1. Arterial Blood Gas
Interpretation
PRESENTER- Dr. Shankerdeep Sondhi
Resident IIInd Yr
Department of Medicine
2. OBJECTIVES
ABG Sampling
Interpretation of ABG
Case Scenarios
3. ABG – Procedure and Precautions
Site- (Ideally) Radial Artery
Brachial Artery
Femoral Artery
Ideally - Pre-heparinised ABG syringes
- Syringe should be FLUSHED with 0.5ml
of 1:1000 Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE
SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
Only small 0.5ml Heparin for flushing and discard it
Syringes must have > 50% blood.
4. Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
◦ Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN
5. ABG ELECTRODES
A. pH (Sanz Electrode)
Measures H+ ion concentration of sample against a
known pH in a reference electrode, hence potential
difference. Calibration with solutions of known pH (6.384
to 7.384)
B. P CO2 (Severinghaus Electrode)
CO2 reacts with solution to produce H+
higher C02- more H+ higher P CO2 measured
C. P 02 (Clark Electrode)
02 diffuses across membrane producing an electrical
current measured as P 02.
7. Acid Base Homeostasis
1. Plasma Acid Homeomostasis: Chemical
buffering
◦ H+ influenced by
Rate of endogenous production
Rate of excretion
Buffering capacity of body
◦ Buffers effective at physiologic pH are
Hemoglobin
Phosphate
Proteins
Bicarbonate
8. 2. Alveolar Ventilation:
pCO2 action is immediate. Stimulation of respiratory
center washes off the excess CO2 increasing pH, and
vice versa
3. Excretion:
Liver: uses HCO3– to make urea which further
prevents accumulation of ammonia and traps H+ in
renal distal tubule
Kidney: regulate plasma [HCO3–] through three main
processes:
• reabsorption of filtered HCO3–
• formation of titratable acid
• excretion of NH4+ in the urine.
Proximal tubule reclaims 85% filtered HCO3–
Distal tubule reclaims 15%, and excretes H+
40–60 mmol/d of protons is excreted to maintain balance
9. Acid Base Balance
H+ ion concentration in the body is
precisely regulated
The body understands the importance of H+
and hence devised DEFENCES against any
change in its concentration-
BICARBONATE RESPIRATORY RENAL
BUFFER REGULATION REGULATION
SYSTEM Acts in few Acts in hours to
Acts in few minutes days
seconds
10. BUFFER SYSTEM
1st line of defence in pH regulation.
Determine capacity of ECF to
transport acids from site of production
to site of excretion without undue
change in pH.
They resist change in pH on addition
of acid/alkali in media wherever they
are.
12. BICARBONATE BUFFER
NAHCO3/H2CO3 = 20/1 = Alkali reserve.
conversion of strong & non volatile acid
in ECF, in weak & volatile acid at the
expense of NaHCO3 component of
buffer.
H2CO3 thus formed is eliminated by lung
as CO2.Directly linked with respiration &
healthy lungs essential for its function.
High concentration in blood,so very good
physiological buffer.
Weak chemical buffer.
13. Bicarbonate Buffer System
CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3-
In Acidosis - Acid = H+
H+ + HCO3 H2CO3 CO2 + H2O
In Alkalosis - Alkali + Weak Acid = H2CO3
CO2 + H20 H2CO3 HCO3- + H+
+
ALKALI
14. PHOSPHATE BUFFER
Na2HPO4/NaH2PO4 =
AlkPO4/AcidPO4 = 4/1.
NaH2PO4 excreted by kidneys.
Directly linked with kidneys & healthy
kidneys necessary for its functioning.
Concentration in blood is low so not
good physiological buffer.
Very good chemical buffer as pKa
aprroches pH.
15. PROTEIN BUFFER
Na+Pr- / H+Pr- = salt/acid.
Proteins can act as a base In acidic
medium nd as an acid in basic
medium..with COOH& NH2 group.
Buffering capacity of plasma proteins
is much less than Hb.
16. Respiratory Regulation of Acid Base
Balance-
ALVEOLAR
H+ VENTILATION PaCO2
ALVEOLAR
H+ VENTILATION PaCO2
17. Renal Regulation of Acid Base Balance
Kidneys control the acid-base balance by excreting
either an acidic or a basic urine,
This is achieved in the following ways-
Reabsorption Secretion of H+
of HCO3 ions in tubules
in blood and excretion
PCO2 K+
in ECF
Aldosterone
H+ ion •Proximal Convulated
Tubules (85%)
•Thick Ascending Limb of
ECF Volume Loop of Henle (10%)
Angiotensin II
•Distal Convulated Tubule
•Collecting Tubules(5%)
18. Definitions and Terminology
ACIDOSIS – presence of a process which tends to
pH by virtue of gain of H + or loss of HCO3-
ALKALOSIS – presence of a process which tends
to pH by virtue of loss of H+ or gain of HCO3-
If these changes, change pH, suffix ‘emia’ is added
ACIDEMIA – reduction in arterial pH (pH<7.35)
ALKALEMIA – increase in arterial pH (pH>7.45)
19. Simple Acid Base Disorder/ Primary Acid Base
disorder – a single primary process of acidosis or
alkalosis due to an initial change in PCO2 and HCO3.
Compensation - The normal response of
the respiratory system or kidneys to change in pH
induced by a primary acid-base disorder
The Compensatory responses to a primary Acid Base
disturbance are never enough to correct the change in
pH , they only act to reduce the severity.
Mixed Acid Base Disorder – Presence of more than
one acid base disorder simultaneously .
22. Compensation
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2
METABOLIC
ACIDOSIS • For every 1mmol/l in HCO3 the
PCO2 falls by 1.25 mm Hg
METABOLIC
ALKALOSIS • For every 1mol/l in HCO3 the
PCO2 by 0.75 mm Hg
23. In Respiratory Disorders
PCO2 Kidney HCO3 Reabsorption
Compensation begins to appear in 6 – 12 hrs and is fully
developed only after a few days.
1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l
2.CHRONIC (>24 hrs)
After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
24. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
BUT never overshoots,
If a overshoot pH is there,
Take it granted it is a MIXED disorder
26. Normal Values
ANALYTE Normal Value Units
pH 7.35 - 7.45
PCO2 35 – 45 mm Hg
PO2 80 – 100 mm Hg`
[HCO3] 22 – 26 meq/L
SaO2 95-100 %
Anion Gap 10 + 2 meq/L
∆HCO3 +2 to -2 meq/L
27. STEP 0 • Is this ABG Authentic?
STEP 1 • ACIDEMIA or ALKALEMIA?
• RESPIRATORY or METABOLIC?
STEP 2
STEP 3 • Is COMPENSATION adequate?
STEP 4 • If METABOLIC – ANION GAP?
• If High gap Metabolic Acidosis–
STEP 5 GAP GAP?
28. Step 0 – Authentic or Not?
Verify that the ABG values are internally
accurate.
◦ The accuracy of the values can be established
by confirming that they satisfy a simplified form
of the Henderson-Hasselbalch equation:
[H+](nmol/L) = 24 × pCO2(mm Hg) ∕ [HCO3-]
(mEq/L)
◦ [H+] = 10 exp(-pH). Within the pH range of 7.26
to 7.45 [H+] in nmol/L = 80 − the decimal of the
pH
(e.g., for pH = 7.25, [H+] = 80 − 25 = 55
30. STEP 1 ACIDEMIA OR ALKALEMIA?
Look at pH
<7.35 - acidemia
>7.45 – alkalemia
RULE – An acid base abnormality is present even if
either the pH or PCO2 are Normal.
31. STEP 2 RESPIRATORY or METABOLIC?
IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
pH HCO3 or pH HCO3 METABOLIC
pH PCO2 or pH PCO2 RESPIRATORY
RULE- If either the pH or PCO2 is Normal, there is a
mixed metabolic and respiratory acid base disorder.
33. Disorder Prediction of Compensation pH HCO3– PaCO2
Metabolic PaCO2 will 1.25 mmHg per mmol/L in
acidosis [HCO3-] Low Low Low
Metabolic PaCO2 will 0.75 mmHg per mmol/L in High High High
alkalosis [HCO3-]
34. Disorder Prediction of Compensation pH HCO3– PaCO2
Respiratory High Low Low
alkalosis
Acute [HCO3-] will 0.2 mmol/L per mmHg in
PaCO2
Chronic [HCO3-] will 0.4 mmol/L per mmHg in
PaCO2
Respiratory Low High High
acidosis
Acute [HCO3-] will 0.1 mmol/L per mmHg in
PaCO2
Chronic [HCO3-] will 0.4 mmol/L per mmHg in
PaCO2
35. STEP 0 • Is this ABG Authentic?
STEP 1 • ACIDEMIA or ALKALEMIA?
• RESPIRATORY or METABOLIC?
STEP 2
STEP 3 • If Respiratory – ACUTE or CHRONIC?
STEP 4 • Is COMPENSATION adequate?
STEP 4 • If METABOLIC – ANION GAP?
• If High gap Metabolic Acidosis–
STEP 6 GAP GAP?
36. Electrochemical Balance in Blood
100% UC
UA
90%
80% HCO3
Na Sulfate
70% Phosphate
60% Mg- OA
Cl
50% K - Proteins
40% Ca-HCO3
30% Na- Cl
20%
10%
0%
CATIONS ANIONS
37. Anion Gap
AG based on principle of electroneutrality:
Total Serum Cations = Total Serum Anions
M cations + U cations = M anions + U anions
Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
Na + UC = HCO3 + Cl + UA
But in Blood there is a relative abundance of Anions, hence
Anions > Cations
Na – (HCO3 + Cl) = UA – UC
Na – (HCO3 + Cl) = Anion Gap
38. METABOLIC ACIDOSIS-
STEP 4
ANION GAP?
IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP?
ANION GAP(AG) = Na – (HCO3 + Cl)
Normal Value = 10 + 2
Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)
50% in S. Albumin 75% in Anion Gap !!!
High Anion Gap Metabolic Acidosis
Metabolic Acidosis
Normal Anion Gap Acidosis
39. STEP 5 CO EXISTANT METABOLIC
DISORDER – “Gap Gap‖?
C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER?
∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
∆AG/ HCO3- = 1 Pure High AG Met Acidosis
AG/ HCO3- > 1 Assoc Metabolic Alkalosis
AG/ HCO3- < 1 Assoc N AG Met Acidosis
41. Case Scenario
A patient with a severe postoperative
ileus requires the insertion of a
nasogastric (NG) tube for
decompression. After several days on
the floor, he develops a line infection and
is moved to the ICU once he becomes
pressor dependent. The patient's ABG
reveals a pH = 7.44, pCO2 = 12, and
[HCO3-] = 8. The [Na+] = 145 with [Cl-] =
102.
42. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8,
[Na+] = 145 with [Cl-] = 102
◦ With knowledge of the common clinical
scenarios leading to acid-base
disturbances, this patient is at risk for
developing a metabolic alkalosis from NG
suction and a metabolic acidosis and
respiratory alkalosis from sepsis.
◦ Step 1. [H+] = 80 − 44 = 36.
Does 36 = 24 × 12 / 8? It does.
◦ Step 2. The patient is mildly alkalemic, which
can be explained by the low pCO2 but not by
the low [HCO3-], suggesting that a respiratory
alkalosis may be the primary derangement.
43. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8,
[Na+] = 145 with [Cl-] = 102
◦ Step 3
a. The drop in [HCO3-] might be an appropriate
compensation for a chronic respiratory alkalosis
([HCO3-] is 0.4 mmol/L per mmHg in PaCO2)
However, 24 − [(40 − 12) × 0.4] = 12.8, which is not
close to the observed [HCO3-] of 8. A mixed disorder is
implied.
b. AG = 145 − 102 − 8 = 35. There is an elevated
AG, suggests a concomitant metabolic acidosis.
c. Delta anion gap=35 − 10 = 25.
d. Delta bicarbonate= 24 − 8 =16.
Ratio of above two is more than 1 suggestive of
associated metabolic alkalosis. This has proven to be
a triple acid-base disorder with an elevated anion
gap acidosis, a metabolic alkalosis, and a
respiratory alkalosis, as was alluded to in Step 1
44. Metabolic Acidosis
Metabolic acidosis can occur because of
◦ increase in endogenous acid production (lactate and ketoacids)
◦ loss of bicarbonate (as in diarrhea)
◦ accumulation of endogenous acids (as in renal failure).
Effects on the respiratory, cardiac, and nervous
systems.
◦ Kussmaul respiration
◦ Intrinsic cardiac contractility may be depressed, but inotropic
function can be normal because of catecholamine release.
◦ Both peripheral arterial vasodilation and central
venoconstriction can be present
◦ The decrease in central and pulmonary vascular compliance
predisposes to pulmonary edema with even minimal volume
overload.
◦ Central nervous system function is depressed, with
headache, lethargy, stupor, and, in some cases, even coma.
45. Metabolic Acidosis: Essentials of
Diagnosis
Decreased HCO3– with acidemia.
Classified into high anion gap acidosis
and normal anion gap (hyperchloremic)
acidosis.
The high anion gap acidoses are seen in
lactic acidosis, ketoacidosis, renal failure
or toxins.
Normal anion gap acidosis is mainly
caused by gastrointestinal HCO3– loss or
RTA.
Urinary anion gap may help distinguish
between these causes.
46. Causes of High-Anion-Gap
Metabolic Acidosis
1. Lactic acidosis
Poor tissue perfusion (type A)
Aerobic disorders (type B)
2. Ketoacidosis
Diabetic
Alcoholic
Starvation
3. Toxins
Ethylene glycol
Methanol
Salicylates
Propylene glycol: as vehicle of medications
Pyroglutamic acid: acetaminophen toxicity
4. Renal failure (acute and chronic)
47. Ketacidosis –
Diabetic Ketoacidosis (DKA):
DKA is caused by increased fatty acid
metabolism and the accumulation of ketoacids
(acetoacetate and -hydroxybutyrate).
DKA usually occurs in insulin-dependent
diabetes mellitus in association with
cessation of insulin or
an intercurrent illness, such as an
infection, gastroenteritis, pancreatitis, or
myocardial infarction, which increases insulin
requirements temporarily and acutely.
The accumulation of ketoacids accounts for the
increment in the Anion Gap and is
accompanied most often by hyperglycemia
[glucose > 17 mmol/L (300 mg/dL)].
48. Glucose,a mmol/L (mg/dL) 13.9–33.3 (250–600)
Sodium, meq/L 125–135
Potassiuma Normal to ↑
Magnesiuma Normal ( plasma levels may be normal or high at
presentation, total-body stores are usually
depleted)
Chloridea Normal
Phosphatea ↓
Creatinine Slightly ↑
Osmolality (mOsm/mL) 300–320
Plasma ketonesa ++++
Serum bicarbonate,a meq/L <15 meq/L
Arterial pH 6.8–7.3
Arterial PCO2,a mmHg 20–30
Anion gapa[Na - (Cl + HCO3)] ↑
49. Management
Confirm diagnosis (plasma glucose, positive serum
ketones, metabolic acidosis).
Admit to hospital; intensive-care setting may be necessary for
frequent monitoring or if pH < 7.00 or unconscious.
Assess:
Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate)
Acid-base status—pH, HCO3-, PCO2, b-hydroxybutyrate
Renal function (creatinine, urine output)
Replace fluids:
2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour);
subsequently, 0.45% saline at 150–300 mL/h;
change to 5% glucose and 0.45% saline at 100–200 mL/h when
plasma glucose reaches 250 mg/dL (14 mmol/L).
Administer short-acting insulin:
IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by
continuous IV infusion;
increase 2- to 3-fold if no response by 2–4 h.
If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do not
administer insulin until the potassium is corrected to > 3.3 mmol/L
50. Management
Assess patient: What precipitated the episode
(noncompliance, infection, trauma, infarction, cocaine)?
Initiate appropriate workup for precipitating event
(cultures, CXR, ECG).
Measure
capillary glucose every 1–2 h;
electrolytes (especially K+, bicarbonate, phosphate) and anion
gap every 4 h for first 24 h.
Monitor blood pressure, pulse, respirations, mental
status, fluid intake and output every 1–4 h.
Replace K+:
10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flow
and normal creatinine documented;
administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if
bicarbonate is given.
Continue above until patient is stable, glucose goal is 150–
250 mg/dL, and acidosis is resolved. Insulin infusion may be
decreased to 0.05–0.1 units/kg per hour.
Administer intermediate or long-acting insulin as soon as
patient is eating. Allow for overlap in insulin infusion and
51. since insulin prevents production of
ketones, bicarbonate therapy is rarely
needed except with extreme acidemia (pH <
7.1), and then in only limited amounts.
Patients with DKA are typically volume
depleted and require fluid resuscitation with
isotonic saline.
Volume overexpansion is not uncommon
after IV fluid administration, and contributes
to the development of a hyperchloremic
acidosis during treatment of DKA because
volume expansion increases urinary
ketoacid anion excretion (loss of potential
bicarbonate).
The mainstay for treatment of this condition
is IV regular insulin
52. Drug, Toxin-Induced Acidosis
Plasma osmolality is calculated according to the following
expression:
Posm = 2Na+ + Glu + BUN (all in mmol/L)
Posm = 2Na+ + Glu/18 + BUN/2.8 (milligrams per deciliter)
The calculated and determined osmolality should be within
10–15 mmol/kg H2O
When the measured osmolality exceeds the calculated
osmolality by >15–20 mmol/kg H2O, either prevails.
Either the serum sodium is spuriously low, as with
hyperlipidemia or hyperproteinemia
(pseudohyponatremia)
Osmolytes other than sodium salts, glucose, or urea
have accumulated in plasma. Examples include
mannitol, radiocontrast media, isopropyl
alcohol, ethylene glycol, propylene
53. In this situation, the difference between the
calculated osmolality and the measured osmolality
(osmolar gap) is proportional to the concentration of
the unmeasured solute.
Alcohols: With an appropriate clinical history and index
of suspicion, identification of an osmolar gap is helpful
in identifying the presence of poison-associated AG
acidosis. Three alcohols may cause fatal intoxications:
ethylene glycol, methanol, and isopropyl alcohol
Salicylates: Salicylate intoxication in adults usually
causes respiratory alkalosis or a mixture of high-AG
metabolic acidosis and respiratory alkalosis. Only a
portion of the AG is due to salicylates. Lactic acid
production is also often increased
54. Renal failure Acidosis
The hyperchloremic acidosis of moderate renal
insufficiency is eventually converted to the
high-AG acidosis of advanced renal failure.
At GFRs below 20 mL/min, the inability to
excrete H+ with retention of acid anions such
as PO43– and SO42– results in an increased
anion gap acidosis
[HCO3–] rarely falls to <15 mmol/L, and the AG
is rarely >20 mmol/L, indicating that the acid
retained in chronic renal disease is buffered by
alkaline salts from bone.
Results in significant loss of bone mass due to
reduction in bone calcium carbonate and
increases urinary calcium excretion.
55. Treatment of high anion gap
acidosis
Treatment is aimed at the underlying disorder, such as
insulin and fluid therapy for diabetes and appropriate
volume resuscitation to restore tissue perfusion. The
metabolism of lactate will produce HCO3– and increase
pH.
Controversy regarding administration of large
amounts of HCO3–
may have deleterious effects, including hypernatremia and
hyperosmolality.
Intracellular pH may decrease because administered HCO3–
is converted to CO2, which easily diffuses into cells, combines
with water to create additional hydrogen ions and worsening
of intracellular acidosis and this could impair cellular function
Alkali administration is known to stimulate
phosphofructokinase activity, thus exacerbating lactic acidosis
via enhanced lactate production. Ketogenesis is also
augmented by alkali therapy.
56. Treatment of high anion gap
acidosis…..
◦ In salicylate intoxication, alkali therapy must be started unless blood
pH is already alkalinized by respiratory alkalosis, since the
increment in pH converts salicylate to more impermeable salicylic
acid and thus prevents central nervous system damage.
◦ In DKA, alkali must be administered in extreme alkalemia (pH<7.1)
◦ In alcoholic ketoacidosis, thiamine should be given together with
glucose to avoid the development of Wernicke's encephalopathy.
The amount of HCO3– deficit can be calculated as follows:
Amount of HCO3– deficit = 0.5 X body weight X (24 - HCO3–)
◦ Half of the calculated deficit should be administered within the first
3–4 hours to avoid overcorrection and volume overload.
In methanol intoxication
◦ ethanol has been used as a competitive substrate for alcohol
dehydrogenase, which metabolizes methanol to formaldehyde
◦ or through direct inhibition of alcohol dehydrogenase by fomepizole
57. Hyperchloremic (Nongap)
Metabolic Acidoses: causes
I. Gastrointestinal bicarbonate loss
Diarrhea
External pancreatic or small-bowel drainage
Ureterosigmoidostomy, jejunal loop, ileal loop
Drugs - Calcium chloride , Magnesium sulfate
(diarrhea), Cholestyramine (bile acid diarrhea)
II. Renal acidosis
Hypokalemia
Proximal RTA (type 2)
Distal (classic) RTA (type 1)
Hyperkalemia
Generalized distal nephron dysfunction (type 4 RTA)
a. Mineralocorticoid deficiency
b. Mineralocorticoid resistance (autosomal dominant PHA I)
c. Voltage defect (autosomal dominant PHA I and PHA II)
d. Tubulointerstitial disease
58. III. Drug-induced hyperkalemia (with renal insufficiency)
◦ Potassium-sparing diuretics
(amiloride, triamterene, spironolactone)
◦ Trimethoprim
◦ Pentamidine
◦ ACE-Is and ARBs
◦ Nonsteroidal anti-inflammatory drugs
◦ Cyclosporine and tacrolimus
IV. Other
◦ Acid loads (ammonium chloride, hyperalimentation)
◦ Loss of potential bicarbonate: ketosis with ketone excretion
◦ Expansion /dilutional acidosis (rapid saline administration)
◦ Hippurate
◦ Cation exchange resins
59. Approach: Urinary Anion Gap
Increased renal NH4+Cl– excretion to enhance H+ removal is a normal
physiologic response to metabolic acidosis. NH3 reacts with H+ to
form NH4+, which is accompanied by the anion Cl– for excretion.
Urinary anion gap from a random urine sample ([Na++ K+]– Cl–)
reflects the ability of the kidney to excrete NH4Cl as in the following
equation:
Na+ + K+ + NH4+ = Cl– + 80
urinary anion gap is equal to (80 – NH4+)
Gastrointestinal HCO3– loss (diarrhea), the renal acidification ability
remains normal and NH4Cl excretion increases in response to the
acidosis. urinary anion gap is negative (eg, –30 mEq/L).
Distal RTA, the urinary anion gap is positive (eg, +25 mEq/L), since
the basic lesion in the disorder is the inability of the kidney to excrete
H+ and thus the inability to increase NH4Cl excretion.
Proximal (type II) RTA, the kidney has defective HCO3–
reabsorption, leading to increased HCO3– excretion rather than
decreased NH4Cl excretion. Thus, the urinary anion gap is negative
60. Urinary pH may not as readily differentiate
between the two causes because volume
depletion or potassium depletion, which can
accompany diarrhea (and surreptitious laxative
abuse) may impair renal acidification.
Thus, when volume depletion is present, the
urinary anion gap is a better measurement of
ability to acidify the urine than urinary pH.
When large amounts of other anions are present
in the urine, the urinary anion gap may not be
reliable. In such a situation, NH4+ excretion can
be estimated using the urinary osmolar gap.
NH4+ excretion (mmol/L) = 0.5 x Urinary osmolar
gap = 0.5 [U osm – 2(U Na++U K+) + U urea + U
glucose]
where urinary (U) concentrations and osmolality
are in millimoles per liter.
61. Renal Serum Urinary Titratable Urinary Treatment
Defect [K+] NH4+ Plus Acid Anion
Minimal Gap
Urine pH
Gastrointestinal None ↓ < 5.5 ↑↑ Negative Na+, K+, and
HCO3– loss HCO3– as
required
Renal tubular
acidosis
I. Classic distal Distal H+ ↓ > 5.5 ↓ Positive NaHCO3 (1–3
secretion mEq/kg/d)
II. Proximal Proximal ↓ < 5.5 Normal Negative NaHCO3 or
secretion HCO3– KHCO3 (10–15
abspn mEq/kg/d),
thiazide
IV. Distal Na+ ↑ < 5.5 ↓ Positive Fludrocortisone
Hyporeninemic reabsorption (0.1–0.5 mg/d),
+ dietary K+ rstrn,
hypoaldosteroni K secretion,
and H+ furosemide (40–
sm
secretion 160 mg/d),
NaHCO3 (1–3
mEq/kg/d)
62. Treatment of normal Anion gap
Acidosis
Gastrointestinal: Correction of the contracted ECFV with NaCl
and repair of K+ deficits corrects the acid-base disorder, and
chloride deficiency.
RTA : administration of alkali (either as bicarbonate or citrate) to
correct metabolic abnormalities and prevent nephrocalcinosis and
renal failure.
◦ Proximal RTA : Large amounts of alkali (10–15 mEq/kg/d) may
be required to treat proximal RTA because most of the alkali is
excreted into the urine, which exacerbates hypokalemia. Thus, a
mixture of sodium and potassium salts, such as K-Shohl
solution, is preferred. The addition of thiazides may reduce the
amount of alkali required, but hypokalemia may develop.
◦ Distal RTA : Correction of type 1 distal RTA requires a smaller
amount of alkali (1–3 mEq/kg/d) and potassium supplementation
as needed.
◦ Type IV RTA: dietary potassium restriction may be needed and
potassium-retaining drugs should be withdrawn. Fludrocortisone
may be effective in cases with hypoaldosteronism, but should be
used with care, preferably in combination with loop diuretics.
alkali supplementation (1–3 mEq/kg/d) may be required.
63.
64. Metabolic Alkalosis
Essentials of Diagnosis
◦ High HCO3– with alkalemia.
◦ Evaluate effective circulating volume by
physical examination and check urinary
chloride concentration. This will help
differentiate saline-responsive metabolic
alkalosis from saline-unresponsive
alkalosis
65. Metabolic Alkalosis
Occurs as a result of net gain of [HCO3–] or loss
of nonvolatile acid (usually HCl by vomiting) from
the extracellular fluid.
The disorder involves
a generative stage, in which the loss of acid usually
causes alkalosis
maintenance stage, in which the kidneys fail to
compensate by excreting HCO3–.
Classified based on "saline responsiveness" or
urinary Cl–, which are markers for volume status
Saline-responsive metabolic alkalosis is a sign
of extracellular volume contraction
Saline-unresponsive alkalosis implies a volume-
expanded state
66. Symptoms
With metabolic alkalosis, changes in central and
peripheral nervous system function are similar to
those of hypocalcemia : symptoms include
Mental confusion
Obtundation
Predisposition to seizures
Paresthesia
Muscular cramping
Tetany
Aggravation of arrhythmias
Hypoxemia in chronic obstructive pulmonary
disease.
Related electrolyte abnormalities include
Hypokalemia- Weakness and hyporeflexia
hypophosphatemia.
67. Classification and etiology
I. Saline-Responsive (UCl < 10 mEq/d)
Excessive body bicarbonate content
Renal alkalosis
Diuretic therapy
Poorly reabsorbable anion therapy:
carbenicillin, penicillin, sulfate, phosphate
Posthypercapnia
Gastrointestinal alkalosis
Loss of HCl from vomiting or nasogastric suction
Intestinal alkalosis: chloride diarrhea
Exogenous alkali
NaHCO3 (baking soda)
Sodium citrate, lactate, gluconate, acetate
Transfusions
Antacids
Normal body bicarbonate content
"Contraction alkalosis"
68. II. Saline-Unresponsive (UCl > 10 mEq/d)
Excessive body bicarbonate content
Renal alkalosis
Normotensive
Bartter's syndrome (renal salt wasting and
secondary hyperaldosteronism)
Severe potassium depletion
Refeeding alkalosis
Hypercalcemia and hypoparathyroidism
Hypertensive
Endogenous mineralocorticoids
Primary aldosteronism
Hyperreninism
Adrenal enzyme deficiency: 11- and 17-
hydroxylase
Liddle's syndrome
Exogenous mineralocorticoids
Licorice
69.
70. Treatment
Mild alkalosis is generally well tolerated. Severe or
symptomatic alkalosis (pH > 7.60) requires urgent
treatment.
Saline-Responsive Metabolic Alkalosis
◦ Aimed at correction of extracellular volume
deficit.
◦ Depending on the degree of
hypovolemia, adequate amounts of 0.9%
NaCl and KCl should be administered.
◦ Discontinuation of diuretics and
administration of H2-blockers in patients
whose alkalosis is due to nasogastric suction
can be useful.
◦ If impaired pulmonary or cardiovascular
status prohibits adequate volume
repletion, acetazolamide, 250–500 mg
intravenously every 4–6 hours, can be used.
71. Treatment…..
One must be alert to the possible development of
hypokalemia, since potassium depletion can be
induced by forced kaliuresis via bicarbonaturia.
Administration of acid can be used as emergency
therapy. HCl, 0.1 mol/L, is infused via a central vein
(the solution is sclerosing). Dosage is calculated to
decrease the HCO3– level by 50% over 2–4
hours, assuming an HCO3– volume of distribution (L)
of 0.5% body weight (kg).
Patients with marked renal failure may require dialysis.
Saline-Unresponsive Metabolic Alkalosis
surgical removal of a mineralocorticoid-producing
tumor
blockage of aldosterone effect with an ACE inhibitor or
with spironolactone.
primary aldosteronism can be treated only with
potassium repletion.
72. Respiratory Acidosis
Results from decreased alveolar ventilation and hypercapnia
both due to pulmonary and non pulmonary disorders
Central Neuromuscular
◦ Drugs ◦ Poliomyelitis
(anesthetics, morphine, sedatives) ◦ Kyphoscoliosis
◦ Stroke ◦ Myasthenia
◦ Infection ◦ Muscular dystrophies
Airway Miscellaneous
◦ Obstruction ◦ Obesity
◦ Asthma ◦ Hypoventilation
Parenchyma ◦ Permissive hypercapnia
◦ Emphysema
◦ Pneumoconiosis
◦ Bronchitis
◦ Adult respiratory distress
syndrome
◦ Barotrauma
73. Respiratory Acidosis
Acute respiratory failure
associated with severe acidosis and only a small increase
in the plasma bicarbonate.
After 6–12 hours, the primary increase in PCO2 evokes a
renal compensatory response to generate more HCO3–
, which tends to ameliorate the respiratory acidosis. This
takes several days to complete.
Chronic respiratory acidosis
seen in patients with underlying lung disease, such as
chronic obstructive pulmonary disease.
Urinary excretion of acid in the form of NH4+ and Cl– ions
results in the characteristic hypochloremia of chronic
respiratory acidosis.
When chronic respiratory acidosis is corrected
suddenly, especially in patients who receive mechanical
ventilation, there is a 2- to 3-day lag in renal bicarbonate
excretion, resulting in posthypercapnic metabolic
alkalosis.
74. Symptoms and Signs
◦ With acute onset, there is somnolence and confusion, and
myoclonus with asterixis
◦ Coma from CO2 narcosis may ensue
◦ Severe hypercapnia increases cerebral blood flow and
cerebrospinal fluid pressure. Signs of increased intracranial
pressure (papilledema, pseudotumor cerebri) may be seen.
Laboratory Findings
◦ Arterial pH is low
◦ PCO2 is increased
◦ Serum HCO3– is elevated, but not enough to completely
compensate for the hypercapnia.
◦ If the disorder is chronic, hypochloremia is seen.
Treatment
◦ In all forms of respiratory acidosis, treatment is directed at the
underlying disorder to improve ventilation.
◦ Because opioid drug overdose is an important reversible cause of
acute respiratory acidosis, naloxone, 0.04–2 mg intravenously is
administered to all such patients if no obvious cause for
respiratory depression is present.
◦ Mechanical ventilation for oxygenation till it restores back to
normal maybe needed
75. Respiratory Alkalosis(Hypocapnia)
Respiratory alkalosis, or hypocapnia, occurs when hyperventilation
reduces the PCO2, which increases the pH
Symptoms and Signs
In acute cases (hyperventilation), there is light-headedness,
anxiety, paresthesias, numbness about the mouth, and a tingling
sensation in the hands and feet. Tetany occurs in more severe
alkalosis from a fall in ionized calcium.
In chronic cases, findings are those of the responsible condition.
Laboratory Findings
Arterial blood pH is elevated, and PCO2 is low. Serum
bicarbonate is decreased in chronic respiratory alkalosis.
Determination of appropriate compensatory changes in the
HCO3– is useful to sort out the presence of an associated
metabolic disorder
the changes in HCO3– values are greater if the respiratory
alkalosis is chronic
Although serum HCO3– is frequently below 15 mEq/L in
metabolic acidosis, it is unusual to see such a low level in
respiratory alkalosis, and its presence would imply a
superimposed (noncompensatory) metabolic acidosis.
78. Treatment
Treatment is directed toward the underlying cause.
In acute hyperventilation syndrome from
anxiety, reassurance , attention to underlying psychological
stress and rebreathing into a paper bag will increase the
PCO2.
The processes are usually self-limited since muscle
weakness caused by hyperventilation-induced alkalemia will
suppress ventilation.
Sedation may be necessary if the process persists however
Antidepressants and sedatives should be avoided
Adrenergic blockers may ameliorate peripheral
manifestations of the hyperadrenergic state.
Rapid correction of chronic respiratory alkalosis may result
in metabolic acidosis as PCO2 is increased in the setting of
previous compensatory decrease in HCO3–.
If respiratory alkalosis complicates ventilator
management, changes in dead space, tidal volume, and
frequency can minimize the hypocapnia
79. Conclusion
Clinical suspicion according to scenario
Primary disorder from pH and bicarbonate or CO2
values
Degree of compensation…? Inappropriate? mixed
disorder
Anion gap (corrected for serum albumin
change)…? Primary metabolic acidosis
Corrected bicarbonate levels…?
More than normal- associated metabolic alkalosis
Less - associated metabolic non-anion gap acidosis
Review compensation for metabolic ds…confirm if
initially suspected respiratory disorder exists
80. Metabolic acidosis: ..see AG
High AG: …plasma osmolal gap
more.. Toxins
Less.. KA, RF, LA,
Normal AG acidosis:
urine AG….negative..GI
urinary pH ….high..RTA 1
serum potassium….high..RTA4
Metabolic alkalosis:
◦ Urinary Chloride…
Less..saline responsive…ECF contraction
more ..saline non responsive
Plasma Potassium…low..K depletion
High…Blood pressure
Plasma renin
81. 1.PaCO2 equation:
VCO2 x 0.863 VCO2 = CO2 production
PaCO2 = ----------------- VA = VE – VD
VA VE = minute (total) ventilation
VD = dead space ventilation
0.863 converts units to mm Hg
Condition State of
PaCO2 in blood alveolar ventilation
>45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
<35 mm Hg Hypocapnia Hyperventilation
PaCO2 reflects ratio of metabolic CO2 production to alveolar
ventilation
82. Hypercapnia
VCO2 x 0.863
PaCO2 = ------------------
VA
The only physiologic reason for elevated PaCO2 is
inadequate alveolar ventilation (VA) for the amount of the
body‘s CO2 production (VCO2). Since alveolar ventilation
(VA) equals minute ventilation (VE) minus dead space
ventilation (VD), hypercapnia can arise from insufficient
VE, increased VD, or a combination.
83. Hypercapnia
VCO2 x 0.863
PaCO2 = ------------------
VA VA = VE – VD
Examples of inadequate VE leading to decreased VA and
increased PaCO2: sedative drug overdose; respiratory muscle
paralysis; central hypoventilation
Examples of increased VD leading to decreased VA and
increased PaCO2: chronic obstructive pulmonary disease;
severe pulmonary embolism, pulmonary edema.
84. Physiologic effects of
hypercapnia
◦ 1) An elevated PaCO2 will lower the PAO2 (see Alveolar gas
equation), and as a result lower the PaO2.
◦ 2) An elevated PaCO2 will lower the pH (see Henderson-
Hasselbalch equation).
◦ 3) The higher the baseline PaCO2, the greater it will rise for a
given fall in alveolar ventilation, e.g., a 1 L/min decrease in
VA will raise PaCO2 a greater amount when baseline PaCO2
is 50 mm Hg than when it is 40 mm Hg.
86. Oxygenation
-----XXXX Diagnostics----- Parameters: /limitations
Blood Gas Report
328
Pt ID
03:44
3245 / 00
Feb 5 2006 O2 Content of blood:
(Hb x1.34x O2 Sat + 0.003x Dissolved O2 )
Measured 37.0 0C
pH 7.452 Remember Hemoglobin
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Corrected 38.6 0C Oxygen Saturation:
pH 7.436
pCO2 47.6 mm Hg ( remember this is calculated …error prone)
pO2 122.4 mm Hg
Calculated Data Alveolar / arterial gradient:
HCO3 act 31.2 mmol / L ( classify respiratory failure)
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 % Arterial / alveolar ratio:
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg Proposed to be less variable
pO2 (a/A) 0.78
Same limitations as A-a gradient
Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
87. Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
where PAO2 is the average alveolar PO2, and PIO2 is the partial pressure
of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47
mm Hg is the water vapor pressure at normal body temperature.
88. Alveolar Gas Equation
If FIO2 and PB are constant, then as PaCO2 increases
both PAO2 and PaO2 will decrease (hypercapnia causes
hypoxemia).
If FIO2 decreases and PB and PaCO2 are constant, both
PAO2 and PaO2 will decrease.
If PB decreases (e.g., with altitude), and PaCO2 and FIO2
are constant, both PAO2 and PaO2 will decrease
(mountain climbing causes hypoxemia).
89. P(A-a)O2
P(A-a)O2 is the alveolar-arterial difference in partial pressure of
oxygen. It is commonly called the ―A-a gradient‖. It results from
gravity-related blood flow changes within the lungs (normal
ventilation-perfusion imbalance).
Normal P(A-a)O2 ranges from 5 to 25 mm Hg breathing room air
(it increases with age). A higher than normal P(A-a)O2 means the
lungs are not transferring oxygen properly from alveoli into the
pulmonary capillaries. Except for right to left cardiac shunts, an
elevated P(A-a)O2 signifies some sort of problem within the lungs.
90. Physiologic causes of low PaO2
NON-RESPIRATORY P(A-a)O2
Cardiac right to left shunt Increased
Decreased PIO2 Normal
RESPIRATORY
Pulmonary right to left shunt Increased
Ventilation-perfusion imbalance Increased
Diffusion barrier Increased
Hypoventilation (increased PaCO2) Normal
91. Ventilation-Perfusion imbalance
A normal amount of ventilation-perfusion (V-Q)
imbalance accounts for the normal P(A-a)O2.
By far the most common cause of low PaO2 is an
abnormal degree of ventilation-perfusion imbalance
within the hundreds of millions of alveolar-capillary
units. Virtually all lung disease lowers PaO2 via V-Q
imbalance, e.g., asthma, pneumonia, atelectasis,
pulmonary edema, COPD.
Diffusion barrier is seldom a major cause of low PaO2
(it can lead to a low PaO2 during exercise).
92. SaO2 and oxygen content
How much oxygen is in the blood? Oxygen content = CaO2 (mlO2/dl).
CaO2 = quantity O2 bound + quantity O2 dissolved
to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of
Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is
solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg
PO2.
93. Given arterial oxygen saturation (SpO2) =
100%, Hb = 15 g/100 ml and arterial partial
pressure of oxygen (PaO2) = 13.3 kPa, then
the oxygen content of arterial blood (CaO2) is:
CaO2 = 20.1 +0.3 = 20.4 ml/100 ml
Similarly the oxygen content of mixed venous
blood can be calculated. Given normal
values of mixed venous oxygen saturation
(SvO2) = 75% and venous partial pressure of
oxygen (PvO2) = 6 kPa, so:
CvO2 = 15.2 + 0.1 = 15.2 ml/100 ml
94. Oxygen dissociation curve: SaO2 vs. PaO2
Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm%
and 10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 is 50%.
95. SaO2 – is it calculated or measured?
SaO2 is measured in a ‗co-oximeter‘. The traditional ‗blood gas
machine‘ measures only pH, PaCO2 and PaO2,, whereas the co-
oximeter measures SaO2, carboxyhemoglobin, methemoglobin and
hemoglobin content. Newer ‗blood gas‘ consoles incorporate a co-
oximeter, and so offer the latter group of measurements as well as
pH, PaCO2 and PaO2.
Always make sure the SaO2 is measured, not calculated. If it is
calculated from the PaO2 and the O2-dissociation curve, it
provides no new information, and could be inaccurate --
especially in states of CO intoxication or excess
methemoglobin. CO and metHb do not affect PaO2, but do lower
the SaO2.
96. Carbon monoxide – an important cause
of hypoxemia
Normal %COHb in the blood is 1-2%, from metabolism and small
amount of ambient CO (higher in traffic-congested areas)
All smokers have excess CO in their blood.
CO binds @ 200x more avidly to hemoglobin than O2, displacing O2
from the heme binding sites.
CO : 1) decreases SaO2 by the amount of %COHb present, and 2)
shifts the O2-dissociation curve to the left, retarding unloading of
oxygen to the tissues.
CO does not affect PaO2, only SaO2. To detect CO
poisoning, SaO2 and/or COHb must be measured (requires co-
oximeter). In the presence of excess CO, SaO2 (when measured)
will be lower than expected from the PaO2.
97. CO does not affect PaO2!
A patient presented to the ER with headache and dyspnea.
His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH
7.43. SaO2 on this first set was calculated from the O2-dissociation
curve at 97%, and oxygenation was judged normal.
He was sent out from the ER and returned a few hours later with mental
confusion; this time both SaO2 and COHb were measured (SaO2 shown
by ‗X‘): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2
53%, carboxyhemoglobin 46%.
CO poisoning was missed on the first set of blood gases
because SaO2 was not measured!
98. Causes of Hypoxia
1. Hypoxemia (=low PaO2 and/or low CaO2)
◦ a. reduced PaO2 – usually from lung disease (most common
physiologic mechanism: V-Q imbalance)
◦ b. reduced SaO2 -- most commonly from reduced PaO2; other
causes include carbon monoxide
poisoning, methemoglobinemia, or rightward shift of the O2-
dissociation curve
◦ c. reduced hemoglobin content -- anemia
2. Reduced oxygen delivery to the tissues
◦ a. reduced cardiac output -- shock, congestive heart failure
◦ b. left to right systemic shunt (as may be seen in septic shock)
3. Decreased tissue oxygen uptake
◦ a. mitochondrial poisoning (e.g., cyanide poisoning)
◦ b. left-shifted hemoglobin dissociation curve (e.g., from acute
alkalosis, excess CO, or abnormal hemoglobin structure)
99. Arterial Oxygen Tension (PaO2)
Normal value in healthy adult breathing
room air at sea level 97 mm Hg.
progressively with age
Dependant upon
1. FiO2
2. Patm
Hypoxemia is PaO2 < 80 mm Hg at RA
Most pts who need ABG usually req O2
therapy
O2 therapy should not be
withheld/interrupted ‗to determine PaO2
on RA‘
100. Acceptable PaO2 Values on Room
Air
Age Group Accepable PaO2
(mm Hg)
Adults upto 60 yrs > 80
& Children
Newborn 40-70
70 yrs > 70
80 yrs > 60
90 yrs > 50
60 yrs 80 mm Hg 1mm Hg/yr
101. Inspired O2 – PaO2 Relationship
FIO2 (%) Predicted Min
PaO2 (mm Hg)
30 150
40 200
50 250
80 400
100 500
If PaO2 < FIO2 x 5, pt probably hypoxemic at RA
102. Hypoxemia on O2 therapy
Uncorrected: PaO2 < 80 mm Hg
(< expected on RA & FIO2)
Corrected: PaO2 = 80-100 mm Hg
(= expected on RA but < expected for FIO2)
Excessively Corrected: PaO2 > 100 mm Hg
(> expected on RA but < expected for FIO2)
PaO2 > expected for FIO2:
1. Error in sample/analyzer
2. Pt‘s O2 consumption reduced
3. Pt does not req O2 therapy (if 1 & 2 NA)
