Actual base excess is the concentration of titratable base when the blood is titrated with a strong base or acid to a plasma pH of 7.40 at a pCO2 of 40 mmHg (5.3 kPa) and 37 °C at the actual oxygen saturation.
“ Base excess” is the absolute deviation (in mmol/L) of the buffer base amount from the normal level in blood.
“Buffer base” , represents the , blood’s total buffer capacity, comprising the bicarbonate, hemoglobin, plasma protein, and ,phosphate buffer systems ,normal buffer base level
2. HANDERSON’S AND HASSELBACH’S EQUATION:
• PH = PKA + LOG10 [HCO3
-
]
[H2CO3]
PH= 7.35-7.45 HCO3
-
= 24-28 MMOL/L
PO2= 80-100 MMHG PCO2= 35-45 MMHG
• BICARBONATE IS SECOND LARGEST ANION OF PLASMA
• COMPOSED OF TRUE BICARBONATE, CARBONATE AND CO2
BOUND TO CARBAMINO COMPOUND (RCNHCOOH)
• DISSOLVED CO2 (DCO2) IS UNDISSOCIATED CARBONIC ACID AND
FREE CO2 (PHYSICALLY DCO2)
• H2CO3= ∞ X P CO2 = 0.03X 40 MMHG= 1.224 MMOL/L
• [HCO3
-
] = 25 = 20
[H2CO3] 1.25 1
3. BASE EXCESS OF ECF OR STANDARD BASE
EXCESS:
• ACTUAL BASE EXCESS IS THE CONCENTRATION OF
TITRATABLE BASE WHEN THE BLOOD IS TITRATED
WITH A STRONG BASE OR ACID TO A PLASMA PH OF
7.40 AT A PCO2 OF 40 MMHG (5.3 KPA) AND 37 °C AT THE
ACTUAL OXYGEN SATURATION.
• “ BASE EXCESS” IS THE ABSOLUTE DEVIATION (IN
MMOL/L) OF THE BUFFER BASE AMOUNT FROM THE
NORMAL LEVEL IN BLOOD.
• “BUFFER BASE” REPRESENTS THE BLOOD’S TOTAL
BUFFER CAPACITY, COMPRISING THE BICARBONATE,
HEMOGLOBIN, PLASMA PROTEIN, AND PHOSPHATE
BUFFER SYSTEMS. THE NORMAL BUFFER BASE LEVEL
IS 48 ± 2 MMOL/L.
4. • BE WAS MODIFIED TO ‘STANDARDIZE’ THE
EFFECT OF HEMOGLOBIN IN ORDER TO
IMPROVE THE ACCURACY OF BE INVIVO .
• THIS EFFECT IS UNDERSTOOD TO BE DUE
TO EQUILIBRATION ACROSS THE ENTIRE
EXTRACELLULAR FLUID SPACE (WHOLE
BLOOD PLUS INTERSTITIAL FLUID).
• THUS, THE TERM ‘STANDARD BASE EXCESS’
(SBE) HAS BEEN GIVEN TO THIS VARIABLE,
WHICH BETTER QUANTIFIES THE CHANGE IN
METABOLIC ACID–BASE STATUS INVIVO .
• SBE = 0.9287 × (HCO3
–
– 24.4 + 14.83 × [PH –
7.4])
5. BUFFERS:
• WEAK ACID AND SALT OF STRONG BASE OR
WEAK BASE AND SALT OF STRONG ACID
• RESIST THE CHANGE IN PH
• BUFFERING CAPACITY: PH = PKA ± 1
MAJORBODY BUFFER:
• BICARBONATE BUFFER: PRINCIPLE ECF BUFFER
CONSISTING OF CARBONIC ACID (THE PROTON
DONOR) AND BICARBONATE (THE PROTON
ACCEPTOR)
• EFFECTIVE BUFFER AT PHYSIOLOGICAL PH
BECAUSE:
• MOST ABUNDANT BUFFERING SYSTEM (60%)
• CO2 CAN READILY BE DISPOSED OR RETAINED BY LUNGS
• THE RENAL TUBULES CAN INCREASE OR DECREASE THE RATE OF
RECLAMATION OF HCO3
-
FROM GLOMERULAR FILTRATE.
6. PHOSPHATE BUFFER:
• INTRACELLULAR BUFFER PI : 5% ORG.P:16%
(2,3BPG)
• PKA : 6.86, VERY EFFECTIVE INTRACELLULARLY
• H2PO4
-
IS PROTON DONOR HPO4
--
AS PROTON
ACCEPTOR
PROTEIN BUFFER: ALBUMIN CONTAINING IMIDAZOLE
GROUPS OF HISTIDINE (PKA 7.3) OF WHICH 16 ARE
PRESENT FOR EACH ALBUMIN.
HEMOGLOBIN BUFFER: MAJOR PART OF BUFFERING
IN RBC
• HIGH CONTENT OF HISTIDINE (IMIDAZOLE GROUPS)
• PKA VALUES OF OXYGEN LINKED ACID BASE
GROUPS DECREASE WHEN DHB IS OXYGENATED
• THE PKA SHIFT ALSO CAUSES A LIBERATION OF H+
UPON OXYGENATION OF HEMOGLOBIN, A
PHENOMENON IS CALLED HALDANE EFFECT
• BUFFERING OF HB= 4 X BUFFERING OF PROTEIN
7. METABOLIC ACIDOSIS
A. INCREASED ANION GAP METABOLIC ACIDOSIS
(NORMOCHLOREMIC ACIDOSIS):
1.INCREASED PRODUCTION OF ORGANIC ACIDS THAT
EXCEEDS RATE OF ELIMINATION
• DIABETIC KETOACIDOSIS:
INCREASED PRODUCTION OF KETONE BODIES LIKE
ACETOACETATE, ß HYDROXYBUTYRATE
• LACTIC ACIDOSIS: INCREASED PRODUCTION OF
LACTIC ACID (>2MMOL/L) IN CASES OF:
• TISSUE HYPOXIA
• LIVER DISEASE
• ETHANOL INTOXIFICATION
8. 2.IMPAIRED EXCRETION OF H+
IONS BY KIDNEY:
• RENAL FAILURE (GFR< 20ML/MIN) :
• DECREASE GFR AND LOSS OF FUNCTIONAL
RENAL TUBULES
• DECREASE NH3 FORMATION AND NA+
-H+
EXCHANGE
• DECREASE H+
ION EXCRETION METABOLIC
ACIDOSIS
3.INGESTION OF ACIDIC DRUGS OR TOXINS
WHICH ARE METABOLIZED TO ACIDS:
SALICYLATE INTOXIFICATION :
• MIXED ACID BASE DISORDER (RESPIRATORY
ALKALOSIS AND METABOLIC ACIDOSIS)
9. TOXIN AND OTHER CHEMICALS
• METHANOL HCHO + HCOOH
• ETHYLENE GLYCOL GLYCOLIC ACID +
OXALIC ACID
B. NORMAL ANION GAP ACIDOSIS
(HYPERCHLOREMIC ACIDOSIS)
• LOSS OF HCO3
-
FROM GI OR URINE:
• DIARRHEA
• RENAL TUBULAR ACIDOSIS(RTA)
• CARBONIC ANHYDRASE INHIBITORS (DIURETICS)
EG. ACETAZOLAMIDE, MAFENIDE
10. ANION GAP
• THE TOTAL BODY CONCENTRATION OF ANIONS = CATIONS
• AG = NA+
+(K+
) – (CL-
+ HCO3
-
)
• THE AG ACCOUNTS FOR UNMEASURED ANIONS SUCH AS
ENDOGENOUS ACIDS (PHOSPHATES, LACTATE, SULFATES,
ETC) AND ALBUMIN (PROTEINATE-
)
• NORMALLY THE UNMEASURED ANIONS EXCEED THE
UNMEASURED CATIONS.
• NORMAL VALUE IS 12±4.
• INCREASED AG CAN BE CAUSED TO INCREASED ACIDS.
• LOW ANION GAP CAN BE CAUSED BY LOW SERUM ALBUMIN.
11. (REMEMBER “MUDPILES” & “DRC” FOR
OVERALL CAUSES OF METABOLIC ACIDOSIS
BUT START WITH MAJOR ONE!!)
COMPENSATION OF METABOLIC ACIDOSIS:
• RESPIRATORY COMPENSATION:
• PCO2 < 40MMHG: HYPERVENTILATION
• KIDNEY: FULLY COMPENSATED BY
INCREASED NA+
-H+
EXCHANGE INCREASED
AMMONIA AND HCO3
-
REABSORPTION.
• COMPENSATION VALUE FOR METABOLIC ACIDOSIS
PCO2 =(1.5 X HCO3
-
) +8±2
15. LOOP DIURETICS
BLOCK NA+
REABSORPTION FROM RENAL TUBULES:
LOOP OF HENLE
STIMULATE ALDOSTERONE SECRETION
INCREASED NA+
REABSORPTION IN TUBULAR FLUIDS
AT DCT
SECRETION AND LOSS OF K+
INCREASED HCO3
-
RECLAMATION
COMPENSATION OF METABOLIC ALKALOSIS:
• RESPIRATORY COMPENSATION PCO2 >40MM HG
• METABOLIC ALKALOSIS
PCO2 = 40 + 0.6 X ΔHCO3-
16. RESPIRATORY ACIDOSIS:
1. FACTORS THAT DIRECTLY DEPRESS THE
RESPIRATORY CENTRE:
• CENTRALLY ACTING DRUGS
• SEDATIVES AND GENERAL ANESTHESIA
• CNS TRAUMA AND INFECTION
2. FACTORS THAT AFFECT RESPIRATION
APPARATUS OR CAUSE MECHANICAL
OBSTRUCTION OF THE AIRWAYS:
• CHRONIC OBSTRUCTIVE AIRWAY DISEASE
• BRONCHOPNEUMONIA
• BRONCHITIS
• ACUTE EXACERBATION OF ASTHMA
• EMPHYSEMA
17. 3.PULMONARY DISEASES:
• RESPIRATORY DISTRESS SYNDROME (RDS),
• SEVERE PNEUMONIA
4.THORACIC DISEASES:
• KYPOSCOLIOSIS
• FLAIL CHEST
COMPENSATION OF RESPIRATORY ACIDOSIS:
• RENAL COMPENSATION, LATE 48-72 HRS, HCO3
-
>24 MM HG, RECLAMATION OF HCO3
-
, INCREASE
PULMONARY RATE AND DEPTH.
• RESPIRATORY ACIDOSIS
ACUTE: HCO3- = 24 + 0.1 X Δ PCO2
CHRONIC: HCO3- = 24 + 0.3 X Δ PCO2
18.
19. RESPIRATORY ALKALOSIS
1.PHYSIOLOGICAL
• HIGH ALTITUDE
• MECHANICAL OVER VENTILATION
2.PATHOLOGICAL
THOSE WITH A DIRECT EFFECT OF
RESPIRATION CENTRE STIMULATION
• HYSTERIA (HYSTERICAL OVER BREATHING)
• FEVER
• CNS INFECTIONS/RAISED INTRACRANIAL PRESSURE
• HYPOXIA: PROFOUND ANEMIA
• DRUGS: SALICYLATES, MEDROXYPROGESTERONE,
CATECHOLAMINES.
20. 3.THOSE DUE TO EFFECTS ON PULMONARY MECHANISM
• PNEUMONIA
• ASTHMA
• PULMONARY EMBOLI
4. MISCELLANEOUS: SEPSIS, PREGNANCY, LIVER DISEASE,
HYPERTHYROIDISM.
22. KEY CONCEPT FOR COMPENSATORY MECHANISMS:
• SINCE ABNORMAL CONDITION DIRECTLY ALTERS ONE TERM OF
CHCO3: PCO2 RATIO, PLASMA PH CAN BE READJUSTED BACK
TOWARD NORMAL BY A COMPENSATORY ALTERATION OF THE
OTHER TERM.
23. STORAGE ANDTRANSPORT
• IDEALLY SPECIMENS SHOULD NEVER BE STORED BEFORE ANALYSIS (DELAYED UP
TO 1 HR WILL HAVE MINIMAL EFFECT)
• PH DECREASES ON STANDING AT A RATE OF 0.04 TO 0.08 PH UNIT /HR AT 370
C, 0.02
TO 0.03/HR AT 220
C AND <0.01/HR AT 40
C
• PCO2 INCREASES BY -5MMHG/HR AT 370
C, 1MMHG/HR AT 220
C AND 0.5MMHG AT 40
C
• PO2 DECREASES AT RATE OF 2MMHG/HR AT 220
C AND 5 TO 10MMHG /HR AT 370
C
• BUT PO2 DECREASES 20MMHG IN JUST 2 MIN AND 40 MMHG IN 5 MIN WHEN WBC
COUNT IS VERY HIGH
• IF ANALYSIS MUST BE DELAYED BY CIRCUMSTANCES, THE SYRINGE OR TUBE
CONTAINING THE BLOOD SHOULD BE IMMERSED IN A MIXTURE OF ICE AND
WATER UNTIL ANALYSIS IS POSSIBLE. SYRINGE WAS INITIALLY HEPARINIZED AND
MADE AIR TIGHT.
24. ARTERIAL SAMPLE TYPES
• ARTERIAL SAMPLES CAN BE COLLECTED EITHER BY
ARTERIAL PUNCTURE OR BY ASPIRATION FROM AN
INDWELLING ARTERIAL CATHETER
Arterial punctures
Advantages Disadvantages
• Less risk of bias than arterial-line and
capillaries, if performed correctly
• Can be carried out in an emergency
situation
• No catheter needed
• Requires less blood volume than catheter
sampling
• Painful to the patient, hyperventilation
can potentially change blood gas values
• It can be difficult to locate arteries
• Risk of complications for the patient, not
always advisable to perform arterial
puncture
• Requires trained/authorized personnel
25. DIAGNOSIS
• ABG (ATERIAL BLOOD GAS)
• SERUM ELECTROLYTES
• ANION GAP
• COMPENSATORY CHANGES
• THE ABG DIRECTLY MEASURES ARTERIAL PH AND PCO2. HCO3
−
LEVELS ON
ABG ARE CALCULATED USING THE HENDERSON-HASSELBALCH EQUATION.
• ACID-BASE BALANCE IS GENERALLY MOST ACCURATELY ASSESSED WITH
MEASUREMENT OF PH AND PCO2 ON ARTERIAL BLOOD.
• THE PH ESTABLISHES THE PRIMARY PROCESS (ACIDOSIS OR ALKALOSIS),
ALTHOUGH IT MOVES TOWARD THE NORMAL RANGE WITH
COMPENSATION.
• CHANGES IN PCO2 REFLECT THE RESPIRATORY COMPONENT, AND CHANGES
IN HCO3
−
REFLECT THE METABOLIC COMPONENT
26. PH= 6.1+LOG(CHCO3
-
/0.0301*CO2)
• PO2 IS THE OXYGEN PARTIAL PRESSURE (OR TENSION) IN A
GAS PHASE IN EQUILIBRIUM WITH THE BLOOD.
• HIGH PO2 : HYPEROXEMIA
• LOW PO2 : HYPOXEMIA.
• SO2 IS CALLED OXYGEN SATURATION AND IS DEFINED AS
THE RATIO BETWEEN THE CONCENTRATIONS OF O2HB
AND HHB + O2HB:
SO2= O2HB/HHB+O2HB
• CLINICAL INTERPRETATION
HIGH (NORMAL) SO2: SUFFICIENT UTILIZATION OF
ACTUAL OXYGEN TRANSPORT CAPACITY. POTENTIAL
RISK OF HYPEROXIA
LOW SO : IMPAIRED OXYGEN UPTAKE, RIGHT SHIFT OF
27. • CARBON DIOXIDE READILY DIFFUSES ACROSS
CELL MEMBRANES, AND THE TENSION OF
PCO2 IN NORMAL INSPIRED AIR IS NEGLIGIBLE
• HIGH AND LOW VALUES OF PCO2 IN ARTERIAL
BLOOD INDICATE BLOOD HYPERCAPNIA AND
HYPOCAPNIA, RESPECTIVELY.
28. • CHCO3
-
IS THE CONCENTRATION OF
BICARBONATE (HYDROGEN CARBONATE) IN THE
PLASMA OF THE SAMPLE.
• AN INCREASED LEVEL OF CHCO3
-
MAY BE DUE TO
A PRIMARY METABOLIC ALKALOSIS OR A
COMPENSATORY RESPONSE TO PRIMARY
RESPIRATORY ACIDOSIS.
• DECREASED LEVELS OF CHCO3
-
ARE SEEN IN
METABOLIC ACIDOSIS AND AS A COMPENSATORY
MECHANISM TO PRIMARY RESPIRATORY
ALKALOSIS
29. • STANDARD BICARBONATE (CHCO3
-
(ST) IS THE
CONCENTRATION OF HYDROGEN CARBONATE IN PLASMA
FROM BLOOD WHICH HAS BEEN EQUILIBRATED WITH A
GAS MIXTURE WITH PCO2 = 40 MMHG (5.3 KPA) AND PO2 =
100 MMHG (13.3 KPA) AT 37 °C.
• THUS, “STANDARDIZING” MEASUREMENT CONDITIONS
ELIMINATES ANY RESPIRATORY INFLUENCE ON THE
BICARBONATE CONCENTRATION.
• A LOW (NEGATIVE) BE SIGNIFIES METABOLIC ACIDOSIS
• HIGH BE SIGNIFIES METABOLIC ALKALOSIS
30. DIAGNOSIS & MANAGEMENT
• FROM HISTORY & CLINICAL EXAMINATION CONSIDER LIKELY
DIAGNOSIS
• COLLECT ARTERIAL BLOOD SAMPLE WITH APPROPRIATE
PRECAUTIONS
• EXAMINE RESULTS TO CLASSIFY PRIMARY ACID-BASE DISORDER
32. • IS COMPENSATION PRESENT?
• EXAMINE COMPONENT PCO2 OR HCO3
-
• PCO2+HCO3
-
CHANGED IN SAME DIRECTION THAN CONSIDER
DEGREE OF COMPENSATION
• PCO2+HCO3
-
CHANGED IN OPPOSITE DIRECTION THAN
CONSIDER MIXED ACID BASE DISORDER
• DO BIOCHEMICAL RESULTS CONFIRM CLINICAL DIAGNOSIS?
• YES DECIDE ON MANAGEMENT
• NO REPEAT TEST OR RECONSIDER DIAGNOSIS
33. CASE 1
• A 25 Y OLD ASTHMATIC PRESENTS ACUTELY SHORT OF BREATH
TO THE ER WITH A PH OF 7.56, PA CO2 20 MMHG, HCO3
-
21 MMOL/L
AND
02 SAT. 96%.
34. CASE 2
• A 50 Y OLD MAN WITH A HISTORY OF RENAL
TRANSPLANT AND BASELINE CREATININE 2.0, IS
BROUGHT TO THE ICU WITH TACHYPNEA AND
LETHARGIC AFTER SURGER. HIS RR IS 35, HIS BP
WAS 120/70, HR 120. HE UNDERWENT CATARACTS
SURGERY 10 DAYS AGO.
• CREATININE IS 3.0 MG/DL, UREA 80 MG/DL, HCO3
-
8
MMOL/L,
PH 7.10, PACO2 25 MMHG, PAO2 90 MMHG ON ROOM
AIR, NA 134 MMOL/L, CL 96 MMOL/L.
35. DISORDER OF SODIUM AND WATER METABOLISM
COMBINEDSODIUMANDWATERDEPLETION:
• LOSSES FROM GIT AND SKIN: AS IN SEVERE VOMITING, DIARRHOEA,
ABDOMINAL SEQUESTRATION IN PERITONITIS, SWEATING, BURNS.
• LOSSES FROM KIDNEY: DIURETIC ABUSE, CRF, SALT WASTING TUBULAR
DISEASE, MINERALOCORTICOIDS DEFICIENCY(ADDISION’S DISEASE)
HYPONATREMIA: <136 MMOL/L (RR: 136-145 MMOL/L)
HYPONATREMIA MAY OCCUR IN THREE DIFFERENT SETTING IN ASSOCIATION WITH:
1. ECF VOLUME DEPLETION
2. ECF VOLUME EXCESS AND EDEMA
3. NORMAL ECF VOLUME
36. DIFFERENTIAL DIAGNOSIS OF HYPONATREMIA
PLASMA OSMOLALITY(MOSMOL/KG):1.86(NA+
)+GLUCOSE/18+BUN/2.8+9
NORMAL (280-295) DECREASED INCREASED
PSEUDOHYPONATREMIA HYPERGLYCEMIA
HYPERLIPIDEMIA VOLUME MANNITOL THERAPY
HYPERPROTEINEMIA STATUS UREMIA
HYPERVOLEMIA EUVOLEMIA HYPOVOLEMIA
URINE NA+
(MMOL/L) URINE NA+
(MMOL/L)
>20 <10 SIADH >20 <10
DIURETICS
RENAL FAILURE CONGESTIVE HYPOTHYROIDISM RENAL LOSS: EXTRA
HEART FAILURE HYPOADRENALISM DIURETICS RENAL
CIRRHOSIS ADDISON’S LOSS:
(WITH ASCITES) MET. ALKALOSIS GI LOSS
NEPHROTIC SYNDROME PROXIMAL RTA SKIN LOSS
CA INHIBITORS
SALT LOSING
RENAL DISEASE
37. HYPERNATREMIA(>150 MMOL/L)
• HYPERNATREMIA IS DUE TO DEFICIT OF BODY WATER RELATIVE TO THE TOAL
BODY SOLUTE(SODIUM CONTENT).
• NORMALLY INCREASED IN TONICITY IS CONTROLLED BY THE THRIST
MECHANISM AND RELEASE OF ADH.
• HYPERNATREMIA MAY OCCURS UNDER FOLLOWING SETTINGS:
1. LOSS OF WATER ALONE:
• THROUGH SKIN: FEVER, BURNS
• RENAL: DIABETES INSIPIDUS
• DISORDERS OF THIRST MECHANISM
2. WATER AND SODIUM DEFICITS WITH PROPORTIONATELY HIGHER LOSSES OF
WATER
• EXCESSIVE SWEATING SINCE SWEAT IS HYPOTONIC, PROPORTIONATELY
HIGHER AMOUNT OF WATER IS LOST
3. SODIUM GAIN:
• EXCESSIVE SALINE THERAPY
• ADRENAL HYPERFUNCTION AS HYPERALDOSTERONISM AND CUSHING’S
SYNDROME
38. DIFFERENTIAL DIAGNOSIS OF HYPERNATREMIA
VOLUME STATUS
HYPERVOLEMIA EUVOLEMIA HYPOVOLEMIA
HYPERALDOSTERONISM
CUSHING’S SYNDROME URINE NA+
VARIABLE
HYPERTONIC IV FLUID THERAPY URINE NA+
(MMOL/L)
URINARY OSMOLALITY
(MOSM/KG) >20 <10
<800 >800 DIURETICS GI LOSS,
THERAPY AND SKIN LOSS
DECREASED WITH
CENTRAL INCREASE WATER INTAKE DECREASE
OR INSENSIBLE LOSS: OSMOTIC WATER
NEPHROGENIC LUNG DIURESIS INTAKE
DIABETES INSIPIDUS SKIN
![HANDERSON’S AND HASSELBACH’S EQUATION:
• PH = PKA + LOG10 [HCO3
-
]
[H2CO3]
PH= 7.35-7.45 HCO3
-
= 24-28 MMOL/L
PO2= 80-100 MMHG PCO2= 35-45 MMHG
• BICARBONATE IS SECOND LARGEST ANION OF PLASMA
• COMPOSED OF TRUE BICARBONATE, CARBONATE AND CO2
BOUND TO CARBAMINO COMPOUND (RCNHCOOH)
• DISSOLVED CO2 (DCO2) IS UNDISSOCIATED CARBONIC ACID AND
FREE CO2 (PHYSICALLY DCO2)
• H2CO3= ∞ X P CO2 = 0.03X 40 MMHG= 1.224 MMOL/L
• [HCO3
-
] = 25 = 20
[H2CO3] 1.25 1](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)