Arterial Blood Gas Interpretation PRESENTER- Dr. Shankerdeep Sondhi Resident IIInd Yr Department of Medicine
OBJECTIVESABG SamplingInterpretation of ABGCase Scenarios
ABG – Procedure and Precautions Site- (Ideally) Radial Artery Brachial Artery Femoral Artery Ideally - Pre-heparinised ABG syringes - Syringe should be FLUSHED with 0.5ml of 1:1000 Heparin solution and emptied. DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGEHEPARIN DILUTIONAL HCO3 EFFECT PCO2 Only small 0.5ml Heparin for flushing and discard it Syringes must have > 50% blood.
Ensure No Air Bubbles. Syringe must be sealed immediately after withdrawing sample. ◦ Contact with AIR BUBBLES Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg Air Bubble + Blood = PO2 PCO2 ABG Syringe must be transported at the earliest to the laboratory for EARLY analysis via COLD CHAIN
ABG ELECTRODESA. pH (Sanz Electrode) Measures H+ ion concentration of sample against a known pH in a reference electrode, hence potential difference. Calibration with solutions of known pH (6.384 to 7.384)B. P CO2 (Severinghaus Electrode) CO2 reacts with solution to produce H+ higher C02- more H+ higher P CO2 measuredC. P 02 (Clark Electrode) 02 diffuses across membrane producing an electrical current measured as P 02.
Interpretation of ABG
Acid Base Homeostasis1. Plasma Acid Homeomostasis: Chemical buffering ◦ H+ influenced by Rate of endogenous production Rate of excretion Buffering capacity of body ◦ Buffers effective at physiologic pH are Hemoglobin Phosphate Proteins Bicarbonate
2. Alveolar Ventilation: pCO2 action is immediate. Stimulation of respiratory center washes off the excess CO2 increasing pH, and vice versa3. Excretion: Liver: uses HCO3– to make urea which further prevents accumulation of ammonia and traps H+ in renal distal tubule Kidney: regulate plasma [HCO3–] through three main processes: • reabsorption of filtered HCO3– • formation of titratable acid • excretion of NH4+ in the urine. Proximal tubule reclaims 85% filtered HCO3– Distal tubule reclaims 15%, and excretes H+ 40–60 mmol/d of protons is excreted to maintain balance
Acid Base Balance H+ ion concentration in the body is precisely regulated The body understands the importance of H+ and hence devised DEFENCES against any change in its concentration-BICARBONATE RESPIRATORY RENALBUFFER REGULATION REGULATIONSYSTEM Acts in few Acts in hours toActs in few minutes daysseconds
BUFFER SYSTEM 1st line of defence in pH regulation. Determine capacity of ECF to transport acids from site of production to site of excretion without undue change in pH. They resist change in pH on addition of acid/alkali in media wherever they are.
BICARBONATE BUFFER NAHCO3/H2CO3 = 20/1 = Alkali reserve. conversion of strong & non volatile acid in ECF, in weak & volatile acid at the expense of NaHCO3 component of buffer. H2CO3 thus formed is eliminated by lung as CO2.Directly linked with respiration & healthy lungs essential for its function. High concentration in blood,so very good physiological buffer. Weak chemical buffer.
PHOSPHATE BUFFER Na2HPO4/NaH2PO4 = AlkPO4/AcidPO4 = 4/1. NaH2PO4 excreted by kidneys. Directly linked with kidneys & healthy kidneys necessary for its functioning. Concentration in blood is low so not good physiological buffer. Very good chemical buffer as pKa aprroches pH.
PROTEIN BUFFER Na+Pr- / H+Pr- = salt/acid. Proteins can act as a base In acidic medium nd as an acid in basic medium..with COOH& NH2 group. Buffering capacity of plasma proteins is much less than Hb.
Respiratory Regulation of Acid Base Balance- ALVEOLAR H+ VENTILATION PaCO2 ALVEOLAR H+ VENTILATION PaCO2
Renal Regulation of Acid Base BalanceKidneys control the acid-base balance by excreting either an acidic or a basic urine,This is achieved in the following ways-Reabsorption Secretion of H+ of HCO3 ions in tubules in blood and excretion PCO2 K+ in ECF Aldosterone H+ ion •Proximal Convulated Tubules (85%) •Thick Ascending Limb ofECF Volume Loop of Henle (10%) Angiotensin II •Distal Convulated Tubule •Collecting Tubules(5%)
Definitions and Terminology ACIDOSIS – presence of a process which tends to pH by virtue of gain of H + or loss of HCO3- ALKALOSIS – presence of a process which tends to pH by virtue of loss of H+ or gain of HCO3-If these changes, change pH, suffix ‘emia’ is added ACIDEMIA – reduction in arterial pH (pH<7.35) ALKALEMIA – increase in arterial pH (pH>7.45)
Simple Acid Base Disorder/ Primary Acid Base disorder – a single primary process of acidosis or alkalosis due to an initial change in PCO2 and HCO3. Compensation - The normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder The Compensatory responses to a primary Acid Base disturbance are never enough to correct the change in pH , they only act to reduce the severity. Mixed Acid Base Disorder – Presence of more than one acid base disorder simultaneously .
CompensationMetabolic Disorders – Compensation in these disorders leads toa change in PCO2 METABOLIC ACIDOSIS • For every 1mmol/l in HCO3 the PCO2 falls by 1.25 mm Hg METABOLIC ALKALOSIS • For every 1mol/l in HCO3 the PCO2 by 0.75 mm Hg
In Respiratory Disorders PCO2 Kidney HCO3 Reabsorption Compensation begins to appear in 6 – 12 hrs and is fully developed only after a few days.1.ACUTEBefore the onset of compensationResp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/lResp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l2.CHRONIC (>24 hrs)After compensation is fully developedResp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/lResp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Body’s physiologic response to Primary disorderin order to bring pH towards NORMAL limitFull compensationPartial compensationNo compensation…. (uncompensated)BUT never overshoots,If a overshoot pH is there,Take it granted it is a MIXED disorder
STEP WISE APPROACH to Interpretation Of ABG reports
Normal ValuesANALYTE Normal Value Units pH 7.35 - 7.45 PCO2 35 – 45 mm Hg PO2 80 – 100 mm Hg` [HCO3] 22 – 26 meq/L SaO2 95-100 %Anion Gap 10 + 2 meq/L ∆HCO3 +2 to -2 meq/L
STEP 0 • Is this ABG Authentic?STEP 1 • ACIDEMIA or ALKALEMIA? • RESPIRATORY or METABOLIC?STEP 2STEP 3 • Is COMPENSATION adequate?STEP 4 • If METABOLIC – ANION GAP? • If High gap Metabolic Acidosis–STEP 5 GAP GAP?
Step 0 – Authentic or Not? Verify that the ABG values are internally accurate. ◦ The accuracy of the values can be established by confirming that they satisfy a simplified form of the Henderson-Hasselbalch equation: [H+](nmol/L) = 24 × pCO2(mm Hg) ∕ [HCO3-] (mEq/L) ◦ [H+] = 10 exp(-pH). Within the pH range of 7.26 to 7.45 [H+] in nmol/L = 80 − the decimal of the pH (e.g., for pH = 7.25, [H+] = 80 − 25 = 55
STEP 1 ACIDEMIA OR ALKALEMIA? Look at pH <7.35 - acidemia >7.45 – alkalemia RULE – An acid base abnormality is present even if either the pH or PCO2 are Normal.
STEP 2 RESPIRATORY or METABOLIC?IS PRIMARY DISTURBANCE RESPIRATORY ORMETABOLIC?pH HCO3 or pH HCO3 METABOLICpH PCO2 or pH PCO2 RESPIRATORY RULE- If either the pH or PCO2 is Normal, there is a mixed metabolic and respiratory acid base disorder.
Step 3 Is CompensationAdequate?
Disorder Prediction of Compensation pH HCO3– PaCO2Metabolic PaCO2 will 1.25 mmHg per mmol/L inacidosis [HCO3-] Low Low LowMetabolic PaCO2 will 0.75 mmHg per mmol/L in High High Highalkalosis [HCO3-]
Disorder Prediction of Compensation pH HCO3– PaCO2Respiratory High Low LowalkalosisAcute [HCO3-] will 0.2 mmol/L per mmHg in PaCO2 Chronic [HCO3-] will 0.4 mmol/L per mmHg in PaCO2Respiratory Low High HighacidosisAcute [HCO3-] will 0.1 mmol/L per mmHg in PaCO2 Chronic [HCO3-] will 0.4 mmol/L per mmHg in PaCO2
STEP 0 • Is this ABG Authentic?STEP 1 • ACIDEMIA or ALKALEMIA? • RESPIRATORY or METABOLIC?STEP 2STEP 3 • If Respiratory – ACUTE or CHRONIC?STEP 4 • Is COMPENSATION adequate?STEP 4 • If METABOLIC – ANION GAP? • If High gap Metabolic Acidosis–STEP 6 GAP GAP?
Electrochemical Balance in Blood100% UC UA 90% 80% HCO3 Na Sulfate 70% Phosphate 60% Mg- OA Cl 50% K - Proteins 40% Ca-HCO3 30% Na- Cl 20% 10% 0% CATIONS ANIONS
Anion GapAG based on principle of electroneutrality: Total Serum Cations = Total Serum Anions M cations + U cations = M anions + U anions Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids) Na + UC = HCO3 + Cl + UA But in Blood there is a relative abundance of Anions, hence Anions > Cations Na – (HCO3 + Cl) = UA – UC Na – (HCO3 + Cl) = Anion Gap
METABOLIC ACIDOSIS- STEP 4 ANION GAP?IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP? ANION GAP(AG) = Na – (HCO3 + Cl) Normal Value = 10 + 2Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)50% in S. Albumin 75% in Anion Gap !!! High Anion Gap Metabolic AcidosisMetabolic Acidosis Normal Anion Gap Acidosis
STEP 5 CO EXISTANT METABOLIC DISORDER – “Gap Gap‖?C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER? ∆ Anion Gap = Measured AG – Normal AG Measured AG – 12∆ HCO3 = Normal HCO3 – Measured HCO3 24 – Measured HCO3Ideally, ∆Anion Gap = ∆HCO3For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L∆AG/ HCO3- = 1 Pure High AG Met Acidosis AG/ HCO3- > 1 Assoc Metabolic Alkalosis AG/ HCO3- < 1 Assoc N AG Met Acidosis
CLINICAL CASE SCENARIO
Case ScenarioA patient with a severe postoperativeileus requires the insertion of anasogastric (NG) tube fordecompression. After several days onthe floor, he develops a line infection andis moved to the ICU once he becomespressor dependent. The patients ABGreveals a pH = 7.44, pCO2 = 12, and[HCO3-] = 8. The [Na+] = 145 with [Cl-] =102.
ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8, [Na+] = 145 with [Cl-] = 102◦ With knowledge of the common clinical scenarios leading to acid-base disturbances, this patient is at risk for developing a metabolic alkalosis from NG suction and a metabolic acidosis and respiratory alkalosis from sepsis.◦ Step 1. [H+] = 80 − 44 = 36. Does 36 = 24 × 12 / 8? It does.◦ Step 2. The patient is mildly alkalemic, which can be explained by the low pCO2 but not by the low [HCO3-], suggesting that a respiratory alkalosis may be the primary derangement.
ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8, [Na+] = 145 with [Cl-] = 102◦ Step 3 a. The drop in [HCO3-] might be an appropriate compensation for a chronic respiratory alkalosis ([HCO3-] is 0.4 mmol/L per mmHg in PaCO2) However, 24 − [(40 − 12) × 0.4] = 12.8, which is not close to the observed [HCO3-] of 8. A mixed disorder is implied. b. AG = 145 − 102 − 8 = 35. There is an elevated AG, suggests a concomitant metabolic acidosis. c. Delta anion gap=35 − 10 = 25. d. Delta bicarbonate= 24 − 8 =16. Ratio of above two is more than 1 suggestive of associated metabolic alkalosis. This has proven to be a triple acid-base disorder with an elevated anion gap acidosis, a metabolic alkalosis, and a respiratory alkalosis, as was alluded to in Step 1
Metabolic Acidosis Metabolic acidosis can occur because of ◦ increase in endogenous acid production (lactate and ketoacids) ◦ loss of bicarbonate (as in diarrhea) ◦ accumulation of endogenous acids (as in renal failure). Effects on the respiratory, cardiac, and nervous systems. ◦ Kussmaul respiration ◦ Intrinsic cardiac contractility may be depressed, but inotropic function can be normal because of catecholamine release. ◦ Both peripheral arterial vasodilation and central venoconstriction can be present ◦ The decrease in central and pulmonary vascular compliance predisposes to pulmonary edema with even minimal volume overload. ◦ Central nervous system function is depressed, with headache, lethargy, stupor, and, in some cases, even coma.
Metabolic Acidosis: Essentials ofDiagnosis Decreased HCO3– with acidemia. Classified into high anion gap acidosis and normal anion gap (hyperchloremic) acidosis. The high anion gap acidoses are seen in lactic acidosis, ketoacidosis, renal failure or toxins. Normal anion gap acidosis is mainly caused by gastrointestinal HCO3– loss or RTA. Urinary anion gap may help distinguish between these causes.
Causes of High-Anion-Gap Metabolic Acidosis1. Lactic acidosis Poor tissue perfusion (type A) Aerobic disorders (type B)2. Ketoacidosis Diabetic Alcoholic Starvation3. Toxins Ethylene glycol Methanol Salicylates Propylene glycol: as vehicle of medications Pyroglutamic acid: acetaminophen toxicity4. Renal failure (acute and chronic)
Ketacidosis – Diabetic Ketoacidosis (DKA): DKA is caused by increased fatty acid metabolism and the accumulation of ketoacids (acetoacetate and -hydroxybutyrate). DKA usually occurs in insulin-dependent diabetes mellitus in association with cessation of insulin or an intercurrent illness, such as an infection, gastroenteritis, pancreatitis, or myocardial infarction, which increases insulin requirements temporarily and acutely. The accumulation of ketoacids accounts for the increment in the Anion Gap and is accompanied most often by hyperglycemia [glucose > 17 mmol/L (300 mg/dL)].
Glucose,a mmol/L (mg/dL) 13.9–33.3 (250–600)Sodium, meq/L 125–135Potassiuma Normal to ↑Magnesiuma Normal ( plasma levels may be normal or high at presentation, total-body stores are usually depleted)Chloridea NormalPhosphatea ↓Creatinine Slightly ↑Osmolality (mOsm/mL) 300–320Plasma ketonesa ++++Serum bicarbonate,a meq/L <15 meq/LArterial pH 6.8–7.3Arterial PCO2,a mmHg 20–30Anion gapa[Na - (Cl + HCO3)] ↑
Management Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis). Admit to hospital; intensive-care setting may be necessary for frequent monitoring or if pH < 7.00 or unconscious. Assess: Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate) Acid-base status—pH, HCO3-, PCO2, b-hydroxybutyrate Renal function (creatinine, urine output) Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour); subsequently, 0.45% saline at 150–300 mL/h; change to 5% glucose and 0.45% saline at 100–200 mL/h when plasma glucose reaches 250 mg/dL (14 mmol/L). Administer short-acting insulin: IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h. If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do not administer insulin until the potassium is corrected to > 3.3 mmol/L
Management Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG). Measure capillary glucose every 1–2 h; electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h. Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h. Replace K+: 10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flow and normal creatinine documented; administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if bicarbonate is given. Continue above until patient is stable, glucose goal is 150– 250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour. Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and
since insulin prevents production of ketones, bicarbonate therapy is rarely needed except with extreme acidemia (pH < 7.1), and then in only limited amounts. Patients with DKA are typically volume depleted and require fluid resuscitation with isotonic saline. Volume overexpansion is not uncommon after IV fluid administration, and contributes to the development of a hyperchloremic acidosis during treatment of DKA because volume expansion increases urinary ketoacid anion excretion (loss of potential bicarbonate). The mainstay for treatment of this condition is IV regular insulin
Drug, Toxin-Induced Acidosis Plasma osmolality is calculated according to the following expression: Posm = 2Na+ + Glu + BUN (all in mmol/L) Posm = 2Na+ + Glu/18 + BUN/2.8 (milligrams per deciliter) The calculated and determined osmolality should be within 10–15 mmol/kg H2O When the measured osmolality exceeds the calculated osmolality by >15–20 mmol/kg H2O, either prevails. Either the serum sodium is spuriously low, as with hyperlipidemia or hyperproteinemia (pseudohyponatremia) Osmolytes other than sodium salts, glucose, or urea have accumulated in plasma. Examples include mannitol, radiocontrast media, isopropyl alcohol, ethylene glycol, propylene
In this situation, the difference between the calculated osmolality and the measured osmolality (osmolar gap) is proportional to the concentration of the unmeasured solute. Alcohols: With an appropriate clinical history and index of suspicion, identification of an osmolar gap is helpful in identifying the presence of poison-associated AG acidosis. Three alcohols may cause fatal intoxications: ethylene glycol, methanol, and isopropyl alcohol Salicylates: Salicylate intoxication in adults usually causes respiratory alkalosis or a mixture of high-AG metabolic acidosis and respiratory alkalosis. Only a portion of the AG is due to salicylates. Lactic acid production is also often increased
Renal failure Acidosis The hyperchloremic acidosis of moderate renal insufficiency is eventually converted to the high-AG acidosis of advanced renal failure. At GFRs below 20 mL/min, the inability to excrete H+ with retention of acid anions such as PO43– and SO42– results in an increased anion gap acidosis [HCO3–] rarely falls to <15 mmol/L, and the AG is rarely >20 mmol/L, indicating that the acid retained in chronic renal disease is buffered by alkaline salts from bone. Results in significant loss of bone mass due to reduction in bone calcium carbonate and increases urinary calcium excretion.
Treatment of high anion gapacidosis Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion. The metabolism of lactate will produce HCO3– and increase pH. Controversy regarding administration of large amounts of HCO3– may have deleterious effects, including hypernatremia and hyperosmolality. Intracellular pH may decrease because administered HCO3– is converted to CO2, which easily diffuses into cells, combines with water to create additional hydrogen ions and worsening of intracellular acidosis and this could impair cellular function Alkali administration is known to stimulate phosphofructokinase activity, thus exacerbating lactic acidosis via enhanced lactate production. Ketogenesis is also augmented by alkali therapy.
Treatment of high anion gap acidosis….. ◦ In salicylate intoxication, alkali therapy must be started unless blood pH is already alkalinized by respiratory alkalosis, since the increment in pH converts salicylate to more impermeable salicylic acid and thus prevents central nervous system damage. ◦ In DKA, alkali must be administered in extreme alkalemia (pH<7.1) ◦ In alcoholic ketoacidosis, thiamine should be given together with glucose to avoid the development of Wernickes encephalopathy. The amount of HCO3– deficit can be calculated as follows: Amount of HCO3– deficit = 0.5 X body weight X (24 - HCO3–) ◦ Half of the calculated deficit should be administered within the first 3–4 hours to avoid overcorrection and volume overload. In methanol intoxication ◦ ethanol has been used as a competitive substrate for alcohol dehydrogenase, which metabolizes methanol to formaldehyde ◦ or through direct inhibition of alcohol dehydrogenase by fomepizole
Hyperchloremic (Nongap)Metabolic Acidoses: causes I. Gastrointestinal bicarbonate loss Diarrhea External pancreatic or small-bowel drainage Ureterosigmoidostomy, jejunal loop, ileal loop Drugs - Calcium chloride , Magnesium sulfate (diarrhea), Cholestyramine (bile acid diarrhea) II. Renal acidosis Hypokalemia Proximal RTA (type 2) Distal (classic) RTA (type 1) Hyperkalemia Generalized distal nephron dysfunction (type 4 RTA) a. Mineralocorticoid deficiency b. Mineralocorticoid resistance (autosomal dominant PHA I) c. Voltage defect (autosomal dominant PHA I and PHA II) d. Tubulointerstitial disease
III. Drug-induced hyperkalemia (with renal insufficiency) ◦ Potassium-sparing diuretics (amiloride, triamterene, spironolactone) ◦ Trimethoprim ◦ Pentamidine ◦ ACE-Is and ARBs ◦ Nonsteroidal anti-inflammatory drugs ◦ Cyclosporine and tacrolimusIV. Other ◦ Acid loads (ammonium chloride, hyperalimentation) ◦ Loss of potential bicarbonate: ketosis with ketone excretion ◦ Expansion /dilutional acidosis (rapid saline administration) ◦ Hippurate ◦ Cation exchange resins
Approach: Urinary Anion Gap Increased renal NH4+Cl– excretion to enhance H+ removal is a normal physiologic response to metabolic acidosis. NH3 reacts with H+ to form NH4+, which is accompanied by the anion Cl– for excretion. Urinary anion gap from a random urine sample ([Na++ K+]– Cl–) reflects the ability of the kidney to excrete NH4Cl as in the following equation: Na+ + K+ + NH4+ = Cl– + 80 urinary anion gap is equal to (80 – NH4+) Gastrointestinal HCO3– loss (diarrhea), the renal acidification ability remains normal and NH4Cl excretion increases in response to the acidosis. urinary anion gap is negative (eg, –30 mEq/L). Distal RTA, the urinary anion gap is positive (eg, +25 mEq/L), since the basic lesion in the disorder is the inability of the kidney to excrete H+ and thus the inability to increase NH4Cl excretion. Proximal (type II) RTA, the kidney has defective HCO3– reabsorption, leading to increased HCO3– excretion rather than decreased NH4Cl excretion. Thus, the urinary anion gap is negative
Urinary pH may not as readily differentiate between the two causes because volume depletion or potassium depletion, which can accompany diarrhea (and surreptitious laxative abuse) may impair renal acidification. Thus, when volume depletion is present, the urinary anion gap is a better measurement of ability to acidify the urine than urinary pH. When large amounts of other anions are present in the urine, the urinary anion gap may not be reliable. In such a situation, NH4+ excretion can be estimated using the urinary osmolar gap. NH4+ excretion (mmol/L) = 0.5 x Urinary osmolar gap = 0.5 [U osm – 2(U Na++U K+) + U urea + U glucose] where urinary (U) concentrations and osmolality are in millimoles per liter.
Renal Serum Urinary Titratable Urinary Treatment Defect [K+] NH4+ Plus Acid Anion Minimal Gap Urine pHGastrointestinal None ↓ < 5.5 ↑↑ Negative Na+, K+, andHCO3– loss HCO3– as requiredRenal tubularacidosis I. Classic distal Distal H+ ↓ > 5.5 ↓ Positive NaHCO3 (1–3 secretion mEq/kg/d) II. Proximal Proximal ↓ < 5.5 Normal Negative NaHCO3 orsecretion HCO3– KHCO3 (10–15 abspn mEq/kg/d), thiazide IV. Distal Na+ ↑ < 5.5 ↓ Positive FludrocortisoneHyporeninemic reabsorption (0.1–0.5 mg/d), + dietary K+ rstrn,hypoaldosteroni K secretion, and H+ furosemide (40–sm secretion 160 mg/d), NaHCO3 (1–3 mEq/kg/d)
Treatment of normal Anion gap Acidosis Gastrointestinal: Correction of the contracted ECFV with NaCl and repair of K+ deficits corrects the acid-base disorder, and chloride deficiency. RTA : administration of alkali (either as bicarbonate or citrate) to correct metabolic abnormalities and prevent nephrocalcinosis and renal failure. ◦ Proximal RTA : Large amounts of alkali (10–15 mEq/kg/d) may be required to treat proximal RTA because most of the alkali is excreted into the urine, which exacerbates hypokalemia. Thus, a mixture of sodium and potassium salts, such as K-Shohl solution, is preferred. The addition of thiazides may reduce the amount of alkali required, but hypokalemia may develop. ◦ Distal RTA : Correction of type 1 distal RTA requires a smaller amount of alkali (1–3 mEq/kg/d) and potassium supplementation as needed. ◦ Type IV RTA: dietary potassium restriction may be needed and potassium-retaining drugs should be withdrawn. Fludrocortisone may be effective in cases with hypoaldosteronism, but should be used with care, preferably in combination with loop diuretics. alkali supplementation (1–3 mEq/kg/d) may be required.
Metabolic Alkalosis Essentials of Diagnosis ◦ High HCO3– with alkalemia. ◦ Evaluate effective circulating volume by physical examination and check urinary chloride concentration. This will help differentiate saline-responsive metabolic alkalosis from saline-unresponsive alkalosis
Metabolic Alkalosis Occurs as a result of net gain of [HCO3–] or loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid. The disorder involves a generative stage, in which the loss of acid usually causes alkalosis maintenance stage, in which the kidneys fail to compensate by excreting HCO3–. Classified based on "saline responsiveness" or urinary Cl–, which are markers for volume status Saline-responsive metabolic alkalosis is a sign of extracellular volume contraction Saline-unresponsive alkalosis implies a volume- expanded state
Symptoms With metabolic alkalosis, changes in central and peripheral nervous system function are similar to those of hypocalcemia : symptoms include Mental confusion Obtundation Predisposition to seizures Paresthesia Muscular cramping Tetany Aggravation of arrhythmias Hypoxemia in chronic obstructive pulmonary disease. Related electrolyte abnormalities include Hypokalemia- Weakness and hyporeflexia hypophosphatemia.
Classification and etiology I. Saline-Responsive (UCl < 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Diuretic therapy Poorly reabsorbable anion therapy: carbenicillin, penicillin, sulfate, phosphate Posthypercapnia Gastrointestinal alkalosis Loss of HCl from vomiting or nasogastric suction Intestinal alkalosis: chloride diarrhea Exogenous alkali NaHCO3 (baking soda) Sodium citrate, lactate, gluconate, acetate Transfusions Antacids Normal body bicarbonate content "Contraction alkalosis"
II. Saline-Unresponsive (UCl > 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Normotensive Bartters syndrome (renal salt wasting and secondary hyperaldosteronism) Severe potassium depletion Refeeding alkalosis Hypercalcemia and hypoparathyroidism Hypertensive Endogenous mineralocorticoids Primary aldosteronism Hyperreninism Adrenal enzyme deficiency: 11- and 17- hydroxylase Liddles syndrome Exogenous mineralocorticoids Licorice
Treatment Mild alkalosis is generally well tolerated. Severe or symptomatic alkalosis (pH > 7.60) requires urgent treatment. Saline-Responsive Metabolic Alkalosis ◦ Aimed at correction of extracellular volume deficit. ◦ Depending on the degree of hypovolemia, adequate amounts of 0.9% NaCl and KCl should be administered. ◦ Discontinuation of diuretics and administration of H2-blockers in patients whose alkalosis is due to nasogastric suction can be useful. ◦ If impaired pulmonary or cardiovascular status prohibits adequate volume repletion, acetazolamide, 250–500 mg intravenously every 4–6 hours, can be used.
Treatment….. One must be alert to the possible development of hypokalemia, since potassium depletion can be induced by forced kaliuresis via bicarbonaturia. Administration of acid can be used as emergency therapy. HCl, 0.1 mol/L, is infused via a central vein (the solution is sclerosing). Dosage is calculated to decrease the HCO3– level by 50% over 2–4 hours, assuming an HCO3– volume of distribution (L) of 0.5% body weight (kg). Patients with marked renal failure may require dialysis. Saline-Unresponsive Metabolic Alkalosis surgical removal of a mineralocorticoid-producing tumor blockage of aldosterone effect with an ACE inhibitor or with spironolactone. primary aldosteronism can be treated only with potassium repletion.
Respiratory AcidosisResults from decreased alveolar ventilation and hypercapniaboth due to pulmonary and non pulmonary disorders Central Neuromuscular ◦ Drugs ◦ Poliomyelitis (anesthetics, morphine, sedatives) ◦ Kyphoscoliosis ◦ Stroke ◦ Myasthenia ◦ Infection ◦ Muscular dystrophies Airway Miscellaneous ◦ Obstruction ◦ Obesity ◦ Asthma ◦ Hypoventilation Parenchyma ◦ Permissive hypercapnia ◦ Emphysema ◦ Pneumoconiosis ◦ Bronchitis ◦ Adult respiratory distress syndrome ◦ Barotrauma
Respiratory Acidosis Acute respiratory failure associated with severe acidosis and only a small increase in the plasma bicarbonate. After 6–12 hours, the primary increase in PCO2 evokes a renal compensatory response to generate more HCO3– , which tends to ameliorate the respiratory acidosis. This takes several days to complete. Chronic respiratory acidosis seen in patients with underlying lung disease, such as chronic obstructive pulmonary disease. Urinary excretion of acid in the form of NH4+ and Cl– ions results in the characteristic hypochloremia of chronic respiratory acidosis. When chronic respiratory acidosis is corrected suddenly, especially in patients who receive mechanical ventilation, there is a 2- to 3-day lag in renal bicarbonate excretion, resulting in posthypercapnic metabolic alkalosis.
Symptoms and Signs ◦ With acute onset, there is somnolence and confusion, and myoclonus with asterixis ◦ Coma from CO2 narcosis may ensue ◦ Severe hypercapnia increases cerebral blood flow and cerebrospinal fluid pressure. Signs of increased intracranial pressure (papilledema, pseudotumor cerebri) may be seen. Laboratory Findings ◦ Arterial pH is low ◦ PCO2 is increased ◦ Serum HCO3– is elevated, but not enough to completely compensate for the hypercapnia. ◦ If the disorder is chronic, hypochloremia is seen. Treatment ◦ In all forms of respiratory acidosis, treatment is directed at the underlying disorder to improve ventilation. ◦ Because opioid drug overdose is an important reversible cause of acute respiratory acidosis, naloxone, 0.04–2 mg intravenously is administered to all such patients if no obvious cause for respiratory depression is present. ◦ Mechanical ventilation for oxygenation till it restores back to normal maybe needed
Respiratory Alkalosis(Hypocapnia) Respiratory alkalosis, or hypocapnia, occurs when hyperventilation reduces the PCO2, which increases the pH Symptoms and Signs In acute cases (hyperventilation), there is light-headedness, anxiety, paresthesias, numbness about the mouth, and a tingling sensation in the hands and feet. Tetany occurs in more severe alkalosis from a fall in ionized calcium. In chronic cases, findings are those of the responsible condition. Laboratory Findings Arterial blood pH is elevated, and PCO2 is low. Serum bicarbonate is decreased in chronic respiratory alkalosis. Determination of appropriate compensatory changes in the HCO3– is useful to sort out the presence of an associated metabolic disorder the changes in HCO3– values are greater if the respiratory alkalosis is chronic Although serum HCO3– is frequently below 15 mEq/L in metabolic acidosis, it is unusual to see such a low level in respiratory alkalosis, and its presence would imply a superimposed (noncompensatory) metabolic acidosis.
Treatment Treatment is directed toward the underlying cause. In acute hyperventilation syndrome from anxiety, reassurance , attention to underlying psychological stress and rebreathing into a paper bag will increase the PCO2. The processes are usually self-limited since muscle weakness caused by hyperventilation-induced alkalemia will suppress ventilation. Sedation may be necessary if the process persists however Antidepressants and sedatives should be avoided Adrenergic blockers may ameliorate peripheral manifestations of the hyperadrenergic state. Rapid correction of chronic respiratory alkalosis may result in metabolic acidosis as PCO2 is increased in the setting of previous compensatory decrease in HCO3–. If respiratory alkalosis complicates ventilator management, changes in dead space, tidal volume, and frequency can minimize the hypocapnia
Conclusion Clinical suspicion according to scenario Primary disorder from pH and bicarbonate or CO2 values Degree of compensation…? Inappropriate? mixed disorder Anion gap (corrected for serum albumin change)…? Primary metabolic acidosis Corrected bicarbonate levels…? More than normal- associated metabolic alkalosis Less - associated metabolic non-anion gap acidosis Review compensation for metabolic ds…confirm if initially suspected respiratory disorder exists
Metabolic acidosis: ..see AG High AG: …plasma osmolal gap more.. Toxins Less.. KA, RF, LA, Normal AG acidosis: urine AG….negative..GI urinary pH ….high..RTA 1 serum potassium….high..RTA4 Metabolic alkalosis: ◦ Urinary Chloride… Less..saline responsive…ECF contraction more ..saline non responsive Plasma Potassium…low..K depletion High…Blood pressure Plasma renin
1.PaCO2 equation: VCO2 x 0.863 VCO2 = CO2 production PaCO2 = ----------------- VA = VE – VD VA VE = minute (total) ventilation VD = dead space ventilation 0.863 converts units to mm Hg Condition State ofPaCO2 in blood alveolar ventilation>45 mm Hg Hypercapnia Hypoventilation35 - 45 mm Hg Eucapnia Normal ventilation<35 mm Hg Hypocapnia HyperventilationPaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation
Hypercapnia VCO2 x 0.863 PaCO2 = ------------------ VA The only physiologic reason for elevated PaCO2 isinadequate alveolar ventilation (VA) for the amount of thebody‘s CO2 production (VCO2). Since alveolar ventilation(VA) equals minute ventilation (VE) minus dead spaceventilation (VD), hypercapnia can arise from insufficientVE, increased VD, or a combination.
Hypercapnia VCO2 x 0.863 PaCO2 = ------------------ VA VA = VE – VD Examples of inadequate VE leading to decreased VA and increased PaCO2: sedative drug overdose; respiratory muscle paralysis; central hypoventilation Examples of increased VD leading to decreased VA and increased PaCO2: chronic obstructive pulmonary disease; severe pulmonary embolism, pulmonary edema.
Physiologic effects of hypercapnia◦ 1) An elevated PaCO2 will lower the PAO2 (see Alveolar gas equation), and as a result lower the PaO2.◦ 2) An elevated PaCO2 will lower the pH (see Henderson- Hasselbalch equation).◦ 3) The higher the baseline PaCO2, the greater it will rise for a given fall in alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO2 a greater amount when baseline PaCO2 is 50 mm Hg than when it is 40 mm Hg.
Assessment of OxygenationStatus2.Alveolar gas equation Oxygenation(alv)3.Oxygen content equation Oxygenation(tissue)
Oxygenation -----XXXX Diagnostics----- Parameters: /limitationsBlood Gas Report328Pt ID 03:44 3245 / 00 Feb 5 2006 O2 Content of blood: (Hb x1.34x O2 Sat + 0.003x Dissolved O2 )Measured 37.0 0CpH 7.452 Remember HemoglobinpCO2 45.1 mm HgpO2 112.3 mm HgCorrected 38.6 0C Oxygen Saturation:pH 7.436pCO2 47.6 mm Hg ( remember this is calculated …error prone)pO2 122.4 mm HgCalculated Data Alveolar / arterial gradient:HCO3 act 31.2 mmol / L ( classify respiratory failure)HCO3 std 30.5 mmol / LBE 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 % Arterial / alveolar ratio:ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg Proposed to be less variablepO2 (a/A) 0.78 Same limitations as A-a gradientEntered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl
Alveolar Gas Equation PAO2 = PIO2 - 1.2 (PaCO2)where PAO2 is the average alveolar PO2, and PIO2 is the partial pressureof inspired oxygen in the trachea PIO2 = FIO2 (PB – 47 mm Hg)FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47mm Hg is the water vapor pressure at normal body temperature.
Alveolar Gas Equation If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia). If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease. If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing causes hypoxemia).
P(A-a)O2 P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the ―A-a gradient‖. It results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance). Normal P(A-a)O2 ranges from 5 to 25 mm Hg 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. Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs.
Physiologic causes of low PaO2NON-RESPIRATORY P(A-a)O2 Cardiac right to left shunt Increased Decreased PIO2 NormalRESPIRATORY Pulmonary right to left shunt Increased Ventilation-perfusion imbalance Increased Diffusion barrier Increased Hypoventilation (increased PaCO2) Normal
Ventilation-Perfusion imbalance A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2. By far the most common cause of low PaO2 is an abnormal degree of ventilation-perfusion imbalance within the hundreds of millions of alveolar-capillary units. Virtually all lung disease lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD. Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise).
SaO2 and oxygen contentHow much oxygen is in the blood? Oxygen content = CaO2 (mlO2/dl). CaO2 = quantity O2 bound + quantity O2 dissolved to hemoglobin in plasma CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2) Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.
Given arterial oxygen saturation (SpO2) = 100%, Hb = 15 g/100 ml and arterial partial pressure of oxygen (PaO2) = 13.3 kPa, then the oxygen content of arterial blood (CaO2) is: CaO2 = 20.1 +0.3 = 20.4 ml/100 ml Similarly the oxygen content of mixed venous blood can be calculated. Given normal values of mixed venous oxygen saturation (SvO2) = 75% and venous partial pressure of oxygen (PvO2) = 6 kPa, so: CvO2 = 15.2 + 0.1 = 15.2 ml/100 ml
Oxygen dissociation curve: SaO2 vs. PaO2Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm%and 10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 is 50%.
SaO2 – is it calculated or measured? SaO2 is measured in a ‗co-oximeter‘. The traditional ‗blood gas machine‘ measures only pH, PaCO2 and PaO2,, whereas the co- oximeter measures SaO2, carboxyhemoglobin, methemoglobin and hemoglobin content. Newer ‗blood gas‘ consoles incorporate a co- oximeter, and so offer the latter group of measurements as well as pH, PaCO2 and PaO2. Always make sure the SaO2 is measured, not calculated. If it is calculated from the PaO2 and the O2-dissociation curve, it provides no new information, and could be inaccurate -- especially in states of CO intoxication or excess methemoglobin. CO and metHb do not affect PaO2, but do lower the SaO2.
Carbon monoxide – an important cause of hypoxemia Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas) All smokers have excess CO in their blood. CO binds @ 200x more avidly to hemoglobin than O2, displacing O2 from the heme binding sites. CO : 1) decreases SaO2 by the amount of %COHb present, and 2) shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues. CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or COHb must be measured (requires co- oximeter). In the presence of excess CO, SaO2 (when measured) will be lower than expected from the PaO2.
CO does not affect PaO2!A patient presented to the ER with headache and dyspnea. His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH 7.43. SaO2 on this first set was calculated from the O2-dissociation curve at 97%, and oxygenation was judged normal. He was sent out from the ER and returned a few hours later with mental confusion; this time both SaO2 and COHb were measured (SaO2 shown by ‗X‘): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2 53%, carboxyhemoglobin 46%. CO poisoning was missed on the first set of blood gases because SaO2 was not measured!
Causes of Hypoxia1. Hypoxemia (=low PaO2 and/or low CaO2) ◦ a. reduced PaO2 – usually from lung disease (most common physiologic mechanism: V-Q imbalance) ◦ b. reduced SaO2 -- most commonly from reduced PaO2; other causes include carbon monoxide poisoning, methemoglobinemia, or rightward shift of the O2- dissociation curve ◦ c. reduced hemoglobin content -- anemia2. Reduced oxygen delivery to the tissues ◦ a. reduced cardiac output -- shock, congestive heart failure ◦ b. left to right systemic shunt (as may be seen in septic shock)3. Decreased tissue oxygen uptake ◦ a. mitochondrial poisoning (e.g., cyanide poisoning) ◦ b. left-shifted hemoglobin dissociation curve (e.g., from acute alkalosis, excess CO, or abnormal hemoglobin structure)
Arterial Oxygen Tension (PaO2) Normal value in healthy adult breathing room air at sea level 97 mm Hg. progressively with age Dependant upon 1. FiO2 2. Patm Hypoxemia is PaO2 < 80 mm Hg at RA Most pts who need ABG usually req O2 therapy O2 therapy should not be withheld/interrupted ‗to determine PaO2 on RA‘
Acceptable PaO2 Values on RoomAir Age Group Accepable PaO2 (mm Hg) Adults upto 60 yrs > 80 & Children Newborn 40-70 70 yrs > 70 80 yrs > 60 90 yrs > 50 60 yrs 80 mm Hg 1mm Hg/yr
Inspired O2 – PaO2 Relationship FIO2 (%) Predicted Min PaO2 (mm Hg) 30 150 40 200 50 250 80 400 100 500 If PaO2 < FIO2 x 5, pt probably hypoxemic at RA
Hypoxemia on O2 therapy Uncorrected: PaO2 < 80 mm Hg (< expected on RA & FIO2) Corrected: PaO2 = 80-100 mm Hg (= expected on RA but < expected for FIO2) Excessively Corrected: PaO2 > 100 mm Hg (> expected on RA but < expected for FIO2) PaO2 > expected for FIO2: 1. Error in sample/analyzer 2. Pt‘s O2 consumption reduced 3. Pt does not req O2 therapy (if 1 & 2 NA)