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Blood Gas Interpretation
Before beginning…
Allen’s test for radial and ulnar artery Common errors of arterial blood sampling
Air in 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
CO2 + H2O H2CO3 H+ + HCO3-
Oral intake
Kidney
Metabolism
Oral intake
Kidney
Stomach
Metabolism
Lung
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 tubule
Distal tubule: reabsorption of remained bicarbonate 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
Respiratory acidosis
pH PaCo2 HC03
normal
Respiratory
Alkalosis
normal
Metabolic Acidosis
normal
Metabolic Alkalosis
normal
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 directionFor 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 acidosisrespiratory 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 Increased unmeasured
anions Decreased unmeasured
cations (Ca++, K+, Mg++) Increase in anionic
albumin
Decrease Increase in unmeasured cations Addition of abnormal cations Reduction in albumin concentra
tion Decrease in the effective anioni
c 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 defectIII. 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. CyclosporineIV. 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 vomiting) from the extracellular fluid
Kidneys fail to compensate by excreting HCO3-
(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 syndromeII. 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 tabletsIV. 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, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis
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
N
Respiratory alkalosis
Metabolic alkalosis
Metabolic acidosis
Respiratory acidosis
7.4
7.6
7.2
pH
30 40 50
PCO2 (mmHg)
Determination of primary acid-base disorders
Compensatory Mechanisms
Respiratory compensationComplete within 24 hrs
Metabolic compensationComplete within several days
Both the respiratory or renal compensation almost never over-compensates
Prediction of Compensatory Responses on SimpleAcid-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
Primary
Secondary
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic 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-a gradient 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 respiratoryLook 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 calculationsFor 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 3PH 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 PAO2 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 compensation
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 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
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