Acid Base�in PICU�
ACID - BASE
KISS
Step approach to acid base problems
1. pH?
Alkalosis : pH > 7.45
PaCO2 < 35 mm Hg ? : Respiratory
[HCO3] > 26 mM ? Metabolic
Acidosis: pH < 7.35
PaCO2 > 45 mmHg? : Respiratory
[HCO3] < 22 mM/L? : Metabolic
Step approach to acid base problems
2. If Respiratory
is it acute or chronic: ? (HCO3/PaCO2)
3. If Metabolic
what is anion gap? > 20, then I ۫ metabolic acidosis
Is respiratory compensation (fall in PaCO2/HCO3) as predicted ?
4. What is excess AG ( ∆ Gap or gap-gap)
ACID – BASE�20:1 rule
Metabolic (kidney)
pH = __________________
Ventilation (lung)
HCO3 20
pH = ___________ = ________
0.03 x PaC02 1
ACID – BASE�balance between compensated HCO3 and PaCO2 is nearly 20:1
pH = 6.1+ log HCO3 / 0.03 PaC02
normal HC03 = ~ 24
normal PaC02 = ~ 40
(PaC02) 40 x 0.03 = 1.2
24/1.2 = 20
ACID – BASE�
Predicted change in pH
Acute Respiratory Acidosis 0.08 x [PaCO2-40÷10]
Chronic Respiratory Acidosis 0.03 x [PaCO2- 40÷10]
Acute Respiratory Alkalosis 0.08 x [40 - PaCO2÷10]
Chronic Respiratory Alkalosis 0.03 x [40-PaCO2÷10]
ACID – BASE�balance between compensated HCO3 and PaCO2 is nearly 20:1
Cherniak, RM, Pulmonary Function Testing, WB Saunders Co., ed 2,1992
PaC02 40
ACID – BASE�Metabolic Acidosis�balance between compensated HCO3 and PaCO2 is nearly 20:1
Cherniak, RM, Pulmonary Function Testing, WB Saunders Co., ed 2,1992
PaCO2 falls by 1 -1.5 mm Hg times the fall in [HCO3]
pH
PaC02 20
Metabolic Acidosis
ACID – BASE�Metabolic Alkalosis�balance between compensated HCO3 and PaCO2 is nearly 20:1
Cherniak, RM, Pulmonary Function Testing, WB Saunders Co., ed 2,1992
PaC02 should rise by 0.25 – 1.0 mm Hg times the rise in [HCO3]
PaC02 ~45
Metabolic Alkalosis
ACID – BASE� Respiratory Acidosis �balance between compensated HCO3 and PaCO2 is nearly 20:1
Cherniak, RM, Pulmonary Function Testing, WB Saunders Co., ed 2,1992
ACUTE
↑ [HCO3] by 1 mM for each 10 mm Hg In PaCO2
CHRONIC
↑ [HCO3] by 4 mM for each 10 mm Hg in PaCO2
Respiratory Acidosis
ACID – BASE� Respiratory Alkalosis�balance between compensated HCO3 and PaCO2 is nearly 20:1
Cherniak, RM, Pulmonary Function Testing, WB Saunders Co., ed 2,1992
ACUTE
↓ [HCO3] by 1 - 3 mM for each 10 mm Hg ↓ In PaCO2, but usually to no lower than ~ 18 mM/L
CHRONIC
↓ [HCO3] of 2-5 for each 10 mm Hg ↓ In PaCO2, but not to less than 14
PaC02 20
Respiratory Alkalosis
Step approach to acid base problems
1. pH?
Alkalosis : pH > 7.45
PaCO2 < 35 mm Hg ? : Respiratory
[HCO3] > 26 mM ? Metabolic
Acidosis: pH < 7.35
PaCO2 > 45 mmHg? : Respiratory
[HCO3] < 22 mM/L? : Metabolic
Step approach to acid base problems
2. If Respiratory
is it acute or chronic: ? (HCO3/PaCO2)
3. If Metabolic
what is anion gap? > 20, then I ۫ metabolic acidosis
Is respiratory compensation (fall in PaCO2/HCO3) as predicted ?
4. What is excess AG ( ∆ Gap or gap-gap)
Step approach to acid base problems
∆ gap = [calculated AG – nl AG (~12)] +measured HC03
if ∆ gap > nl Serum HCO3 (30), there is underlying metabolic alkalosis
if ∆ gap less than normal [HC03] (23), there is an underlying metabolic, non anion gap, acidosis
< 15 mM/L
> 20 mM/L
Metabolic Alkalosis�acid loss
Metabolic Alkalosis
Retention of bicarbonate
Metabolic Alkalosis�Diagnosis:�Urinary Chloride
Chloride Responsive
Urinary Cl < 10
Vomiting
NG loss
Post hypercapnea
Prolonged diuretic
Chloride Resistant
Urine Cl : 10 – 15
Mineralocorticoid excess
Cushing’s
Licorice
Severe K depletion
Bartter’s
Treatment of alkalosis
Generally due to diuretics
Replace Cl- to enhance renal HCO3- clearance
Treatment of alkalosis
Saline administration
Renal retention of NaCl in distal tubules
Allows secretion of HCO3-
fall in urine pH with treatment
Treatment of alkalosis
Arginine Hydrochloride
Ammonium Chloride- beware in liver failure- metabolized to NH3
HCl 0.1-.2N - need central catheter
calculated doses
acid required in mEq/kg=
0.2 L/kg X [103-Cl-] or
0.5 L/kg X [HCO3- - 24]
give 1/2 dose over 3 hours then reassess
Metabolic acidosis
Sodium Bicarbonate for Acidosis�or not!!!!!!!!!!!!!!!!!
The data supporting treatment of pH alone does NOT EXIST …………………. pause ………………..icons fall,
ACLS : no data
In two RCT’s no difference between volume replacement and NaHCO3 therapy in improvement in global hemodynamics or response to catecholamines
Mathieu D, et al. Effects of bicarbonate therapy on hemodynamics and tissue oygenation in patients with Lactic Acidosis: a prospective controlled clinical study. Crit Care Med 19:1352,1991
Cooper DJ, et al. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective controlled clinical study. Ann Int Med 112:492, 1990.
Sodium Bicarbonate for Acidosis�or not!!!!!!!!!!!!!!!!!
Negative side effects of NaHCO3:
Sodium Bicarbonate for Acidosis�or not!!!!!!!!!!!!!!!!!
Recommended treatment if choose to use HCO3:
HCO3 defecit = 0.3 x BW in Kg x [HCO3 exp - HCO3 obs}
Metabolic Acidoisis and Mechanical Ventilation: Hyperventilation in DKA �Tasker RC, etal. Hyperventilation in severe diabetic ketoacidosis Pediatr Crit Care Med 2005; 6 405-411.
pH CSF determines CBF
[HCO3] csf changes slowly over hours
PCO2 changes quickly across BBB
In DKA low [HCO3] csf and compensatory hyperventilation lowers PaCO2, and maintains a relatively increased pH csf
IF DKA patient intubated +/or given HCO3, and goal is normal PaCO2, then Pcsf CO2 ↑ rapidly, pH csf ↓ and brain may become hyperemic
ACID – BASE� Hyperventilation in DKA �Tasker RC, etal. Hyperventilation in severe diabetic ketoacidosis Pediatr Crit Care Med 2005; 6 405-411.
ACID – BASE�∆ Gap, ∆ / ∆, SID
Anion Gap (AG)
= Na – (Cl + HCO3)
= 12 ± 2 mEq/L
∆ Gap
= [calculated AG – Normal AG (12 mM)] + measured serum [HCO3]
∆ Gap > 30 there is underlying metabolic alkalosis
∆ Gap < 23 there is a non anion gap acidosis
ACID – BASE�∆ Gap, ∆ / ∆, SID
Anion Gap (AG)
situations to know to avoid false interpretation
Profound metabolic alkalosis (elevated gap due to HCO3) pH > 7.5
Hypoalbuminemia (<3.0)
Excess or Deficit in Plasma Water (use SID)
Anion gap acidosis
Renal Failure
Lactic Acidosis
Ketoacidosis (DKA, starvation, alcohol)
Rhabdomyolysis
Ingestions
ASA, methanol, ethylene glycol, paraldehyde, toluene
Non gap acidosis
Acid Administration- hydrochloric acid administration, HAL
HCO3- losses
GI
Renal- RTA (proximal type 2), ketoacidosis
Impaired Renal Acid Excretion
RTA Type 1
with elevated K (Type 4 RTA)
Renal insufficiency
Non gap acidosis
RTA
Distal RTA, Type 1
urine pH > 6, mild to moderate acidosis
Proximal RTA, Type 2
urine pH > 6, only mild acidosis
Type 4, (Hyperkalemic)
primary aldosterone deficiency, psuedohypoaldosteronism
Iatrogenic RTA
ampho B, aminoglycosides
Non gap acidosis�RTA?
RTA ?
Urinary anion gap
[uNa +uK ] –[-uCl]
if Na + K is less than Cl, there is another cation, eg NH4, normal distal tubular acidification
If Na + K is greater than Cl, it suggests absence of possibility of distal RTA
ACID – BASE�∆ Gap, ∆ / ∆, SID
Anion Gap (AG) and albumin
AG affected by negative charges on proteins, esp albumin
AG falls 2.5 mEq/L for every 1 g dL ↓ in [albumin]
Note :SID accounts for albumin, PO4
ACID – BASE�metabolic acidosis �∆ / ∆,
∆ / ∆ (∆ anion gap / ∆ HCO3)
In Lactic Acidosis ∆ / ∆ usually 1.6: 1, why?
HL + NaHCO3 → NaL + H2CO3 → CO2 + H2O
looks like AG/HCO3 should be 1:1
But
lactate remains in ECF, whereas H + is 50% buffered by bone and cells (takes several hours)
ACID – BASE�metabolic acidosis �∆ Gap, ∆ / ∆
∆ / ∆ (∆ anion gap / ∆ HCO3)
In Ketoacidosis 1:1 why?
urinary losses of ketoacids as Na and K salts of β Hydroxy buterate and aceto acetate
Lowers AG without affecting the [HCO3]
while in LA, urinary acid loss minimal (renal failure and tubular re uptake of lactate)
ACID – BASE�metabolic acidosis �∆ Gap, ∆ / ∆,
∆ / ∆ (∆ anion gap / ∆ HCO3)
In DKA :AG ~ GFR
IF hypovolemic early on → low GFR
AG is high and ∆ / ∆ > 1.6/1 (looks like LA)
but,
when Volume and GFR restored
lose keto acids in urine and ∆ / ∆ is < 1 and AG near nl
ACID – BASE�metabolic acidosis �∆ Gap, ∆ / ∆
∆ / ∆ (∆ anion gap / ∆ HCO3)
D Lactic Acidosis
Patient on multiple antibiotics post jejuno ileal bypass surgery;
ataxic, slurred speech.
Na 137, Cl 102, HCO3 13, LA 2, pH 7.22
AG = 22 ; ∆ Gap =23
∆ / ∆ (∆ anion gap / ∆ HCO3) = 10-12/ 10-12 = (~1)
????
ACID – BASE�metabolic acidosis , ∆ Gap, ∆ / ∆
∆ / ∆ (∆ anion gap / ∆ HCO3)
D-lactic acidosis
short gut, CHO feeds, antibiotics, jejunal bypass
overgrowth of Gram + eg Lactobacillus
CNS symptoms: confusion, ataxia, slurred speech (drunk)
Episodic metabolic acidosis, AG is increased but
Increase in AG less than predicted (ie ∆ / ∆ low)
nl Lactate, no ketones,
Blood Gases and Temperature�For the hypothermia range that we are using, the distinction is probably not clinically significant.�The implications of knowing which standard is being used...�
the "alpha stat" standard (i.e. all ABG's measured at 37C)
"pH stat" standard (i.e. ABG's corrected for pt temp).
As the body is cooled:
total CO2 stores are constant, more CO2 is dissolved into the blood causing "alkalosis" (increased HCO3, decreased pCO2).
alpha stat standard,
No change in management
although the patient may be "alkalotic", the measured pH will be normal.
pH stat standard
decrease the minute ventilation on the ventilator and allow the pCO2 to rise to regain "normal" pH. As the patient is rewarmed, need to remember to increase the minute ventilation since he/she would become acidotic without any changes.
Blood Gases and Temperature��
Which standard ?
Since humans are mammals (non hibernating) intuitively, could manage hypothermia in a pH stat manner
As cooling occurs "alkalosis" actually preserves the normal H+/OH- ratio, so at say 25C, a 7.4 pH is actually "physiologically acidotic" and the net result is that enzyme function may be impaired. It is believed that this "acidosis“ especially intra cell, is deleterious
So the alpha stat approach provides better cellular protection during deep hypothermic circ arrest.
ABG's ( U of M) are being reported by the alpha stat standard, so no special changes in patient management is needed.
ABGs ( U of M) are reported as PaO2 or PaCO2 measurements at 37 C. Temperature correction can be requested.
PaO2 decreases 7% per degree C lower than 37 C and PaCO2 decreases 4% per degree C lower than 37 C.
For temps > 37 C, opposite happens - PaO2 increases 7% per degree C greater than 37 C and PaCO2 increases 4% per degree C higher than 37 C.
So: appreciate that a PaCO2 of 35 (at 37C) is approximately 28 (at 32C).
ACID – BASE�metabolic acidosis �SID
TWO DIAGNOSTIC SYSTEMS: based on assumptions or are calculated ( SBE)
1. PLASMA HC03 AND AG
2. BASE EXCESS/DEFECIT
NEITHER ACCOUNTS FOR NON HCO3 BUFFERS: ALBUMIN AND PHOSPHORUS, changes in water
ACID – BASE�metabolic acidosis �SID
MAIN NON-HCO3 BUFFERS ARE
PLASMA PROTEIN(ALBUMIN)
INORGANIC PHOSPHORUS
Fencl, V Am J Resp Crit Care Med 2000. 162:2246-51
SID calculations:
SID = [HCO3] +[ALB]+[Pi]
XA= ( [Na]+[K]+[Ca]+[Mg])-[Cl]-SID
CORRECTED CL =
WATER EXCESS/DEFECIT = ABNL Na
[Cl] corrected = [Cl] obs x [Na] nl/[Na]obs
Close enough for jazz calculation
SID =
[HCO3]+ .28x[Alb]gms/dl+1.8 x [Pi]mmol/l
Usually 38 - 42
ACID – BASE�metabolic acidosis �SID
HYPOALBUMINEMIA
ALB IS A WEAK ACID
In traditional analysis:
IN THE HCO3 or AG SYSTEM:
EFFECTS HCO3 ESTIMATE IN AG ESTIMATE
IN THE BE APPROACH
NO DISTINCTION BETWEEN A DEFICIT OR EXCESS OF NON VOLATILE Acid
HYPOALBUMINEMIA HAS AN ALKALIZING EFFECT
(deficit of weak acid)
ACID – BASE�metabolic acidosis �SID
HYPOALBUMINEMIA HAS AN ALKALIZING EFFECT
(deficit of weak acid)
AG affected by negative charges on proteins, esp albumin
AG falls 2.5 mEq/L for every 1 g dL ↓ in [albumin]
Note :SID accounts for albumin, PO4
SID in practice
The strong ion gap predicts mortality in children following cardiopulmonary bypass
Durard,A, Tibby SM, Skellet S et al. Pediatr Crit Care Med 2005; 6:281-285.
Raised Strong Ion Gap > 3 mEq/L correlated with 4 / 5 deaths
SIG was superior to serum Lactate as a predictor
Defining Acidosis in postoperative cardiac patients using Stewart’s method of strong ion difference�Murray DM, Olhsson V, Fraser JI. Pediatr Crit Care Med 2004; 5:240-245.
SID=[HCO3] +[Alb]+[Pi]
Tissue Acids ([Na]+[K]+[Ca]+[Mg]) – [Cl]-SID
Unmeasured acids (UMA) given by:
TA=UMA+Lactate
AG corr = AG + .25 x [44-Alb obs]
Cl corr = Cl obs x [Na] nl/[Na] obs
Defining Acidosis in postoperative cardiac patients using Stewart’s method of strong ion difference�Murray DM, Olhsson V, Fraser JI. Pediatr Crit Care Med 2004; 5:240-245.
150 samples; 44 pts; age: 3.5 months
25/44 CPB
TA in 60/150 samples
due to:
↑ UMA in 44/60(73%)
↑ LA in 6/60
↑ UMA and LA in 10/60
Defining Acidosis in postoperative cardiac patients using Stewart’s method of strong ion difference�Murray DM, Olhsson V, Fraser JI. Pediatr Crit Care Med 2004; 5:240-245.
Hyperchloremia in 19/150
BD gave an apparent acidosis in 44/150, but in 21/44 TA was nl (<5 mEq)
BD was normal in 106, but 14/106 had ↑ in TA
Defining Acidosis in postoperative cardiac patients using Stewart’s method of strong ion difference�Murray DM, Olhsson V, Fraser JI. Pediatr Crit Care Med 2004; 5:240-245.
NOTE
Units for albumin’
Phos,
18: COPD, CHF; low albumin is cause of Met Alkalosis. Traditional method reports a high HCO3 and BE of +9. but, SID, Na, Cl, and XA are nl.
This is simply a hypoalbuminemic metabolic alkalosis.
59: MSOF; SID is ⭣ by ~ 20. this is caused by both plasma H20 ⭡ , ⭡ Cl(corrected), and by ⭡ in XA.
The low albumin mitigates the SID acidosis. BE only detects ½ of change in SID. Note AG is low nl, but abnormal amount of anion showed by high XA. The acidemia is mitigated by the hypocapnea as one would predict.
Fencl, V Am J Resp Crit Care Med 2000. 162:2246-51
18: COPD, CHF; low albumin is cause of Met Alkalosis. Traditional method reports a high HCO3 and BE of +9. but, SID, Na, Cl, and XA are nl.
This is simply a hypoalbuminemic metabolic alkalosis.
59: MSOF; SID is ⭣ by ~ 20. this is caused by both plasma H20 ⭡ , ⭡ Cl(corrected), and by ⭡ in XA.
The low albumin mitigates the SID acidosis. BE only detects ½ of change in SID. Note AG is low nl, but abnormal amount of anion showed by high XA. The acidemia is mitigated by the hypocapnea as one would predict.
Fencl, V Am J Resp Crit Care Med 2000. 162:2246-51
63: Post Cardiac Arrest. There is a ⭣ SID of ~ 10, which results from high XA and low plasma water, which offset. The resultant low SID acidosis is hidden by the alkalinization secondary to the ⭣ albumin. BE misses the high XA acidosis and interprets this as a mild metabolic alkalosis. The HC03 is high end of nl, and AG misses the high abnormal anions. No Cl excess is present even though the Cl observed would suggest it.
The alkalosis is from low PaC02
81: ARDS and Sepsis; SID is reduced by ~12, owing to plasma water excess and very high XA and Pi. These are mitigated by the alkalosis from ⭣Cl, and low albumin thus the [HC03] is only slightly low. AG observed is ⭡, and Base deficit is only – 4. The severity of the acidosis is underestimated by traditional methods
Blood Gases
Blood Gases
Alveolar-arterial gradient
PAO2 – PaO2
(Pb – PH2O) x FiO2 – PaCO2/R
Blood gases
Shunt vs V/Q
Ventilation ~ PaCO2
PaCO2 = .863 x CO2 Production
Rate (tidal volume – dead space)
VCO2 is a constant
Estimating in a close enough for jazz world:
Unless Vd increases, if RR or Vt increase, PaCO2
Falls arithmetically and proportionally
and vice versa