ACID-BASE BALANCE

Introduction:

Limitations of the ABG interpretation “by the numbers” method. 
A. Oversimplification of how the body actually works
1) In many situations, body will not compensate to bring pH back to within normal limits. (i.e.—in a metabolic acidosis, body will try to hyperventilate only so much to compensate)
2) It’s possible that you can have an alkalosis and an acidosis, even though the pH may reflect only an acidemia or alkalemia. (A patient may have a chronic respiratory acidosis due to COPD and an acute metabolic alkalosis secondary to hypokalemia).
B. To properly interpret an ABG, it is important to interpret it not in isolation, but in the context of the entire clinical picture.
C. It is important to remember the interpretation by the numbers and to do that process first. Then refine your interpretation in light of what you will learn in the next couple of weeks and the clinical picture of the patient.

1. Henderson-Hasselbach equation
a. used by blood gas machines to compute bicarbonate
B. pH = pKa + log base/acid salt
C. pH = pKa + log HC03/H2CO3
D. pKa = 6.1 for the bicarbonate/carbonic acid buffer pair
e. pKa is the value of the pH if there were equal concentrations of base and acid
f. normal bicarb. is 24 meq/l
G. Normal H2C03 = PaCO2 X .03 = 40 X .03 = 1.2 Meq/L
H. pH = 6.1 + log HC03/H2C03
= 6.1 + log 24/1.2
= 6.1 + log 20
= 6.1 + 1.3
= 7.4

Co2	C02 X.03	HC03	pH
40	1.2	24	7.4
80	2.4	24	7.1
20	.6	24	7.7
40	1.2	48	7.7
40	1.2	12	7.1
80	2.4	28	7.16
20	.6	20	7.62

As a general rule, every acute rise in PaC02 by 10 mm Hg will drop the pH by .05, assuming no co-existing metabolic problem.

As a general rule, every acute drop in PaC02 by 5 mm Hg will increase the pH by .05, assuming no co-existing metabolic problem.

2. Buffer system- presence of a weak acid and its conjugate base which will combine with exogenous acids and bases to decrease the change in the pH
i.e. add HCL to solution with pH of 7.4 without buffers
pH may drop to 5.7 but only drops to 7.1 because of buffering systems
a. major buffering system:-bicarbonate/C02
1) actually not good because of low pKA
2) however, because pAC02 easily removed by lungs, makes it a good buffer
3) CO2 + H20 ßà(carbonic anhydrase)<-à H2C03 <àH+ + HCO3-
4) Add C02 then bicarb will be produced
5) Add bicarb. then C02 will be produced

B. Hgb, plasma proteins and phosphates all do some buffering

4a.  Predicted Pa02 (ON ROOM AIR) = 103 - (.42 X AGE)
i.e. 80YR. = 103 - (.42 X 80) = 69
103 is the PA02 when the pCO2 is 40.
Predicted A-a gradient = (.42 X AGE)
The more useful formula for this is as follows:
Predicted Pa02 (ON ROOM AIR) = PA02 - (.42 x age) in order to calculate the Pa02 given the age and the PaC02.
i.e. a 73 yr old man has a PaC02 of 28 and a Pa02 of 56. What is his predicted Pa02.
Step 1: PA02 = 150 – (28 x 1.25)
= 115
Step 2: Predicted A-a gradient = 73 x .42 = 31
Step 3: Predicted Pa02 = PA02- Pred. A-a gradient or, in this case, 115 – 31 = 84 torr
This man’s actual Pa02 is 28 torr less than predicted indicating a low V/Q

4b. Classifications of severity for hypoxemia:
Hypoxemia (mild) - 60-75 unless predicted for age
Moderate - 40- 59
Severe - < 40

Clinically one treats low Pa02 if < 55-60 torr.
Only times when justifiable to keep Pa02 > 100:
     1. Head injury
     2. Post stroke
     3. Fresh MI
    4. Carbon monoxide poisoning

4c. Causes of hypoxemia
    a. altitude
    b. hypoventilation
    c. low V/Q
    d. anatomic shunting
    e. capillary shunting

Differential diagnosis- on room air at sea level:
a. IF Pa02 + PaC02 > 140 then pt. not on room air
b. If Pa02 + PaC02 between 110 torr and 140 then hypoxemia due to hypoventilation
c. IF Pa02 + PaC02 < 110, then hypoxemia due to c, d,
or e above

4d. Hypoxia
a. Pt. can be hypoxic and not be hypoxemic and vice versa
b. Signs of hypoxia
1. No way to absolutely determine if hypoxia present(except for perhaps by increased blood lactate levels (> 2.5))
2. signs: confusion, decreased cardiac output, low mean arterial pressure(less than 60 mm Hg), low Pv02 (< 25-35 torr), very low or high Ca-v02, severe hypoxemia (Pa02 < 40 torr) low Hgb levels (less than 10 grams %) and lactic acidosis
c. Types of hypoxia
     1. Hypoxemic hypoxia (Pa02 must be less than 60)
rx- oxygen and/or PEEP
     2. Circulatory or stagnant hypoxia
diagnosis-low cardiac output, low MAP, high Ca-V02
     rx- inotropic agents(i.e. dobutamine and dopamine)
     3. anemic hypoxia
diagnosis-Hgb less than 10 gm% or carbon monoxide poisoning with carboxyhemoglobin levels > 20-30% and low Ca-v02 (< 3.5 VOL %)
      rx. anemia-packed cells
CO poisoning-100% 02 and/or hyperbaric oxygen
     4. Histotoxic hypoxia (cyanide poisoning)

  5. Bicarbonate values
a. Actual
1. Calculated by blood gas machine using H-H equation
2. According to C02 + H20 reaction to make bicarb and H+, actual bicarb will change with changes in C02
a. Increasing C02(for every 10 torr > 40) will increase bicarb by 1 meq.
(actual PaC02 - 40)/10 = predicted bicarb change
b. decreasing PaCO2(for every 5 torr < 40) will decrease bicarb. by 1 meq. (40 - actual PaCO2)/5 = predicted bicarb change
c. These changes have nothing to do with compensation, it's just chemistry
d. These stoiochiometric changes in bicarb. make looking at absolute values of bicarb. misleading when attempting to interpret metabolic component of blood gas

b. Standard bicarb.
1. a calculated value to control to control for "respiratory" changes in bicarb value
2. Designed to allow you to look at bicarb. level
as if the pac02 was 40 torr
3. Normally 22-26 meq/l
c. Base excess-similar to standard bicarb. in intent
d. Problems with b and c above is that they're based on in vitro or test tube changes which are not a perfect picture of what happens in vivo

6. Acid-base disorders
a. Respiratory acidosis (acute hypoventilation)
1. Causes
a. CNS depression (narcotic or barbiturate OD)
b. Neuromuscular diseases
c. Variety of severe pulmonary diseases
d. Fatigue
e. Cardiac arrest or apnea
2. RX-Continuous Mechanical Ventilation unless immediately correctable.

B. Resp. alkalosis(acute hyperventilation)
1. Causes
a. Hypoxemia the most common cause seen in the hospital--think of this first
b. Anxiety-have pt. breathe in paper bag
c. Pain
d. Ventilator induced
e. CNS disorders
2. Treat cause: remember-hypoxemia the most common cause
if caused by anxiety-have pt. breathe in paper bag

 c. Metabolic acidosis
1. Causes
a. Lactic acidosis secondary to anaerobic metabolism in profound hypoxia
b. Diabetic ketoacidosis
c. Ingestion of acids (i.e. aspirin OD
d. Diarrhea
e. Renal disease
f. Methonol or ethylene glycol ingestion
2. Differentiation of cause, use anion gap
a. anion gap = (K + Na) - (Cl + HC03)
= 144 - 129 = 15 (normally 12-18)
Anion gap increased if metabolic acidosis caused by increase in unmeasured anions, (i.e. ketoacidosis, lactic acidosis, and ingestion of acids) You will have a normal anion gap in acidosis caused by a loss of bicarb(diarrhea or renal disease)
b. Lactic acidosis- look for signs of hypoxia or increased blood lactate levels (> 2.5)
c. Ketoacidosis- look at blood glucose levels(> 300)
d. Renal disease look at low urine output or high BUN (> 25) or creatinine (> 1.5)
3. Rx. sodium bicarbonate if ph < 7.20 (somewhat controversial)
also rx causes

D. Metabolic alkalosis
1. Differential diagnosis
a. Hypokalemia (k < 3.0 or lasix without taking k
b. Loss of stomach acid-look for prolonged vomiting or NG tube for more than a few days attached to suction)
c. Massive doses of steroids
d. Iatrogenic (overadministration of bicarb.
2. Rx. diamox or ammonium chloride if severe, otherwise rx. causes

7. Evaluating bicarb in respiratory conditions
1. Acute resp. acidosis and alkalosis given in #5
2. Chronic respiratory acidosis assumes must by at least 48 hours old for significant renal compensation to occur. since bicarb. should increase up to 4 meq for every increase in PaCO2 by 10 torr:
Expected HCO3 = 4 X {(PaC02 - 40)/10} + 24
i.e. If chronic PaCO2 = 65 then:
Expected HCO3 = 4 X {(65 - 40)/10} + 24 = 4 X 2.5 + 24 = 34 Meq
3. Since the lungs will compensate immediately for metabolic problems there is no such thing as an acute or chronic metabolic problem

8. Evaluating PaC02 in metabolic conditions
A. Met. acidosis-
1. Predicted PaC02 = (1.5 X ACT. HC03) + 8 (Winter’s formula)
a. If PaC02 is as predicted, then maximal compensation is present even though pH is < 7.35.
b. If PaC02 > pred., than have a resp. problem in addition to a metabolic problem
c. if PaC02 < predicted, then you have a resp. alk. in addition to met. acidosis
B. Met. alkalosis-PaC02 never goes above 50 to compensate for a met. alkalosis
If PaC02 > 50 torr than a chronic resp. acidosis must be present

8. Normal mixed venous gases (see text)
A. taken via Swan-Ganz catheter in pulmonary artery. Pv02 and Sv02 decreases with low arterial 02 content or low cardiac output

8. Bicarbonate administration given in met. acidosis
a. given only if pH < 7.20 (some say < 7.0)
B. (Base deficit x 1/4 body wt. in kg.)/2 = meq of HCO3 needed
C. Meq of HCO3/44 = number of amps required

9. A. Heparin is acidotic and if too much is used will cause measured pH values to be lower than actual
b. Air bubbles have essentially 0 PC02 and 150 P02 so:
1. measured pH > than actual
2. measured PaCO2 < than actual
3. measured Pa02 usually > than actual unless the actual Pa02 IS > 150