This document provides an overview of arterial blood gas analysis. It discusses how ABGs can indicate ventilation, gas exchange, and acid-base status by measuring pH, pCO2, pO2, oxygen saturation, and bicarbonate levels. Normal ranges for these values are provided. The effects of respiratory and metabolic acidosis and alkalosis on pH, pCO2 and bicarbonate are described. Compensation mechanisms and approaches to interpreting ABG results are also summarized. Three case examples are given to demonstrate how to analyze ABG results and identify the primary acid-base disturbance.
This document provides an overview of arterial blood gas analysis. It discusses how ABGs can indicate ventilation, gas exchange, and acid-base status by measuring pH, pCO2, pO2, oxygen saturation, and bicarbonate levels. Normal ranges for these values are provided. The effects of respiratory and metabolic acidosis and alkalosis on pH, pCO2 and bicarbonate are described. Compensation mechanisms and approaches to interpreting ABG results are also summarized. Three case examples are given to demonstrate how to analyze ABG results and identify the primary acid-base disturbance.
This document provides an overview of arterial blood gas analysis. It discusses how ABGs can indicate ventilation, gas exchange, and acid-base status by measuring pH, pCO2, pO2, oxygen saturation, and bicarbonate levels. Normal ranges for these values are provided. The effects of respiratory and metabolic acidosis and alkalosis on pH, pCO2 and bicarbonate are described. Compensation mechanisms and approaches to interpreting ABG results are also summarized. Three case examples are given to demonstrate how to analyze ABG results and identify the primary acid-base disturbance.
This document provides an overview of arterial blood gas analysis. It discusses how ABGs can indicate ventilation, gas exchange, and acid-base status by measuring pH, pCO2, pO2, oxygen saturation, and bicarbonate levels. Normal ranges for these values are provided. The effects of respiratory and metabolic acidosis and alkalosis on pH, pCO2 and bicarbonate are described. Compensation mechanisms and approaches to interpreting ABG results are also summarized. Three case examples are given to demonstrate how to analyze ABG results and identify the primary acid-base disturbance.
B Y: D R . FA I Z A N U R R E H M A N B U R K I ARTERIAL BLOOD GAS ANALYSIS
• Arterial blood gas measurements give an indication of ventilation, gas exchange and acid-base status. 1. Determine pH is normal? acidotic or alkalotic? 2. Determine cause: Respiratory Metabolic Mixed 3. Check oxygenation ARTERIAL BLOOD GASES
• P02 • partial pressure or tension of oxygen. • Pa02 • partial pressure of oxygen in arterial blood, i.e. oxygen dissolved in plasma • normal: (80-100mmHg) • Sa02 • extent to which haemoglobin in arterial blood is saturated with oxygen, i.e. capacity of blood to carry oxygen • normal: 95-98 % • Oxygen content • total amount of oxygen in blood, i.e. oxygen in both plasma and haemoglobin. • PaC02 • partial pressure of CO2 in arterial blood • the basis of respiratory acid-base balance • normal: 35- 45 mmHg • Hypoxaemia • reduced oxygen in arterial blood • Pa02 < (60 mmHg) or Sa02 <90%. • Hypoxia • reduced oxygen at tissue level • final common pathway of the cardiorespiratory system, more relevant to body function than hypoxaemia but more difficult to measure • Hypocapnia/hypocarbia • reduced CO2 in arterial blood. • Hypercapnia/hypercarbia • increased CO2 in arterial blood. • Fi02 • fraction of inspired oxygen, e.g. Fi02 of 0.6 = 60% inspired oxygen. NORMAL VALUES RANGE
• It responds to metabolic and respiratory change but cannot differentiate between them. BICARBONATE ION CONCENTRATION HC0 3 • measures metabolic acid-base balance. normal: 22-26 Meq/L • metabolic acidosis: < 22 mmol/L • metabolic alkalosis: > 26 mmol/L. CARBON DI OXIDE CONCENTRATION C0 2 • Measures respiratory acid base balance • Respiratory acidosis : > 45mm Hg • Respiratory alkalosis : < 35mmHg BASE EXCESS (BE)
• The quantity of strong acid or base required to restore pH to normal.
• BE is calculated from pH, PaC02 and haematocrit. • normal: minus 2 to plus 2 m mol/L • metabolic acidosis: < -2 m mol /L • • metabolic alkalosis: > 2 m mol /L. ACID-BASE REGULATION
• Three mechanisms to maintain pH
1. Buffer (in the blood: carbonic acid/bicarbonate, phosphate buffers)
2. Respiratory (CO2)
3. Renal (HCO3-) 1. Buffer • Whenever there is an accumulation of metabolically produced acids, the body attempts to neutralize those acids to maintain a constant acid–base balance. • This neutralizing is achieved by using up various "buffering" compounds in the blood stream, to bind the acids, disallowing them from contributing to more acidity. • About half of these buffering compounds come from HCO3, and the other half from plasma and red blood cell proteins and phosphates. 1. If buffering is not adequate, the lungs then present an avenue for regulating CO2, Hyper- or hypoventilation can stabilize the acid-base balance within 1-15 minutes. 2. If this is still not adequate, the kidneys then begin to eliminate acid, but take up to 3 days to normalize pH. Bicarbonate or base excess indicates the extent of renal compensation and quantify the metabolic component of an acidbase disturbance. INTERPRETATION OF ABGS INTERPRETATION OF ABGS INTERPRETATION
• Step 1: look at pH:
• pH means acidosis • pH means alkalosis. • Step 2 : look at PaC02: does it account for the abnormal pH? • PaC02 means respiratory acidosis • PaC02 means respiratory alkalosis. • Step 3: look at HC03 does it account for the abnormal pH? • HC03 – means metabolic alkalosis • HC03 - means metabolic acidosis. PH COMPENSATION
• A change in pH due to respiratory or metabolic disturbance is usually offset by a compensatory
change in the other system so that pH normalizes. When pH is restored to normal, full compensation has occurred. • Abnormal pH + change in PaC02 or bicarbonate/BE = non-compensation, i.e. a recent process • Abnormal pH + change in PaC02 and bicarbonate/BE = partial compensation • Normal pH + change in PaC02 and bicarbonate/BE = full compensation. RESPIRATORY ACIDOSIS • CAUSES: • Hypercarbia from hypoventilation • Sputum retention • Atelectasis
• Findings: – pCO2 increased therefore… pH decreases COMPONSETAION: • IN ACUTE: : Bicarb rises 1 meq/L for every 10 mmHg elevation in PCO2 . • IN CHRONIC: Bicarb rises 3.5 for every 10 mmHg elevation in PCO2. Example: ABG : 7.32/50/ /25 PH/PCO2/PO2/HCO3 RESPIRATORY ALKALOSIS • Hypocarbia from hyperventilation(pain,anxiety)
• Mechanical ventilation
• neurogenic
• Findings:
– pCO2 decreased… therefore pH increases
COMPONSETION:
• ACUTE: Plasma bicarb falls by 2 for every 10mmHg fall in PCO2
• CHRONIC: Bicarb falls by 4 for every 10 mmHg fall in PCO2.
Example:
ABG – 7.5/30/ /25
METABOLIC ACIDOSIS • Decrease in plasma bicarb and decrease in PH. CAUSES: • Gain of acid – e.g. lactic acidosis • Inability to excrete acid – e.g. renal tubular acidosis • Loss of base by GI – e.g. diarrhea COMPONSETION: • Respiratory compensation results in 1.2 mm Hg fall in PCO2 for every 1 meq /L fall in bicarb . • Last two digits of pH should equal PCO2 • if equal = no respiratory disturbances • if PCO2 high = overlapping respiratory acidosis • if PCO2 low = overlapping respiratory alkalosis • Example: – ABG – 7.25/40/ /15 ANION GAP
• Anion Gap = Na-(Cl + HCO3) =10 to 18mmol/L.
METABOLIC ALKALOSIS
• Increase HCO3- CAUSES: • Loss of acid – e.g. perfused vomiting (low Cl and kidney retains HCO3-) • Gain of base – e.g. contraction alkalosis (lasix)
COMPONSETION: • Respiratory compensation raises PCO2 by 0.7 mmHg for every 1 meq /L rise in HCO3 Example: – ABG – 7.55/40/ /35 CASE A • A patient is brought back to the floor from the operating room on a patient controlled analgesia (PCA) pump with hydromorphone. The patient hits his PCA button several times in the first hour. Shortly thereafter, the nurse walks in the room and finds him somnolent and difficult to arouse. • His SpO2 is only 88% so the nurse obtains a blood gas that reveals: • pH 7.25 • PCO2 55 • PO2 60 • HCO3- 25 • Step 1: pH is low (acidemia) • Step 2: The PCO2 is high (respiratory acidosis) and the bicarbonate is normal. A low pH with a high PCO 2 indicates that the primary process is a respiratory acidosis. • Summary • In this case, the patient started hypoventilating because he had likely given himself too much narcotic pain medications. CASE B • A patient presents with a one-day history of productive cough, fevers and increasing dyspnea. In the ER, the chest x- ray shows a right middle lobe opacity. His oxygen saturation is 90% on room air. • An arterial blood gas is obtained and it reveals a • pH 7.55 • PCO2 30 • PO2 63 • HCO3- 22 • Step 1: The pH is high (alkalemia) • Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is on the low side of normal. A high pH with a low PCO2 indicates that the primary process is a respiratory alkalosis. • Summary • In this case, the patient is likely hyperventilating because he is hypoxemic. This is a good example of the hypoxemic ventilatory response CASE C • A patient with Type I diabetes presents to the ER complaining of feeling poorly two days after running out of his insulin. • An arterial blood gas is obtained and shows • pH 7.25 • PCO2 28 • PO2 95 • HCO3- 15. • Step 1: The pH is low (acidemia) • Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). A low pH and low bicarbonate signifies that the metabolic acidosis is the primary process. • Summary • In this case, the patient is likely in diabetic ketoacidosis because he was not taking insulin. THANKYOU
