570 likes | 612 Views
Comprehensive guide on Allen’s test, arterial blood sampling, acid-base physiology, respiratory and metabolic effects. Learn to interpret blood gas results accurately and understand acid-base disturbances efficiently.
E N D
Blood Gas Interpretation 2005/8/25
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↨ • Metabolic effects: PCO2↑, pH↓, PO2↓ • Simultaneous electrolytes panel
Acid Base Physiology • The Law of Mass Action [A] + [B] [C] + [D] K1/K2 = [C][D]/[A][B] • Dissociation constant for an acid Ka = [H+][A-]/[HA] K1 K2
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 Oral intake Oral intake CO2 + H2O H2CO3 H+ + HCO3- Metabolism Kidney Stomach Kidney Lung
Acid Production and Elimination Reaction Products Elimination Glucose H+ + HCO3- Fat H+ + HCO3- Glucose H+ + lactate Cysteine H+ + sulfate Phosphoproteins H+ + phosphate +O2 Lungs 24,000 mEq/day Volatile acid +O2 Anaerobic Kidneys 50-100 mEq/day Non-volatile acid +O2 +O2
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
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
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 concentration Decrease in the effective anionic charge on albumin by acidosis Hyperviscosity and severe hyperlipidemia ( underestimation of sodium and chloride concentration) Anion Gap
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 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+]
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 Respiratory alkalosis Metabolic alkalsosis 7.6 pH N 7.4 Metabolic acidosis Respiratory acidosis 7.2 30 40 50 PCO2 (mmHg)
Compensatory Mechanisms • Respiratory compensation • Complete within 24 hrs • Metabolic compensation • Complete within several days • Both the respiratory or renal compensation almost never over-compensates
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↑