Blood Gas

Interpretation
Before beginning…
 Allen’s test for radial and ulnar artery
 Common errors of arterial blood sampling
 Airin sample: PCO2↓, pH↑, PO2↨
 Venous mixture: PCO2↑, pH↓, PO2↓
 Excess anticoagulant (dilution): PCO2↓, pH↑, PO2↨
(RARE)
 Metabolic effects: PCO2↑, pH↓, PO2↓
 Simultaneous electrolytes panel
Normal Range
 PHa = 7.35-7.45 (7.40)
 PHv = 7.31-7.41 (7.36)
 PaCO2 = 35-45 mmHg (40 mmHg)
 PvCO2= 41-51 mmHg (46 mmHg)
 HCO3- = 22-26 mEq/L (24 mEq/L)
 SaO2 = 95%-100% (97%)
 SvO2 = 68%-77% (75%)
Bicarbonate Buffering System
Metabolism
Oral intake
Metabolism Oral intake

CO2 + H2O  H2CO3  H+ + HCO3-

Kidney Kidney
Lung
Stomach
Henderson-Hasselbalch Equation

pH = 6.1 + log ([HCO3-]/0.0301xPCO2)

Determinants of CO2 in the alveolus

PaCO2 = (0.863) x (VCO2/VA)

(VA = VE – VD )
Physiologic dead space = anatomic dead space
+ alveolar dead space
Renal Regulation of Bicarbonate
 “Reabsorption“ of filtered HCO3- (4000 mmol/day)
 Formation of titratable acid (4000 mmol/day H +)
 Excretion of NH4+ in the urine
 80-90% of HCO3- : reabsorbed in the proximal tub
ule
 Distal tubule: reabsorption of remained bicarbonat
e and secretion of hydrogen ion
 STEPS OF ABG INTERPRETATION

 Classification
Type of disorder (Resp. or Metab.)
 Calculations

Calculate Compensation and Gaps

 Confirmation

Patient History, baseline, check for accuracy

 pH PaCo2 HC03
normal
Respiratory
acidosis

Respiratory normal
Alkalosis
Metabolic normal
Acidosis
Metabolic normal
Alkalosis
So
• PaCO2 > 44 with a pH < 7.35
represents a respiratory acidosis
*PaCO2 < 36 with a pH > 7.45
represents a respiratory alkalosis
For a primary respiratory problem, pH and paCO2
move in the opposite direction
 For each deviation in paCO2 of 10 mm Hg in
either direction, 0.08 pH units change in the
opposite direction
And
*HCO3 < 22 with a pH < 7.35
represents a metabolic acidosis
*HCO3 > 26 with a pH > 7.45
represents a metabolic alkalosis
For a primary metabolic problem, pH and HCO3 are
in the same direction, and paCO2 is also in the
same direction
Compensation
 The body’s attempt to return the acid/base status
to normal (i.e. pH closer to 7.4)
Primary Problem Compensation
respiratory acidosis metabolic alkalosis
respiratory alkalosis metabolic acidosis
metabolic acidosis respiratory alkalosis
metabolic alkalosis respiratory acidosis
Expected Compensation

Respiratory acidosis
 Acute – the pH decreases 0.08 units for every 10 mm
Hg increase in paCO2; HCO3 0.1-1 mEq/liter per
10 mm Hg paCO2
 Chronic – the pH decreases 0.03 units for every 10
mm Hg increase in paCO2; HCO3 1.1-3.5 mEq/liter
per 10 mm Hg paCO2
Expected Compensation

Respiratory alkalosis
 Acute – the pH increases 0.08 units for every 10 mm Hg
decrease in paCO2; HCO3 0-2 mEq/liter per 10 mm Hg
paCO2
 Chronic - the pH increases 0.17 units for every 10 mm Hg
decrease in paCO2; HCO3 2.1-5 mEq/liter per 10 mm Hg
paCO2
Expected Compensation

Metabolic acidosis
 paCO2 = 1.5(HCO3) + 8 (2)

 paCO2 1-1.5 per 1 mEq/liter HCO3

Metabolic alkalosis
 paCO2 = 0.7(HCO3) + 20 (1.5)

 paCO2 0.5-1.0 per 1 mEq/liter HCO3

Metabolic Acidosis
 Causes:
 Indogenous acid production (lactic acidosis, k
etoacidosis)
 Indogenous acid accumulation (renal failure)
 Loss of bicarbonate (diarrhea)
 High anion gap
 Normal (hyperchloremic )
Pathophysiologic Effect of Metabolic Acidosis

 Kussmaul respiration
 Central vasoconstriction  pulmonary edema
 Depressed CNS function
 Glucose intolerance
Anion Gap
 AG = Na+ - (Cl- + HCO3-)
 Unmeasured anions in plasma (normally 10 to
12 mmol/L)
 Anionic proteins, phosphate, sulfate, and
organic anions
 Correction: if albumin < 4
Albumin ↓1  AG ↓ 2.5
Anion Gap
 Increase  Decrease
 Increased
 Increase in unmeasured cations
unmeasured  Addition of abnormal cations
anions  Reduction in albumin concentra
 Decreased unmeasured tion
cations (Ca++, K+, Mg++)  Decrease in the effective anioni
c charge on albumin by acidosi
 Increase in anionic s
albumin  Hyperviscosity and severe hype
rlipidemia ( underestimation of
sodium and chloride concentrat
ion)
Causes of High-Anion-Gap Metabolic Acidosis

Lactic acidosis Toxins

 

Ketoacidosis Ethylene glycol

 

Diabetic Methanol
 

Alcoholic Salicylates
 

Starvation Renal failure (acute and chronic)

 
Causes of Non-Anion-Gap Acidosis
I. Gastrointestinal bicarbonate loss
A. Diarrhea
B. External pancreatic or small-bowel drainage
C. Ureterosigmoidostomy, jejunal loop, ileal loop
D. Drugs
1. Calcium chloride (acidifying agent)
2. Magnesium sulfate (diarrhea)
3. Cholestyramine (bile acid diarrhea)
II. Renal acidosis
A. Hypokalemia
1. Proximal RTA (type 2)
2. Distal (classic) RTA (type 1)
B. Hyperkalemia
1. Generalized distal nephron dysfunction (type 4 RTA)
a. Mineralocorticoid deficiency
b. Mineralocorticoid resistance
c. ØNa+ delivery to distal nephron
d. Tubulointerstitial disease
e. Ammonium excretion defect
III. Drug-induced hyperkalemia (with renal insufficiency)
A. Potassium-sparing diuretics (amiloride, triamterene,
spironolactone)
B. Trimethoprim
C. Pentamidine
D. Angiotensin-converting enzyme inhibitors and AT-II
receptor blockers
E. Nonsteroidal anti-inflammatory drugs
F. Cyclosporine
IV. Other
A. Acid loads (ammonium chloride, hyperalimentation)
B. Loss of potential bicarbonate: ketosis with ketone excretion
C. Expansion acidosis (rapid saline administration)
D. Hippurate
E. Cation exchange resins
Mixed Metabolic Disorders:
 Bicarbonate Gap:
 BG= Patient HCO3+ΔAG
 Normal BG=24 (20-28)
 24 AG met. Acidosis
 <20 AG met Acid. + non AG met. Acid.
 >28 AG met Acid. + Met. Alk
Metabolic Alkalosis
 Net gain of [HCO3- ]
 Loss of nonvolatile acid (usually HCl by vomit
ing) from the extracellular fluid
 Kidneys fail to compensate by excreting HCO 3-
(volume contraction, a low GFR, or depletion
of Cl- or K+)
Causes of Metabolic Alkalosis
I. Exogenous HCO3- loads
A. Acute alkali administration
B. Milk-alkali syndrome
II. Effective ECFV contraction, normotension, K+ deficiency,
and secondary hyperreninemic hyperaldosteronism
A. Gastrointestinal origin
1. Vomiting
2. Gastric aspiration
3. Congenital chloridorrhea
4. Villous adenoma
5. Combined administration of sodium polystyrene
sulfonate (Kayexalate) and aluminum hydroxide
B. Renal origin
1. Diuretics
2. Edematous states
3. Posthypercapnic state
4. Hypercalcemia/hypoparathyroidism
5. Recovery from lactic acidosis or ketoacidosis
6. Nonreabsorbable anions including penicillin, carbenicillin
7. Mg2+ deficiency
8. K+ depletion
9. Bartter's syndrome (loss of function mutations in TALH)
10. Gitelman's syndrome (loss of function mutation in
Na+-Cl- cotransporter in DCT)
Causes of Metabolic Alkalosis
III. ECFV expansion, hypertension, K+ deficiency, and
mineralocorticoid excess
A. High renin
1. Renal artery stenosis
2. Accelerated hypertension
3. Renin-secreting tumor
4. Estrogen therapy
B. Low renin
1. Primary aldosteronism
a. Adenoma
b. Hyperplasia
c. Carcinoma
2. Adrenal enzyme defects
a. 11b-Hydroxylase deficiency
b. 17a-Hydroxylase deficiency
3. Cushing's syndrome or disease
4. Other
a. Licorice
b. Carbenoxolone
c. Chewer's tobacco
d. Lydia Pincham tablets
IV. Gain of function mutation of renal sodium channel with
ECFV expansion, hypertension, K+ deficiency, and
hyporeninemic-hypoaldosteronism
A. Liddle's syndrome
Respiratory Acidosis
 Severe pulmonary disease
 Respiratory muscle fatigue
 Abnormal ventilatory control
 Acute vs. Chronic (> 24 hrs)
Respiratory Acidosis
 Acute: anxiety, dyspnea, confusion, psychosis,
and hallucinations and coma
 Chronic: sleep disturbances, loss of memory, d
aytime somnolence, personality changes, impa
irment of coordination, and motor disturbance
s such as tremor, myoclonic jerks, and asterixi
s
 Headache: vasocontriction
Respiratory Acid-Base Disorders
II. Acidosis
A. Central
1. Drugs (anesthetics, morphine, sedatives)
2. Stroke
3. Infection
B. Airway
1. Obstruction
2. Asthma
C. Parenchyma
1. Emphysema
2. Pneumoconiosis
3. Bronchitis
4. Adult respiratory distress syndrome
5. Barotrauma
D. Neuromuscular
1. Poliomyelitis
2. Kyphoscoliosis
3. Myasthenia
4. Muscular dystrophies
E. Miscellaneous
1. Obesity
2. Hypoventilation
3. Permissive hypercapnia
Respiratory Alkalosis
 Strong ventilatory stimulus with alveolar
hyperventilation
 Consuming HCO3-
 > 2-6 hrs: renal compensation (decrease
NH4+/acid excretion and bicarbonate re-
absorption)
Respiratory Alkalosis
 Reduced cerebral blood flow
 dizziness, mental confusion, and seizures
 Minimal cardiovascular effect in normal health
 Cardiac output and blood pressure may fall in
mechanically ventilated patients
 Bohr effect: left shift of hemoglobin-O2 dissociation
curve  tissue hypoxia (arrhythmia)
 intracellular shifts of Na+, K+, and PO4- and reduces
free [Ca2+]
Respiratory Acid-Base Disorders
I. Alkalosis
A. Central nervous system stimulation
1. Pain
2. Anxiety, psychosis
3. Fever
4. Cerebrovascular accident
5. Meningitis, encephalitis
6. Tumor
7. Trauma
B. Hypoxemia or Tissue hypoxia
1. High altitude, ØPaCO2
2. Pneumonia, pulmonary edema
3. Aspiration
4. Severe anemia
C. Drugs or hormones
1. Pregnancy, progesterone
2. Salicylates
3. Nikethamide
D. Stimulation of chest receptors
1. Hemothorax
2. Flail chest
3. Cardiac failure
4. Pulmonary embolism
E. Miscellaneous
1. Septicemia
2. Hepatic failure
3. Mechanical hyperventilation
4. Heat exposure
5. Recovery from metabolic acidosis
Stepwise Approach
 Do comprehensive history taking and physical
examination
 Assess accuracy of data
 Direction of pH: always indicates the primary
disturbance
 Calculate the expected compensation
 Second or third disorders
 Determination of primary acid-base disorders

Respiratory Metabolic
7.6 alkalosis alkalosis

7.4
pH

7.2 Metabolic Respiratory

acidosis acidosis

30 40 50
PCO2 (mmHg)
Compensatory Mechanisms
 Respiratory compensation
 Complete within 24 hrs
 Metabolic compensation
 Complete within several days
 Both the respiratory or renal compensation
almost never over-compensates
Prediction of Compensatory Responses on Simple
Acid-Base Disturbances

Disorder Prediction of Compensation  

Metabolic acidosis PaCO2 = (1.5x HCO3-) + 8 or  

PaCO2 will ↓ 1.25 mmHg per mmol/L ↓ in [HCO3-] or  

PaCO2 = [HCO3-] + 15  

Metabolic alkalosis PaCO2 will ↑ 0.75 mmHg per mmol/L ↑ in [HCO3-] or  

PaCO2 will ↑ 6 mmHg per 10-mmol/L ↑ in [HCO3-] or  

PaCO2 = [HCO3-] + 15  

Respiratory alkalosis  

Acute [HCO3-] will ↓ 2 mmol/L per 10-mmHg ↓ in PaCO2  

Chronic [HCO3-] will ↓ 4 mmol/L per 10-mmHg ↓ in PaCO2  

Respiratory acidosis  

Acute [HCO3-] will ↑ 1 mmol/L per 10-mmHg ↑ in PaCO2  

Chronic [HCO3-] will ↑ 4 mmol/L per 10-mmHg ↑ in PaCO2  

Mixed Acid Base Disorders
Secondary
Primary
Respiratory Respiratory Metabolic Metabolic
acidosis alkalosis acidosis alkalosis
Respiratory
 
acidosis
Respiratory
 
alkalosis
Metabolic
  
acidosis
Metabolic
  
alkalosis
Mechanisms of Hypoxemia
 Inadequate inspiratory partial pressure of
oxygen
 Hypoventilation
 Right to left shunt
 Ventilation-perfusion mismatch
 Incomplete diffusion equilibrium
Assessment of Gas Exchange
 Alveolar-arterial O2 tension difference
 A-agradient
 PAO2-PaO2
 PAO2 = FIO2(PB - PH2O) - PaCO2/RQ*
 arterial-Alveolar O2 tension ratio
 PaO2/PAO2
 arterial-inspired O2 ratio
 PaO2/FIO2
 P/F ratio
*RQ=respiratory quotient= 0.8
Summary
 First, does the patient have an acidosis or an
alkalosis
 Look at the pH
 Second, what is the primary problem –
metabolic or respiratory
 Look at the pCO2
 If the pCO2 change is in the opposite direction of
the pH change, the primary problem is respiratory
Summary
 Third, is there any compensation by the patient
- do the calculations
 For a primary respiratory problem, is the pH
change completely accounted for by the change in
pCO2
 if yes, then there is no metabolic compensation
 if not, then there is either partial compensation or
concomitant metabolic problem
Summary
 For
a metabolic problem, calculate the expected
pCO2
 if equal to calculated, then there is appropriate
respiratory compensation
 if higher than calculated, there is concomitant
respiratory acidosis
 if lower than calculated, there is concomitant respiratory
alkalosis
Summary
 Next, don’t forget to look at the effectiveness
of oxygenation, (and look at the patient)
 your patient may have a significantly increased
work of breathing in order to maintain a “normal”
blood gas
 metabolic acidosis with a concomitant respiratory
acidosis is concerning
Case 1
Little Boy: He suffers a significant depression of
mental status and respiration. You see him in
the ER 3 hours after ingestion with a
respiratory rate of 4. A blood gas is obtained
(after doing the ABC’s, of course). It shows
pH = 7.16, pCO2 = 70, HCO3 = 22
Case 1
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory acidosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic alkalosis
Case 2
Little girl has had vomiting and diarrhea for 3
days. In her mom’s words, “She can’t keep
anything down and she’s runnin’ out.” She
has had 1 wet diaper in the last 24 hours. She
appears cool to touch with a prolonged
capillary refill time. her blood gas reveals:
pH=7.34, pCO2=26, HCO3=12
Case 2
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory alkalosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic acidosis
Case 2
Compensated metabolic acidosis
 The prolong history of fluid loss through diarrhea has
caused a metabolic acidosis. The mechanisms probably
are twofold. First there is lactic acid production from
the hypovolemia and tissue hypoperfusion. Second,
there may be significant bicarbonate losses in the stool.
The body has compensated by “blowing off” the CO2
with increased respirations.
Case 3
PH 7.52 ,PaCO2 30, HCO3 21,PaO2 62
Na 142, Cl 98:
* Interpretation
• Calculate Anion Gap
• Calculate Bicarbonate Gap
• Oxygenation Status
Oxygenation
 Poor diffusion across alveolar membrane
 Small pressure gradient between P AO2 and
PaO2
 Large alveolar area is required for gas
transfer
 Hemoglobin carries the majority of oxygen in
the blood
Oxygenation
 Ventilation and alveolar disease
 Ventilation↓PAO2 ↓PaO2 ↓, combined PCO2↑
 Alveolar disease
 Reduced alveolar area
 Thickened alveolar membrane
 V/Q mismatch
 Shunt
Alveolar-arterial Oxygen Gradient

PAO2 = FiO2 (PB-PH2O) – PCO2/R

= 0.21(760-47) – 40/0.8
= 100
R: respiratory quotient

P(A-a)O2 = PAO2 – PaO2

(= Age x 0.4)
Oxygen Content and Saturation

O2 content = 1.34 x Hb x Saturation + 0.0031xPO2

Pulse Oximeters
 Percentage of oxygenated hemoglobin in blood
 Absorption of light in the red and infra-red spectra
 Continuous monitor
 Accurate (3%) at high saturation, less below 80%
 Insensitive around the normal PO2
 COHb and MetHb
Clinical Example 1
 72 y/o male, COPD with acute exacerbation
 Under O2 2L/min

pH 7.44, PCO2 54, PO2 60, HCO3 36

 Metabolic alkalosis with respiratory compensa
tion
 Mixed respiratory acidosis
Clinical Example 2
 30 y/o male, sudden onset dyspnea
 Room air
 7.33/24/111/12
 Metabolic acidosis
 Respiratory compensation
 Normal A-a O2 gradient
 O2↑: hyperventilation
Clinical Example 3
 70 y/o male, acute hemoptysis and dyspnea
 Room air
 7.50/31/88/24
 Respiratory alkalosis
 Not been renal compensated yet
 Normal PO2, but A-a O2 gradient↑
Clinical Example 4
 18 y/o female, chest tightness and dyspnea for 4 hrs
 RR 28/min, distressed, widespread wheezing
 O2 mask 6L/min
 7.31/49/115/26
 Respiratory acidosis
 Normal bicarbonate  acute
 May have problems with oxygenation
Clinical Example 5
 37 y/o female, mild asthma history
 Wheezes for 3 weeks, increasing chest tightness and dyspnea f
or 24 hrs, call for ambulance with Oxygen use
 RR 18/min, anxious and distressed
 Room air
 7.37/43/97/27
 Normal?
 r/o CO2 retention
 Low A-a O2: Oxygen use in the ambulance
Clinical Example 6
 19 y/o male, Duchenne muscular dystrophy on wheelc
hair for 7 yrs
 No previous respiratory problems but frequent UTI
 Room air
 7.21/81/44/36
 Respiratory acidosis
 Metabolic compensation
 Normal A-a O2  pure ventilatory failure
Clinical Example 7
 57 y/o male, smoker, one week URI then 36 hrs produ
ctive cough, fever and dyspnea
 RR 36/min, distressed, CXR: RLL pneumonia
 7.33/27/51/22, 2L/min
 7.34/32/58/24, 10L/min mask
 Early metabolic acidosis
 Severe hypoxemic respiratory failure
 Intra-pulmonary shunting
Thank you for your attention