or greater than expected

compensation & mixed disorders

expected compensation in primary metabolic disorders

ACIDOSIS: pCO2 = 1.5 x [HCO3-] + 8 ( 2) (last 2 digits of pH)

ALKALOSIS: pCO2 = 0.9 x [HCO3-] + 16 ( 5) (last 2 digits of pH)

expected compensation in primary respiratory disorders

ACUTE ACIDOSIS: ∆[HCO3-] = 0.1 x ∆pCO2

CHRONIC ACIDOSIS: ∆[HCO3-] = 0.4 x ∆pCO2

ACUTE ALKALOSIS: ∆[HCO3-] = 0.2 x ∆pCO2

CHRONIC ALKALOSIS: ∆[HCO3-] = 0.5 x ∆pCO2


Expected compensation in METABOLIC ACIDOSIS

pCO2 = 1.5 x [HCO3-] + 8 ( 2) (last 2 digits of pH)

Voorbeeld:

Metabolic acidosis pH = 7.31 with [HCO3-] 15 mmol/L

95% CI expected pCO2 in case of maximal respiratory compensation:

1.5 x 15 + 8 ( 2) = 30.5 ( 2), so from 28.5 to 32.5 mmHg

compensation & mixed disorders


STEP 1: interpret the pH!

ACIDOSIS: pH < 7.35

ALKALOSIS: pH > 7.45

STEP 2: define metabolic vs. respiratory!

ACIDOSIS = respiratory when pCO2 > 40 mmHg

ACIDOSIS = metabolic when [HCO3-] < 24 mmol/L

ALKALOSIS = respiratory when pCO2 < 40 mmHg

ALKALOSIS = metabolic when [HCO3-] > 24 mmol/L


Case 1

22-year old woman, type I diabetes

nausea, vomiting, polyuria, polydipsia

abdominal discomfort

hyperventilating, orthostatic hypotension, dry tongue

pH 7.23 [Na+] 132 mmol/L

[HCO3-] 10 mmol/L [K+] 6 mmol/L

pCO2 23 mmHg [Cl-] 93 mmol/L

[Glucose] 720 mg/dL

[Creatinine] 2.6 mg/dL

[Ureum] 70 mg/dL

Which acid-base disorder?

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

1


pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

STEP 1: low pH acidosis

STEP 2: low [HCO3-] metabolic acidosis

1

Compensation?

pCO2 = 1.5 x [HCO3-] + 8 ( 2) (last 2 digits of pH)

pCO2 = 1.5 x 10 + 8 ( 2) (23)

pCO2 = 23 ( 2) (23)

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

metabolic acidosis with

respiratory compensation

1


pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

Which cause?

1



pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

STEP 3: calculate the plasma anion gap

1


Which cause?



STEP 3: calculate the plasma anion gap!

(difference between “measurable cations” and “measurable anions”)

[Na+] – ([HCO3-] + [Cl-]) normal 12

OR

([Na+] + [K+]) – ([HCO3-] + [Cl-]) normal 16

METABOLIC ACIDOSIS


pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

[Na+] – ([HCO3-] + [Cl-]) = 132 – (10 + 93) = 29

1

STEP 3: calculate the anion gap


Which cause?



pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

[Na+] – ([HCO3-] + [Cl-]) = 132 – (10 + 93) = 29

high anion gap

metabolic acidosis

1

STEP 3: calculate the anion gap


Which cause?



Causes

KUSSMALE

high anion gap METABOLIC ACIDOSIS


DIABETIC KETO-ACIDOSIS

UREMIA

SALICYLATE INTOXICATION

STARVATION KETO-ACIDOSIS

METHANOL INTOXICATION

ALCOHOLIC KETO-ACIDOSIS

LACTATE ACIDOSIS

ETHYLENE GLYCOL INTOXICATION

high anion gap METABOLIC ACIDOSIS


KUSSMALE

Which high anion gap metabole acidose?

KUSSMALE

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

1


KUSSMALE

Look for ketonuria!

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

1


KUSSMALE

clinical signs of dehydration,

potential tissue hypoxia

Analyse lactate level (blood gas analysis, central lab)

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

1

Which high anion gap metabolic acidosis?

KUSSMALE

pH 7.23 [Na+] 132 mmol/L



[Glucose] 720 mg/dL


[Urea] 70 mg/dL

1


UREMIA





LACTATE ACIDOSIS


CAVE: high lactate and ketonuria are NON SPECIFIC!


ketonuria

ketonuria, high lactate

ketonuria

ketonuria

lactate

lactate?


UREMIA





LACTATE ACIDOSIS




Consider patient history

+ other lab values

ketonuria


ketonuria

ketonuria

lactate

lactate?


UREMIA





LACTATE ACIDOSIS




ketonuria


ketonuria

ketonuria

lactate

lactate?

• serum salicylate > 40 mg/dL

• often mixed acid base disorder:

metabolic acidosis + respiratory alkalosis

Case 2

22-year old student, no relevant medical history

found at home after being missed for a day, slight drunken

appearance, disorientated in space and time

pH 7.11 [Na+] 138 mmol/L

[HCO3-] 6.8 mmol/L [K+] 6 mmol/L


[Glucose] 110 mg/dL


[Urea] 70 mg/dL

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL

Another high anion gap metabolic acidosis

no ketonuria

no salicylates

elevated lactate

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL


no ketonuria

no salicylates

elevated lactate

KUSSMALE

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL

Lactate acidosis.

But why?

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL

Lactate acidosis.

But why?

Type A hypoperfusion, hypoxia

Type B metabolic disorders, medication,

problematic clearance of lactate (CKD, liver)

D-lactate jejuno-ileal bypass, short bowel…

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL

Lactate acidosis.

But what if you don’t find a reasonable explanation for lactate

overproduction from history or circumstances?

Which simple additional test would you perform?

Calculate the OSMOLAL GAP

= measured osmolality – calculated osmolality


2 (Na+ + K+) + urea + glucose - 10

2 (Na+) + urea + glucose

2 (Na+)

6 18

6 18

Na+, K+: mEq/L ureum, glucose: mg/dL

2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL

osmolality 336 mOsm/L [Creatinine] 2.6 mg/dL

[Urea] 70 mg/dL

Calculate the OSMOLAL GAP

= measured osmolality – calculated osmolality

= 336 – 293

OSMOLAL GAP > 10

OSMOLAL GAP > 10

Consider presence of “abnormal osmoles”, such as

ethanol

isopropyl alcohol

methanol high anion gap acidosis

ethylene glycol high anion gap acidosis



Oxalate crystal formation in urine

BUT late (and aspecific) finding


2 pH 7.11 [Na+] 138 mmol/L



[Glucose] 110 mg/dL


[Urea] 70 mg/dL


no ketonuria

no salicylates

elevated lactate

WHY?

KUSSMALE


Acid-base

Case 3

47 year old diabetic patient admitted to the emergency

room because of symmetrical weakness in the legs

History of hypertension treated with Aldactone®

(spironolactone) en Tritace® (ramipril) since 2006

Case 3

Hypokalemia: pathogenesis

LOW POTASSIUM INTAKE

HIGH POTASSIUM LOSS

SHIFT TO INTRA-CELLULAR COMPARTMENT


HIGH POTASSIUM LOSS

RENAL or EXTRA-RENAL (GI/SKIN)

HOW TO DISTINGUISH?

Case 3

Case 3

URINE POTASSIUM IS LOW

GI or SKIN LOSS? SHIFT? LOW INTAKE?

Case 3

TRANSTUBULAR POTASSIUM GRADIENT

TTKG = [Urine [K] ÷ (Urine osmolality / Plasma osmolality)] ÷ Plasma [K]

TTKG is an estimation of how the kidneys handle potassium.

In case of hypokalemia, expected TTKG < 3

In case of hyperkalemia, expected TTKG > 10

If NOT, a primary RENAL CAUSE should be suspected.


HIGH RENAL POTASSIUM LOSS

DIURETICS

carbonic anhydrase inhibitors (acetazolamide)

lisdiuretics (furosemide, bumetanide)

thiazides (hydrochloorthiazide, chloortalidon)

osmotic diuretics

MECHANISM

- high flow and sodium delivery to the

“DISTAL K+ SECRETORY SYSTEM”

- lowering of ECF volume RAAS high aldosterone

inhibitie Na+ reabsorptie

door blokkade Na+ transport

in specifieke nefronsegmenten

DIURETICA

30

NON-REABSORBABLE ANIONS in glomerular filtrate

keep Na+ in tubular lumen

higher distal Na+ delivery

bv.

HCO3- in case of high GI fluid loss

in case of proximal RTA (type 2)

β-hydroxybutyric acid in diabetic keto-acidosis

Hippuric acid in toluene-poisoning (glue-sniffing)



MINERALOCORTICOID EXCESS SYNDROMES

primair (hyper)aldosteronism (Conn’s syndrome)

Cushing syndrome (excess of glucocorticoids)

licorice, glycyrrhetinic acid

renovascular disease

Na+ balans: RAAS

65



RENAL TUBULAR DEFECTS

Bartter’s syndrome (defect NKCC2 mimics loop diuretic)

Gitelman’s syndrome (defect NCC mimics thiazide)

RTA (type 1 en 2)

Liddle’s syndrome

Liddle’s syndrome (autosomal dominant)

Overexpression of ENac in principal cells

Na+ retention

K+ secretion

Mimics aldosteronism with hypertension,

hypokalemia en alkalosis, but without high

aldosteron levels

(pseudo-aldosteronism)





Further clinical differentiation based on

assessment of volume status.

In the present case, physical examination

suggested

mineralocorticoid excess syndrome.

Case 3

65

Acid-Base DIAGNOSTIC FLOW-CHART

STEP 1: interpretet the pH!

METABOLIC ALKALOSIS


STEP 3: intake/generation of alkali?

YES

NO

STEP 4: assess ECF

volume status!

Zuur-base: pathogenese/oorzaken

47

Oorzaken

milk-alkali syndroom vroeger: melkinfuzen, CaCO3 voor peptisch maaglijden

nu: CaCO3 (of andere alkali) “over the counter”

bicarbonaat infuus

bij oxidatie van zouten van zwakke zuren exogeen of endogeen tijdens herstel lactaat of keto-acidose

NaA + H2CO3 HA + NaHCO

ALKALOSE ontstaat vooral wanneer renale eliminatie van

HCO3- gestoord is: hypokalemie, hypochloremie, hypovolemie.

metabole alkalose door inname/vorming van alkali

ECV contraction

gastro-intestinal

renal

ECV expansion

mineralocorticoids


38

Oorzaken Hoe differentiëren?

GASTRO-INTESTINAAL

RENAAL: nierinsufficiëntie, RTA

DILUTIE

1. Anamnese, KO, dossier (nierinsufficiëntie, dilutie)

2. Urine pH > 6.0 RTA (meestal type 1)

3. Urine pH < 6.0: meet urinaire anion gap ([Na+] + [K+] – [Cl-])

urinaire anion gap > -10 RTA (meestal type 2)

urinaire anion gap < -20 gastro-intestinaal

STAP 4: bekijk urine pH en bepaal urinaire anion gap!

non anion gap METABOLE ACIDOSE

Acid-base DIAGNOSTIC FLOW-CHART


METABOLIC ACIDOSIS


STEP 3: calculate plasma anion gap!

HIGH GAP

NON GAP


14

Oorzaken

KUSSMALE

high anion gap METABOLE ACIDOSE

STEP 4: watch urine pH &

calculate urinary anion gap!



RESPIRATORY ACIDOSIS


STEP 3: differentiate between central causes, nerve

conduction problems and peripheral causes


59

STAP 3: differentieer tussen centrale oorzaken,

geleidingsproblemen en perifere oorzaken!

RESPIRATOIRE ACIDOSE

respiratoire acidose door centraal probleem

Hyponatremie: symptomen

39

Symptomen van hersenoedeem en intracraniële overdruk

bradypnee (Cheyne-Stokes-ademhaling)


60


respiratoire acidose door geleidingsprobleem


61


respiratoire acidose door perifere oorzaken

)


62


respiratoire acidose door perifere oorzaken



RESPIRATORY ALKALOSIS


STEP 3: differentiate between central,

peripheral and iatrogenic causes


68

STAP 3: differentieer tussen centrale oorzaken,

perifere en iatrogene oorzaken!

RESPIRATOIRE ALKALOSE

respiratoire alkalose door centrale oorzaken


69


respiratoire alkalose door perifere oorzaken

Zuur-base: fysiologie

• CPG in hersenstam genereert

het normale (onbewuste) adem-

halingsritme.

• Wijzigingen in pCO2, pH en pO2

worden gedetecteerd door

perifere en centrale

chemoreceptoren.

• Dit leidt tot efferente signalen

die diepte en frequentie van

ademhaling wijzigen.27


70


respiratoire alkalose door iatrogene oorzaken

Thank you!

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