Blood Gas Interpretation

2005/8/25

Before beginning
Allens test for radial and ulnar artery Common errors of arterial blood sampling

in sample: PCO2, pH, PO2 Venous mixture: PCO2, pH, PO2 Excess anticoagulant (dilution): PCO2, pH, PO2 Metabolic effects: PCO2, pH, PO2
Air

Simultaneous electrolytes panel

Acid Base Physiology

The Law of Mass Action

[A] + [B] [C] + [D]
K2 K1

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)

Bicarbonate Buffering System

Metabolism Metabolism Oral intake Oral intake

CO2 + H2O H2CO3 H+ + HCO3Kidney Stomach Kidney

Lung

Acid Production and Elimination

Reaction
Glucose Fat
+O2 +O2

Products
H+ + HCO3H+ + HCO3-

Elimination
Lungs
24,000 mEq/day Volatile acid

Anaerobic Glucose +O2 Cysteine +O2 Phosphoproteins

H+ + lactate H+ + sulfate H+ + phosphate

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)

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

Proximal Renal Tubule

Distal Renal Tubule

Distal Tubule NH4+ excretion

Acid Base Disturbance

Metabolic acidosis: HCO3- Metabolic alkalosis: HCO3- Respiratory acidosis: PCO2 Respiratory alkalosis: PCO2
Simple Primary Secondary mixed

Metabolic Acidosis

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

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

Anion Gap

Increase

Decrease

Increased unmeasured anions Decreased unmeasured cations (Ca++, K+, Mg++) Increase in anionic albumin

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 Ketoacidosis Toxins Ethylene glycol

Diabetic
Alcoholic

Methanol
Salicylates

Starvation

Renal failure (acute and chronic)

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+)

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 Alkalosis
Strong ventilatory stimulus with alveolar hyperventilation Consuming HCO3 > 2-6 hrs: renal compensation (decrease NH4+/acid excretion and bicarbonate reabsorption)

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+]

Stepwise Approach

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

7.6

Respiratory alkalosis

Metabolic alkalsosis

pH

7.4

7.2

Metabolic acidosis

Respiratory acidosis

30

40 PCO2 (mmHg)

50

Compensatory Mechanisms

Respiratory compensation
Complete

within 24 hrs within several days

Metabolic compensation
Complete

Both the respiratory or renal compensation almost never over-compensates

Prediction of Compensatory Responses on Simple Acid-Base Disturbances Disorder Metabolic acidosis Prediction of Compensation 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 Chronic Respiratory acidosis Acute Chronic [HCO3-] will 1 mmol/L per 10-mmHg in PaCO2 [HCO3-] will 4 mmol/L per 10-mmHg in PaCO2 [HCO3-] will 2 mmol/L per 10-mmHg in PaCO2 [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 Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

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 VentilationPAO2 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 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

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