This document summarizes acid-base physiology and interpretation of arterial blood gases. It defines the Henderson-Hasselbalch equation and describes how the respiratory and renal systems regulate pH. Primary respiratory and metabolic acid-base disorders are explained. The anion gap, urinary anion gap, and osmolar gap are defined and their clinical significance discussed. Various acid-base imbalances including respiratory acidosis/alkalosis and metabolic acidosis/alkalosis are outlined along with their causes. Steps for interpreting arterial blood gases and examples of analysis are provided.

1. HENDERSON EQUATION:
HCO3 BUFFERING EQUATION=
HCO3⁻+H⁺↔H2O+CO2
??TO REGULATE PH:
-RESPIRATORY :RR & TV →CONTROL PaCO2
-RENAL – REABSORBTION OF HCO3.
1RY RESPIRATORY DISORDER:ANY CHANGE IN
PaCO2 CAUSES INITIAL CHANGE IN PH – KIDNEYS
SLOWLY RESPONDS IN THE OPPOSITE DIRECTION
BY DUMPPING OR HOLDING ON TO HCO3.
1RY METABOLIC DISORDER : CHANGE IN HCO3
CAUSES CHANGE IN PH & RESPIRATROY RATE
IMMEDIATELY ↑OR ↓.

2. ANION GAP:
IS A DETERMENATION OF UNMEASURED ANIONS , WHICH IF
ELEVATED INDICATES INCREASING IN UNMEASURED ACIDS”
KETOACIDS, LACTATE , METHANOL, ETHYLEN GLYCOL”.
THESE ACIDS COMPOSED AN UNMEASURED ANIONS WITH +VE
CHARGED HYDROGENE.
?WHY ANIONS NOT CATIONS?
AG= Na – “ HCO3 + CL”., N= 10 ±3
?NAGMA ??HAGMA??
URINARY ANG = “Na+K” – CL., N= 0
+VE UAG : SUGGEST LOW URINARY NH4 AS IN RTA
-VE UAG SUGGEST HIGH U NH4 AS IN DIARRHEA
UAG: DETERMINED USING THE MEASURED IONS IN THE
URINE , MAINLY NH4, MOSTLY USED TO DEFFERENTIATE
RTA FROM OTHER CAUSES OF NAGMA .

3. OSMOLAR GAP “OG”:
HELPS TO DETERMINE WHETHER UNMEASURED
OSMOLES ARE CIRCULATING IN THE BLOOD &
POSSIBLY CAUSING ACIDOSIS ?
OG= OSMmeasured”s. osm.”- OSMcalculated
CLCULATED OSM.= 2”Na”+BUN/2.8 +GLUCOSE/18
NORMAL OSM GAP= 0
*IF GLUCOSE & BUN ARE NORMAL ., JUST 2Na
CAN GIVE US THE RESULT OF OSM.

4. ANION GAP OSMOLAR GAP PATHOLOGICAL CONDITION
INCREASING AG INCREASING OG METHANOL & ETHYLENE GLYCOL
KETO & LACTIC ACIDOSIS
CRF
INCREASING AG INCREASING OG SALICYLATE POISINING
NORMAL AG INCREASING OG ISOPROPYL ALCOHOL
ACETON INJESTION
NORMAL AG NORMAL OG CO POISINING

5. ACID BASE ANALYSIS
N PH = 7.35-7.45
N PaCO2= 35-45
IF PH < 7.35= ACIDOSIS
IF PH > 7.45= ALKALOSIS
CO2 IS AN ACIDIC GAS & DIRECTLY RELATED TO
ALVEOLAR VENTILATON.

6. MECHANISM OF
REGULATION
PH < 7.35
ACIDOSIS
PH > 7.45
ALKALOSIS
RESPIRATORY ↑ PCO2 ↓PCO2
IF PCO2 NORMAL OR ↓== ==COMPENSATORY
RESP.
METABOLIC ↓HCO3 ↑HCO3
IF HCO3 NORMAL OR
OPP.=
= COMPENSATORY
METAB.

7. ARTERIAL BLOOD GASE INTERPRETATION:
STEP QUESTION ? ANSWER
PH ? DETERMINE S. PH ACIDOSIS ?? ALKALOSIS ?
ANION GAP “
AG”
? AG
? CHANGE IN AG = ∆ AG =
MEASURED AG – N AG
AG= Na- “ HCO3+CL= 10 ±3
∆ AG = MEASURED – NORMAL
AG
= MEASURED -10
HCO3⁻ ?EXPECTED HCO3⁻??
COMPARE EXPECTED
HCO3 TO ACTUAL HCO3
EXPECTED HCO3 = 25- ∆ AG
Pa CO2 ? EXPECTED PaCO2 ?
COMPARE EXPECTED
PaCO2 TO ACTUAL PaCO2
EXP. PaCO2= 15+MEASURED
HCO3⁻

8. UFFERING SYSTEM
1- EXTRACELLULAR
2- INTRACELLULAR
THE MIN ECS BUFFER IS HCO3⁻
MAIN JOB OF HCO3⁻: IS TO COMPLEX WITH ACIDS TO NEUTRALIZE THEM &
KEEP THE BLOOD PH STABLE .
FOR EACH 1 INCREASING IN ACIDIC ANIONS IN THE BLOOD THE HCO3
DECREASED 1 TO NEUTRALIZE IT

9. →→→ABG INTERPRETATAION:
1-PH--?ACIDOSIS ?ALKALOSIS ?
2-AG =Na-(HCO3+CL)
3-∆AG= AG-10
4- HCO3⁻ : EXPECTED HCO3= 25-∆AG
COPARE EXPECTED HCO3 TO ACTUAL HCO3:
IF ACTUAL HCO3 > EXPECTED =METABOLIC ALKALOSIS
IF ACTUAL HCO3 < EXPECTED =METABOLIC ACIDOSIS “NAGMA”
-PaCO2= EXP. PaCO15+ACTUAL HCO3
COMPARE EXPECTED PaCO2 TO ACTUAL :
IF ACTUAL PaCO2 > EXPECTED =RESPIRATORY ACIDOSIS
IF ACTUAL PaCO< EXPECTED = RESPIRATORY ALKALOSIS .
*ABG & ELECTROLITES SHOULD BE DRAWN AT THE SAME TIME

10. METABOLIC ACIDOSIS :
CAUSES:
1-OVERPRODUCTION OF LACTIC ACIDS OR KETOACIDS.
2-HCO3 WASTING “RTA OR DIARRHOEA”
3-UNDEREXECRETION OF ACID –RF.
4-INGESTION OF AGENTS THAT ARE:
ACIDS “SALICYLATE”, OR MEATBOLIZED TO ACIDS ” METAHANOL ETHYLENE
GLYCOL”, OR
CAUSES ACIDOSIS OR KETOACIDOSIS “ISONIAZIDE OR IRON”

11. TYPES OF METABOLIC ACIDOSIS :
NAGMA & HAGMA
1-NAGMA :ALWAYS HYPERCHLOREMIC:
CAUSES :HARDSS
-RTA , DIARRHOEA –USE URINARY AG
-CARBONIC ANHYDRASE INHIBITOR
-HYPERALIMENATION WITH TPN
-ADDISON DISEASE
-PANCREATIC FISTULA
-NH4CL INGESTION

12. HAGMA :
CAUSES “MEDUSAL OR MUD PELS”
-M=METHANOL INGESTION, Rx.”FOMPEZOLE & HD”
-E= ETHANOL GLYCOL INGESTION, Rx.”FOMPEZOLE & HD”
-D= DKA
-U= UREMIA
-S= SALICYLATE INGESTION
-A = ALCOHOLIC KETOACIDOSIS
-L = LACTIC ACID PRODUCTION.

13. METABOLIC ALKALOSIS :
HIGH PH , HIGH HCO3
CAUSES :
VOLUME CONTRACTION: VOMITING , BURNS ,
INGESTION OF BASE , POTASSIUM DEPLETION-
DIURETICS
URINARY CL >10 –CAUSES:
CUSHING SYNDROME, 1RY
HYPERALDOSTERONISM,SEVER HYPOKALEMIA .

14. RESPIRATORY ACIDOSIS :LOW PH , HIGH PaCO2
CAUSES:
TYPE 2 RESPIRATORY FAILURE “HYPERCAPNIA”
COPD ,
NEUROMASCULAR DISEASE.
RESPIRATORY ALKALOSIS :HIGH PH, LOW PaCO2
CAUSES:
HYPERVENTILATION,
CNS- STROKE, SAH, MENINGITIS
ASTHMA ., ANXIETY, HIGH ALTITUDE, FEVER ,
PREGNANCY, PE, RX LIKE SALICYLATE.

15. EXAMPLES:
1- BLOOD GAS RESULT:
PH 7.5, PaCO2=20., PO2= 15, Na = 140.,
CL=103, HCO3=15
-PH = ALKALOSIS
-AG=140-”103+15”=22—HIGH AG
-∆AG=22-10=12
-HCO3 : EXP. HCO3= 25-∆AG=25-12=13
MEASURED HCO3=15—CLOSED ENOUGH=NO METABOLIC DISORDER.
-PaCO2: EXPECTED PaCO2=15+MEASURED HCO3
= 15+15= 30
ACTUAL PaCO2= 20, LESS CO2 THAN EXPECTED ---
HIGH PH & LOW PaCO2=RESPIRATORY ALKALOSIS .
PATIENT HAS RESPRATORY ALKALOSIS WITH COMPENSATORY HAGMA.....THIS CAN
BE SEEN IN SALICYLATE POISINING , WHICH INITIALLY INCREASE THE RESPIRATORY
DRIVE CAUSING RESPIRATORY ALKALOSIS , THEN METABOLIC ACIDOSIS DEVELOPS.

16. 2- BLOOD GAS RESULT:
PH 7.3., PaCO2= 40, PO2= 24
Na 145, CL 100, HCO3= 24
-PH = ACIDOSIS
-AG = 145- “100+24”=21
-∆AG = 21-10=11
-EXP. HCO3= 25-∆AG=25-11=14, COMPARE TO
ACTUAL HCO3= 24→MORE THAN EXP.=ADDITIONAL METABOLIC
ALKALOSIS .
-EXP. PaCO2=15+ACTUAL HCO3=15+24=39, COMPARE TO ACTUAL PaCO2 –
CLOSE ENOUGH =NO ADDITIONAL RESPIRATORY DISORDER .
Ds.: 1RY HAGMA WITH METABOLIC ALKALOSIS .