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