Transcript Blood Gas Interpretation

Blood Gas
Interpretation
2005/8/25
Before beginning…
Allen’s test for radial and ulnar artery
 Common errors of arterial blood sampling
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in sample: PCO2↓, pH↑, PO2↨
 Venous mixture: PCO2↑, pH↓, PO2↓
 Excess anticoagulant (dilution): PCO2↓, pH↑,
PO2↨
 Metabolic effects: PCO2↑, pH↓, PO2↓
 Air
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Simultaneous electrolytes panel
Acid Base Physiology
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The Law of Mass Action
K1
[A] + [B]  [C] + [D]
K2
K1/K2 = [C][D]/[A][B]

Dissociation constant for an acid
Ka = [H+][A-]/[HA]
Henderson-Hasselbalch Equation
CO2 + H2O  H2CO3  H+ + HCO3[H+] = K x [CO2]/[HCO3-]
= 24 PCO2/[HCO3-]
pH = 6.1 + log ([HCO3-]/0.0301xPCO2)
Normal Range
pH = 7.35-7.45
 PCO2 = 35-45 mmHg (40 mmHg)
 HCO3- = 22-26 mEq/L (24 mEq/L)
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Bicarbonate Buffering System
Metabolism
Metabolism
Oral intake
Oral intake
CO2 + H2O  H2CO3  H+ + HCO3-
Lung
Kidney
Stomach
Kidney
Acid Production and Elimination
Reaction
Glucose
Fat
Products
+O2
+O2
Anaerobic
Glucose
+O2
Cysteine
+O2
Phosphoproteins
Elimination
H+ + HCO3H+ + HCO3-
H+ + lactate
H+ + sulfate
H+ + phosphate
Lungs
24,000 mEq/day
Volatile acid
Kidneys
50-100 mEq/day
Non-volatile acid
Determinants of CO2 in the
alveolus
VA = VE – VD = VT x f (1- VD/VT)
PACO2 = k x (VCO2/VA)
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Physiologic dead space = anatomic dead
space + alveolar dead space
PaCO2
PaCO2 > 40 mmHg, MV = 2x normal
PaCO2 > 80 mmHg  CO2 nacrosis
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 tubule
 Distal tubule: reabsorption of remained
bicarbonate and secretion of hydrogen ion
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Proximal Renal Tubule
Distal Renal Tubule
Distal Tubule – NH4+ excretion
Acid Base Disturbance
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Metabolic acidosis: HCO3-↓
Metabolic alkalosis: HCO3- ↑
Respiratory acidosis: PCO2↑
Respiratory alkalosis: PCO2 ↓
Simple
Primary
Secondary
mixed
Metabolic Acidosis
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Indogenous acid production (lactic acidosis,
ketoacidosis)
Indogenous acid accumulation (renal failure)
Loss of bicarbonate (diarrhea)
High anion gap
Normal (hyperchloremic )
Pathophysiologic Effect of
Metabolic Acidosis
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Kussmaul respiration
Intrinsic cardiac contractility↓, normal inotropic
function
Peripheral vasodilatation
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
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Anion Gap
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Increase
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Increased unmeasured anions
 Decreased unmeasured
cations (Ca++, K+, Mg++)
 Increase in anionic albumin
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Decrease
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Increase in unmeasured
cations
Addition of abnormal cations
Reduction in albumin
concentration
Decrease in the effective
anionic charge on albumin by
acidosis
Hyperviscosity and severe
hyperlipidemia
( underestimation of sodium
and chloride concentration)
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
Metabolic Alkalosis
Net gain of [HCO3- ]
 Loss of nonvolatile acid (usually HCl by
vomiting) from the extracellular fluid
 Kidneys fail to compensate by excreting
HCO3- (volume contraction, a low GFR, or
depletion of Cl- or K+)
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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)
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Respiratory Acidosis
Acute: anxiety, dyspnea, confusion,
psychosis, and hallucinations and coma
 Chronic: sleep disturbances, loss of
memory, daytime somnolence, personality
changes, impairment of coordination, and
motor disturbances such as tremor,
myoclonic jerks, and asterixis
 Headache: vasocontriction
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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 reabsorption)
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Respiratory Alkalosis
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Reduced cerebral blood flow
 dizziness,
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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
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Do comprehensive history taking and physical
examination
Order simultaneous arterial blood gas
measurement and chemistry profiles
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
pH
7.6
Respiratory
alkalosis
7.4
7.2
Metabolic
alkalsosis
N
Metabolic
acidosis
30
Respiratory
acidosis
40
PCO2 (mmHg)
50
Compensatory Mechanisms
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Respiratory compensation
 Complete
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Metabolic compensation
 Complete
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within 24 hrs
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
acidosis
Respiratory
alkalosis
Metabolic
acidosis
Metabolic
alkalosis
Respiratory
acidosis
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Respiratory
alkalosis
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Metabolic
acidosis
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Metabolic
alkalosis
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Oxygenation
Poor diffusion across alveolar membrane
 Small pressure gradient between PAO2
and PaO2
 Large alveolar area is required for gas
transfer
 Hemoglobin carries the majority of oxygen
in the blood
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Oxygenation
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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
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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
compensation
 Mixed respiratory acidosis
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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
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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↑
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Clinical Example 4
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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
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37 y/o female, mild asthma history
Wheezes for 3 weeks, increasing chest tightness and
dyspnea for 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
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19 y/o male, Duchenne muscular dystrophy on
wheelchair 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
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57 y/o male, smoker, one week URI then 36 hrs
productive 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