ARTERIAL BLOOD GASES. DR. ABDULAZIZ AL SHAER CONSULTANT INTENSIVIST 21/2/2010. Indications. Oxygenation Ventilation Acid-base disorders. Normal Arterial Blood Gases. Use of Venous VS. Arterial pH. As compared with arterial blood gases:. Technical Considerations.
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ARTERIAL BLOOD GASES DR. ABDULAZIZ AL SHAER CONSULTANT INTENSIVIST 21/2/2010
Indications • Oxygenation • Ventilation • Acid-base disorders
Use of Venous VS. Arterial pH As compared with arterial blood gases:
Technical Considerations • PaO2, PaCO2, and pH are directly measured with standard electrodes and digital analyzers. • Oxygen saturation is calculated from standard O2 dissociation curves. • Bicarbonate concentration is calculated using the Henderson-Hasselbalch equation: [HCO3-] pH = pKa + log ---------------- 0.03 [PaCO2] pKa is the negative logarithm of the dissociation constant of carbonic acid Simplified equation: [PaCO2] [H] = 24 x ----------- [HCO3-]
Technical considerations • Leukocytosis and thrombocytosis accelerate the decline of PaO2 and pH and elevation of PaCO2 within a stored sample • Significant increases in PaCO2 and decreases in pH occur when samples are stored at room temperature for more than 20 minutes
Technical considerations • Increased dead space in the syringe lowers PaCO2. • Air bubble falsely increases PaO2. • PaCO2 and PaO2 may diffuse out of plastic syringes. • Heparin and liquid solutions cause spuriously low PaCO2. • Dry (sodium or lithium) heparin in ABG kits may interfere with electrolyte measurement and, when concentrated, may lower pH. • Timing of ABG collection relative to ventilator changes should permit equilibration of alveolar and arterial PO2.
Oxygenation • PAO2 = PIO2 – 1.25 (PaCO2) PIO2 = FIO2 (PB – 47 mmHg) • P(A-a)O2 = PAO2 – PaO2 • CaO2 = (Hgb x 1.34 x SaO2)+(0.003 x PaO2) • VDO2 = CaO2 x CO
Oxygenation • PAO2 remains constant with age, but PaO2 decreases with age. • PaO2 (corrected for age): 100 mmHg – 0.3 x age • Normal P(A-a)O2 ranges from 5 to 25 mmHg breathing room air (it increases with age). • A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.
Causes of Hypoxemia NON-RESPIRATORYP(A-a)O2 Cardiac right-to-left shunt Increased Decreased PIO2 Normal Low mixed venous oxygen content Increased RESPIRATORY P(A-a)O2 Pulmonary right-to-left shunt Increased Ventilation-perfusion imbalance Increased Diffusion barrier Increased Hypoventilation (increased PaCO2) Normal
O2 delivery • VDO2 = CaO2 x CO • CaO2 = (Hgb x 1.34 x SaO2)=(0.003 x PaO2) • O2 saturation and not PaO2 is the parameter of oxygenation that contributes most to O2 delivery. • The relationship between PaO2 and SaO2 is demonstrated by the oxygen-hemoglobin dissociation curve.
Oxygen-Hemoglobin dissociation curve Left shift Decreased temp Decreased 2-3 DPG Decreased (H+) CO Right shift Reduced affinity’s Increased temp Increased 2-3 DPG Increased (H+)
Ventilation • The only way to assess ventilation is to check PaCO2 through ABGs. • VA=K x VCO2/PACO2 • VA is alveolar ventilation • K is 0.863 to covert VCO2 and VA units from mmHg • VCO2 is CO2 production • PACO2 is the alveolar CO2 pressure and in general it is equal to PaCO2. • VA = 0.863 x VCO2/PaCO2 • PaCO2 = 0.863 x VCO2/VA
Ventilation • VA = f x (Vt – VD) • The only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of the body’s CO2 production (VCO2). • Since alveolar ventilation (VA) equals minute ventilation (VE) minus dead space ventilation (VD), hypercapnia can arise from insufficient VE, increased VD, or a combination of both.
Ventilation • Examples of inadquate VE: • Sedatives • Respiratory muscle paralysis, weakness, CIM, MS, low Mg/Phos • Neuropathy: GBS, CIPN • Central hypoventilation • Examples of increased VD: • Chronic obstructive pulmonary disease • Severe restrictive lung disease
Acid-base interpretation Simplified Henderson-Hasselbalch equation: [PaCO2] [H] = 24 x ----------- [HCO3-] [H] is normally is 40nEq/L which gives a pH of 7.40 • Acidemia: blood pH < 7.35 • Alkalemia: blood pH > 7.45
Approach to Acid-Base Disorders Do numbers make sense? • Consider the clinical setting! • Is the patient acidemic or alkalemic? • Is the primary process metabolic or respiratory? • If metabolic acidosis, gap or non-gap? • Is compensation appropriate? • Is more than one disorder present?
Acute Respiratory Acidosis • pH will decrease by 0.08 for each 10 mmHg increase is PaCO2. • Compensation by retaining HCO3- by the kidney. • HCO3- will decrease by 1 for each 10mmHg increase in PaCO2.
Chronic Respiratory Acidosis • pH will decrease by 0.03 for each 10 mmHg increase is PaCO2. • Compensation by retaining HCO3- by the kidney. • HCO3- will decrease by 4 for each 10 mmHg increase in PaCO2.
Acute Respiratory Alkalosis • pH will increase by 0.08 for each 10 mmHg increase is PaCO2. • Compensation by dumping HCO3- by the kidney. • HCO3- will increase by 2 for each 10 mmHg decrease in PaCO2.
Chronic Respiratory Alkalosis • pH will increase by 0.03 for each 10 mmHg fall is PaCO2. • Compensation by dumping HCO3- by the kidney. • HCO3- will rise by 5 for each 10 mmHg fall in PaCO2.
Metabolic Acidosis • Primary disorder is low HCO3- • Compensation by decreasing PaCO2 • Expected PaCO2: (1.5 x HCO3-)+8 ± 2 • There are two types • Increased anion gap • Normal anion gap
Metabolic Acidosis: Elevated Anion Gap AG = Na+ - (Cl- + HCO3-) = 12 ± 2
Anion Gap in Hypoalbuminemia • The true anion gap is underestimated in hypoalbuminemia; AG must be adjusted. • Formulas for adjusted AG: • For every 1.0 fall in albumin, increased AG by 2.5 • Consider the patient’s “normal” AG to be (2 x alb) + (0.5 x phosphate) • Adjusted AG = Observed AG + (2.5 x [normal alb – adjusted alb]
Causes AG Acidosis • Ketoacidosis • Lactic acidosis • Intoxications • Renal failure • Rhabdomyolysis
Ketosis • Diabetes • Starvation • Alcoholic • Isopropyl alcohol * *Ketosis with normal AG and HCO3
Lactic Acidosis • Type A: Hypoxic Lactate: pyruvate > 10:1 • Type B: Glycolytic Lactate: pyruvate = 10:1
Intoxications Causing High AG Acidosis • Aspirin • Methanol • Ethylene Glycol • Paraldehyde
The Delta/Delta: Δ AG/Δ HCO3 • Rationale: For each unit INCREASE in AG ( • “Normal” values: • AG = 12 • HCO3 = 24
Osmolar Gap • Measured serum osmolality > Calculated serum osmolality by > 10 mOsm • Calculated osmolality: • 2[Na] + BUN/2.8 + glucose/18 ethanol/4.6 • BUN, glucose and ethanol are converted from mg/dl to mmol/L • If using mmol/L: 2[Na] + BUN + glucose + ethanol
Causes of High Osmolar Gap • Isotonic hyponatremia Hyperlipidemia Hyperproteinemia Mannitol • Glycine infusion • Chronic renal failure • Ingestions: Ethanol, isopropyl alcohol, ethylene glycol, mannitol • Contrast media
High Normal Anion Gap GI Fluid Loss? Osmolar Gap Yes No Normal Increased Diarrhea Illeostomy Enteric fistula Urine pH Uremia Lactate Ketoacids Salicylate Ethylene glycol Methanolol >5.5 <5.5 Serum K Distal RTA (Type 1) Low High Proximal RTA (Type 2) Type 4 RTA Approach to Metabolic Acidosis
Metabolic Alkalosis • Etiology: Requires both generation of metabolic alkalosis (loss of H+ through GI tract or kidneys) and maintenance of alkalosis (impairment in renal HCO3 excretion) • Causes of metabolic alkalosis • Loss of Hydrogen • Retention of bivarbonate • Contraction alkalosis • Maintenance factors: Decrease in GFR, increase in HCO3reabsorption
Urine Chloride Very Low (< 10mEq/L) Vomiting, NG suction Postdiuretic, posthypercapneic Villous adenoma, congenital chloridorrhea, post- alkali > 20 mEq/L Low (< 20mEq/L) Urine Potassium Laxative abuse Other profound K depletion 30 mEq/L Diuretic phase of diuretic Rx, Barter’s, Gitelman’s, primary aldo, Cushings, Liddle’s, secondary aldosteronism Use of Spot Urine Cl and K
Treatment of Metabolic Alkalosis • Remove offending culprits. • Chloride (saline) responsive alkalosis: Replete volume with NaCl. • Chloride non-responsive (saline resistant) alkalosis Acetazolamide (CA inhibitor) Hydrochloric acid infusion Correct hypokalemia if present
Q.1 22 male known D.M. developed sever upper respiratory infection Na 128 K 5.9 Cl 94 Hco3 6 Pco2 = 15 Po2=102 PH =7.19 Glucose = 324
1AR the data internally consistent? yes it is internally consistent Pco2= [H]* [HCO3] /24 Pco2=61*6/24 Pco2=15 1BIs the patient acidemic or alkalemic? < 7.4 so acidemic 1CIs the primary disorder respiratory? Pco2 is not elevated so this metabolic
Q 1 cont. 1D The patient has MA ,is this hyperchloremic or high anion gap MA ? AG = Na-Cl-HCO3 = 28 ( normal 10-12) so high AG MA 1FIs the compensation for the MA is appropriate? Expected Pco2 =1.5*HCO3 +8 -+ 2 so expected 17 -+ 2 so simple compensated MA
1E Is there another ( M alk) acid base disturbance present ? What is the delta anion gap Delta AG=measured AG-normal AG=28-10=18 Adding the delta gap to the measured HCO3 give the predicted starting HCO3 ( before the anion gap acidosis). Here, 18+6=24,normal preacidosis level of HCO3. so NO underlying met alkalosis
Q 1 cont. 1Gwhat a re the causes of an increase AG DKA , alcoholic ketoacidosis, and lactic acidosis Drugs and toxin methanol and ethylene glycol Most likely her is DKA
Q.2 47 female CRF admitted with sever alcoholic intoxication, she is somnolent and febrile, RR 10 /min Na = 134 K=6.1 Cl= 112 HCO3=10 Pco2 =30 Po2=52 PH=7.10 Creatnine =3.7 BUN=62 2AR the data internally consistent? the data are internally consistent Pco2=[H]*[HCO3]/24 Pco2=70*10/24 Pco2=29
2BIs the patient acidemic or alkalemic? PH< 7.4 ,so the patient is acidemic 2CIs the primary disorder respiratory? This MA as the Pco2 is not elevated
2Dthe pt has MA is this hyperchlormic or a high anion gap type MA ? AG 134-112-10=12 so the patient has normal AG or hyperchlormic MA
2EIs the compensation for the MA appropriate? Expected Pco2=1.5*HCO3+8 +- 2 for this degree of acidemia Expected Pco2= 1.5*10+8+- 2= 23 +- 2 The measured Pco2 is 30 which is higher than what is expected with adequate compensation. therefore, this is mixed acid base disturbance , that is combined metabolic and respiratory acidosis. Even though the Pco2 is low it is not low enough