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  Notes
 
 
Slide 1 : SEMINAR IN CRITICAL CARE ARTERIAL BLOOD GAS: INTERPRETATION AND CLINICAL IMPLICATIONS VIRENDER VERMA DEPARTMENT OF PEDIATRICS PGIMS ROHTAK
Slide 2 : Conditions Invalidating or Modifying ABG Results DELAYED ANALYSIS Consumption of O2 & Production of CO2 continues after blood drawn into syringe Iced Sample maintains values for 1-2 hours Uniced sample quickly becomes invalid PaCO2 ? 3-10 mmHg/hour PaO2 ? at a rate related to initial value & dependant on Hb Sat
Slide 3 : EFFECT OF TEMP ON RATE OF CHANGE IN ABG VALUES
Slide 4 : EXCESSIVE HEPARIN Dilutional effect on results ? HCO3- & PaCO2 Syringe be emptied of heparin after flushing Risk of alteration of results ? with: ? size of syringe/needle ? vol of sample 25% lower values if 1ml sample taken in 10 ml syringe (0.25 ml heparin in needle) Syringes must be > 50% full with blood sample HYPERVENTILATION OR BREATH HOLDING May lead to erroneous lab results
Slide 5 : AIR BUBBLES PO2 ?150 mmHg & PCO2 ?0 mm Hg in air bubble(R.A.) Mixing with sample lead to ? PaO2 & ? PaCO2 Mixing/Agitation ? S.A. for diffusion ? more erroneous results Discard sample if excessive air bubbles Seal with cork/cap imm after taking sample FEVER OR HYPOTHERMIA Most ABG analyzers report data at N body temp If severe hyper/hypothermia, values of pH & PCO2 at 37 C can be significantly diff from pt’s actual values Changes in PO2 values with temp predictable
Slide 6 : No significant change of HCO3-, O2 Sat, O2 capacity/content, CO2 content values with temp No consensus regarding reporting of ABG values esp pH & PCO2 after doing ‘temp correction’ ? Interpret values measured at 37 C: Most clinicians do not remember normal values of pH & PCO2 at temp other than 37C In pts with hypo/hyperthermia, body temp usually changes with time (per se/effect of rewarming/cooling strategies) – hence if all calculations done at 37 C easier to compare Values other than pH & PCO2 do not change with temp Hansen JE, Clinics in Chest Med 10(2), 1989 227-237
Slide 7 : ? Use Normograms to convert values at 37C to pt’s temp Some analyzers calculate values at both 37C and pt’s temp automatically if entered Pt’s temp should be mentioned while sending sample & lab should mention whether values being given in report at 37 C/pts actual temp WBC COUNT 0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC Marked increase in pts with very high TLC/plt counts – hence imm chilling/analysis essential
Slide 8 : TYPE OF SYRINGE pH & PCO2 values unaffected PO2 values drop more rapidly in plastic syringes (ONLY if PO2 > 400 mm Hg) Other adv of glass syringes: Min friction of barrel with syringe wall Usually no need to ‘pull back’ barrel – less chance of air bubbles entering syringe Small air bubbles adhere to sides of plastic syringes – difficult to expel Though glass syringes preferred, differences usually not of clinical significance ? plastic syringes can be and continue to be used
Slide 9 : QUALITY CONTROL & CALIBRATION Mechanism of Measurement & Electronic Drift in electrodes Measurement of voltages (potentiometric) – Balance Drift (Shifting of calibration points from baseline though maintain same slope) Sanz (pH) electrode Severinghaus/Stow (PCO2) electrode Measurement of amperage (amperometric) – Slope Drift (Angle of calibration points changes though baseline remains same) Clark (PO2) electrode Recommendations for calibration of each electrode – 2 point calibration every 8 hrs 1 point calibration every 4 hrs
Slide 10 : Approach to ABG Interpretation Assessment of the type of acid base disorder requires at a minimum 2 of the following: Arterial pH pCO2 plasma HCO3- Complete analysis of an ABG requires: pH pO2 pCO2 HCO3- O2 Sat BE/BD Anion Gap (AG) ? AG ? HCO3-
Slide 11 : Assessment of Oxygenation Status
Slide 12 : Arterial Oxygen Tension (PaO2) Normal value in healthy adult breathing room air at sea level ? 97 mm Hg. ? progressively with ? age Dependant upon FiO2 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’
Slide 13 : Acceptable PaO2 Values on Room Air 60 yrs ? 80 mm Hg ? ? 1mm Hg/yr
Slide 14 : Inspired O2 – PaO2 Relationship If PaO2 < FIO2 x 5, pt probably hypoxemic at RA
Slide 15 : 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)
Slide 16 : Assessment of Acid-Base Status
Slide 17 : Bicarbonate (HCO3-) Std HCO3-: HCO3- levels measured in lab after equilibration of blood PCO2 to 40 mm Hg (? routine measurement of other serum electrolytes) Actual HCO3-: HCO3- levels calculated from pH & PCO2 directly Reflection of non respiratory (metabolic) acid-base status. Does not quantify degree of abnormality of buffer base/actual buffering capacity of blood.
Slide 18 : Base Excess/Base Deficit Calculated from pH, PaCO2 and HCT Expressed as mEq/L of base above N buffer base range Negative BE also referred to as Base Deficit True reflection of non respiratory (metabolic) acid base status
Slide 19 : DEFINITIONS AND TERMINOLOGY 3 Component Terminology – Compensated/Uncompensated Respiratory/Metabolic Acidosis/Alkalosis ACIDEMIA – reduction in arterial pH    (pH<7.35) ALKALEMIA – increase in arterial pH (pH>7.45) 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-
Slide 20 : RESPIRATORY VS METABOLIC Respiratory – processes which lead to acidosis or alkalosis through a primary alteration in ventilation and resultant excessive elimination or  retention of CO2 Metabolic – processes which lead to acidosis or alkalosis through their effects on kidneys and the consequent disruption of H + and HCO3- control
Slide 21 : COMPENSATION – The normal response of the  respiratory system or kidneys to change in pH induced by a primary acid-base disorder SIMPLE VS. MIXED ACID-BASE DISORDER Simple acid-base disorder – a single primary process  of acidosis or alkalosis Mixed acid-base disorder – presence of more than one acid base disorder simultaneously
Slide 22 : Characteristics of ?? acid-base disorders
Slide 23 : Compensation In the presence of acidosis or alkalosis, regulatory mechanisms occur which attempt to maintain the arterial pH in the physiologic range. These processes result in the return of pH towards, but generally just outside the normal range Disturbances in HCO3- (metabolic acidosis or alkalosis) result in respiratory compensation while changes in CO2 (respiratory acidosis/alkalosis) are counteracted by renal compensation a. Renal compensation – kidneys adapt to alterations in pH by changing the amount of HCO3- generated/excreted. Full renal compensation takes 2-5 days b. Respiratory compensation – alteration in ventilation allow immediate compensation for metabolic acid-base disorders
Slide 24 : RENAL & RESPIRATORY COMPENSATIONS TO ?? ACID-BASE DISTURBANCES Disorder Compensatory response Metabolic acidosis PCO2 ? 1.2 mmHg per 1.0 mEq/L ? HCO3- Metabolic alkalosis PCO2 ? 0.7 mmHg per 1.0 mEq/L ?HCO3- Respiratory acidosis [HCO3-] ? Acute 1.0 mEq/L per 10 mmHg ? Pco2 Chronic 3.5 mEq/L per 10 mmHg ? Pco2 Respiratory alkalosis [HCO3-] ? Acute 2.0 mEq/L per 10 mmHg ? Pco2 Chronic 4.0 mEq/L per 10 mmHg ? Pco2
Slide 25 : Stepwise approach to ABG Analysis Determine whether patient is alkalemic or acidemic using the arterial pH measurement Determine whether the acid-base disorder is a primary respiratory or metabolic disturbance based on the pCO2 and serum HCO3- level If a primary respiratory disorder is present, determine whether it is chronic or acute In metabolic disorders, determine if there is adequate compensation of the respiratory system In respiratory disorders, determine if there is adequate compensation of the metabolic system
Slide 26 : Determine pt’s oxygenation status (PaO2 & SaO2) – hypoxemic or not If a metabolic acidosis is present, determine the anion gap and osmolar gap In high anion gap acidosis, determine the change in anion gap (? AG) & ? HCO3- in order to assess for the presence of coexisting metabolic disturbances In normal (non) anion gap acidosis, determine the urinary anion gap - helpful to distinguish renal from non renal causes
Slide 27 : Interpretation: pH Normal arterial pH = 7.36 to 7.44 Determine Acidosis versus Alkalosis 1. pH <7.35: Acidosis 2. pH >7.45: Alkalosis Metabolic Conditions are suggested if pH changes in the same direction as pCO2/HCO3- pH is abnormal but pCO2 remains unchanged Respiratory Conditions are suggested if: pH changes in the pop direction as pCO2/HCO3- pH is abnormal but HCO3- remains unchanged
Slide 28 : pH ? N ? Acidemia Resp and/or Met Acidosis Alkalemia Resp and/or Met Alkalosis No acidemia /alkalemia Resp Acidosis and Met Alkalosis Met Acidosis and Resp Alkalosis No A-B Dis
Slide 29 : pH ? pCO2 ?, HCO3 ? pCO2 ?, HCO3 N Resp + Met Alkalosis Uncomp Resp Alkalosis pCO2 N, HCO3 ? Uncomp Met Alkalosis pCO2 ?, HCO3 ? Comp(F/P) Met Alkalosis pCO2 ?, HCO3 ? Comp(F/P) Resp Alkalosis
Slide 30 : pH ? pCO2 ?, HCO3 ? pCO2 ?, HCO3 N Resp + Met Acidosis Uncomp Resp Acidosis pCO2 N, HCO3 ? Uncomp Met Acidosis pCO2 ?, HCO3 ? Comp(F/P) Resp Acidosis pCO2 ?, HCO3 ? Comp(F/P) Met Acidosis
Slide 31 : pH N or ?N pCO2 ?, HCO3 ? Comp(F) Met Alkalosis pCO2 N, HCO3 N N Acid Base Homeostasis pCO2 ?, HCO3 ? Met acidosis + Resp alkalosis Comp(F) Met Acidosis Comp(F) Resp Alkalosis Comp(F) Resp Acidosis Resp Acidosis + Met Alkalosis
Slide 32 : Respiratory Acid Base Disorders Respiratory alkalosis most common of all the 4 acid base disorders (23-46%) -followed by met alkalosis - review of 8289 ABG analysis in ICU pts Kaehny WD, MCNA 67(4), 1983 p 915-928 Resp acidosis seen in 14-22% of pts Attention to possibility of hypoxemia and its correction always assumes priority in analysis of pts with a possible respiratory acid-base disorder
Slide 33 : RESPIRATORY ALKALOSIS
Slide 34 : Causes of Respiratory Alkalosis CENTRAL RESPIRATORY STIMULATION (Direct Stimulation of Resp Center): Structural Causes Non Structural Causes Head trauma Pain Brain tumor Anxiety CVA Fever Voluntary PERIPHERAL RESPIRATORY STIMULATION (Hypoxemia ? Reflex Stimulation of Resp Center via Peripheral Chemoreceptors) Pul V/Q imbalance Pul Diffusion Defects Hypotension Pul Shunts High Altitude
Slide 35 : INTRATHORACIC STRUCTURAL CAUSES: Reduced movement of chest wall & diaphragm Reduced compliance of lungs Irritative lesions of conducting airways MIXED/UNKNOWN MECHANISMS: Drugs – Salicylates Nicotine Progesterone Thyroid hormone Catecholamines Xanthines (Aminophylline & related compounds) Cirrhosis Gram –ve Sepsis Pregnancy Heat exposure Mechanical Ventilation
Slide 36 : Manifestations of Resp Alkalosis NEUROMUSCULAR: Related to cerebral A vasoconstriction & ? Cerebral BF Lightheadedness Confusion Decreased intellectual function Syncope Seizures Paraesthesias (circumoral, extremities) Muscle twitching, cramps, tetany Hyperreflexia Strokes in pts with sickle cell disease
Slide 37 : CARDIOVASCULAR: Related to coronary vasoconstriction Tachycardia with ? N BP Angina ECG changes (ST depression) Ventricular arrythmias GASTROINTESTINAL: Nausea & Vomiting (cerebral hypoxia) BIOCHEMICAL ABNORMALITIES: ? tCO2 ?PO43- ?Cl- ? Ca2+
Slide 38 : Homeostatic Response to Resp Alkalosis In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) ? release of H+ by blood and tissue buffers ? react with HCO3- ? fall in HCO3- (usually not less than 18) and fall in pH Cellular uptake of HCO3- in exchange for Cl- Steady state in 15 min - persists for 6 hrs After 6 hrs kidneys increase excretion of HCO3- (usually not less than 12-14) Steady state reached in 11/2 to 3 days. Timing of onset of hypocapnia usually not known except for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice
Slide 39 : Treatment of Respiratory Alkalosis Resp alkalosis by itself not a cause of resp failure unless work of increased breathing not sustained by resp muscles Rx underlying cause Usually extent of alkalemia produced not dangerous. Admn of O2 if hypoxemia If pH>7.55 pt may be sedated/anesthetized/ paralyzed and/or put on MV.
Slide 40 : Pseudo respiratory Alkalosis Arterial hypocapnia can be observed in an idiotypic form of respiratory acidosis. Occurs in patients with profound depression of cardiac function and pulmonary perfusion but with relative preservation of alveolar ventilation ( incl pts undergoing CPR). Severely reduced pul BF limits CO2 delivered to lungs for excretion ? ?PvCO2. Increased V/Q ratio causes removal of a larger-than-normal amount of CO2 per unit of blood traversing the pulmonary circulation ?arterial eucapnia or frank hypocapnia.
Slide 41 : Absolute excretion of CO2 decreased and CO2 balance of body +ve — the hallmark of respiratory acidosis. Pts may have severe venous acidemia (often due to mixed respiratory and metabolic acidosis) accompanied by an arterial pH that ranges from mildly acidic to the frankly alkaline. Extreme oxygen deprivation prevailing in the tissues may be completely disguised by the reasonably preserved values of arterial oxygen. To rule out pseudo respiratory alkalosis in a patient with circulatory failure, blood gas monitoring must include sampling of mixed (or central) venous blood. Mx must be directed toward optimizing systemic hemodynamics.
Slide 42 : RESPIRATORY ACIDOSIS
Slide 43 : Causes of Acute Respiratory Acidosis EXCRETORY COMPONENT PROBLEMS: Perfusion: Massive PTE Cardiac Arrest Ventilation: Severe pul edema Severe pneumonia ARDS Airway obstruction Restriction of lung/thorax: Flail chest Pneumothorax Hemothorax Bronchospasm (severe) Aspiration Laryngospasm OSA
Slide 44 : Muscular defects: Severe hypokalemia Myasthenic crisis Failure of Mechanical Ventilator CONTROL COMPONENT PROBLEMS: CNS: CSA Drugs (Anesthetics, Sedatives) Trauma Stroke Spinal Cord & Peripheral Nerves: Cervical Cord injury LGBS Neurotoxins (Botulism, Tetanus, OPC) Drugs causing Sk. m.paralysis (SCh, Curare, Pancuronium & allied drugs, aminoglycosides)
Slide 45 : Causes of Chronic Respiratory Acidosis EXCRETORY COMPONENT PROBLEMS: Ventilation: COPD Advanced ILD Restriction of thorax/chest wall: Kyphoscoliosis, Arthritis Fibrothorax Hydrothorax Muscular dystrophy Polymyositis
Slide 46 : CONTROL COMPONENT PROBLEMS: CNS: Obesity Hypoventilation Syndrome Tumors Brainstem infarcts Myxedema Ch sedative abuse Bulbar Poliomyelitis Spinal Cord & Peripheral Nerves: Poliomyelitis Multiple Sclerosis ALS Diaphragmatic paralysis
Slide 47 : Manifestations of Resp Acidosis NEUROMUSCULAR: Related to cerebral A vasodilatation & ? Cerebral BF Anxiety Asterixis Lethargy, Stupor, Coma Delirium Seizures Headache Papilledema Focal Paresis Tremors, myoclonus
Slide 48 : CARDIOVASCULAR: Related to coronary vasodilation Tachycardia with ? N BP Ventricular arrythmias (related to hypoxemia and not hypercapnia per se) Sensitivity to digitalis BIOCHEMICAL ABNORMALITIES: ? tCO2 ? Cl- ? PO43-
Slide 49 : Homeostatic Response to Respiratory Acidosis Imm response to rise in CO2 (& H2CO3) ? blood and tissue buffers take up H+ ions, H2CO3 dissociates and HCO3- increases with rise in pH. Steady state reached in 10 min & lasts for 8 hours. PCO2 of CSF changes rapidly to match PaCO2. Hypercapnia that persists > few hours induces an increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH. After 8 hrs, kidneys generate HCO3- Steady state reached in 3-5 d
Slide 50 : Alveolar-gas equation predicts rise in PaCO2 ? obligatory hypoxemia in pts breathing R.A. Resultant fall in PaO2 limits hypercapnia to ? 80 to 90 mm Hg Higher PaCO2 leads to PaO2 incompatible with life. Hypoxemia, not hypercapnia or acidemia, that poses the principal threat to life. Consequently, oxygen administration represents a critical element in the management
Slide 51 : Treatment of Respiratory Acidosis Ensure adequate oxygenation - care to avoid inadequate oxygenation while preventing worsening of hypercapnia due to suppression of hypoxemic resp drive Correct underlying disorder if possible Avoid rapid decrease in ch elevated PCO2 to avoid post hypercapnic met alkalosis (arrythmias, seizures ? adequate intake of Cl-)
Slide 52 : Alkali (HCO3) therapy rarely in ac and never in ch resp acidosis ? only if acidemia directly inhibiting cardiac functions Problems with alkali therapy: Decreased alv ventilation by decrease in pH mediated ventilatory drive Enhanced carbon dioxide production from bicarbonate decomposition Volume expansion. COPD pts on diuretics who develop met alkalosis often benefited by acetazolamide
Slide 53 : ACID PRODUCTION Volatile Acids – metabolism produces 15,000-20,000 mmol of CO2 per day. Henderson Hasselbach Equation pH = pK + log base acid pH = 6.1 + log HCO3- H2CO3 pH = 6.1 + log HCO3- 0.03 pCO2 H+ = 24 x pCO2 HCO3- Free H+ will be produced if the CO2 is not eliminated. Overview of Acid-Base Physiology
Slide 54 : Non-Volatile Acids – 50-100 mEq/day of non-volatile acids produced daily. The primary source is from metabolism of sulfur containing amino acids (cystine, methionine) and resultant formation of sulfuric acid. Other sources are non metabolized organic acids, phosphoric acid and other acids
Slide 55 : Range of ECF [H+] variation very small pH Vs. [H+] pH nanoeq [H+]/L 7.00-7.38 Acidemia 100-44 7.38-7.44 Normal 44-36 7.44-7.80 Alkalemia 36-16 Relationship between pH and [H] at physiologic pH pH 7.00 7.10 7.20 7.30 7.40 7.50 7.60 7.70 [H+] (nM) 100 79 63 50 40 32 25 20
Slide 56 : Importance of pH Control pH (intracellular and ECF incl blood) maintained in narrow range to preserve N cell, tissue and organ fx Intracellular pH (pHi) Maintained at ? 7.2: To keep imp metabolic intermediates in ionized state and limit tendency to move out of cell Most intracellular enzymes taking part in cellular metabolism have pH optimum close to this value DNA, RNA & Protein synthesis ? at slightly higher pH
Slide 57 : Maintained with help of plasma memb H+/base transporters (activated in response to acidemia) Blood pH Maintained at ? 7.4: To keep pHi in optimal range Enable optimal binding of hormones to receptors Enable optimal activity of enzymes present in blood Kraut et al AJKD 2001; 38(4): 703-727
Slide 58 : 1. BUFFERS – presence of buffer systems minimize the change in pH resulting from production of acid and provide imm protection from acid load. Main buffer system in humans is HCO3- HCO3- + H+ ? H2CO3 ? H2O + CO2 2. ROLE OF THE RESPIRATORY SYSTEM – elimination  of volatile acid -- CO2. a. Respiratory centers in the brain respond  to changes in pH of CSF and blood to  affect ventilatory rate. b. Ventilation directly controls the elimination of CO2. Regulation of arterial pH
Slide 59 : 3. ROLE OF THE KIDNEY - To retain and regenerate HCO3- thereby regenerating the body buffer with the net effect of eliminating the non-volatile acid load a. H+ secretion 1. Free urinary H+ - minimal contribution 2. Ammonia 3. Phosphorus b. HCO3- reabsorption 1. Proximal tubule – 90% 2. Distal tubule Factors affecting H+ secretion/reabsorption HCO3- a. CO2 concentration, pH b. Aldosterone d. Potassium concentration c. ECF volume e. Chloride
Slide 60 : Anion Gap AG traditionally used to assess acid-base status esp in D/D of met acidosis ? AG & ? HCO3- used to assess mixed acid-base disorders AG based on principle of electroneutrality: Total Serum Cations = Total Serum Anions Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids) Na + UC = HCO3 + Cl + UA Na – (HCO3 + Cl) = UA – UC Na – (HCO3 + Cl) = AG
Slide 61 : Normal value of AG = 12 +/- 4 mEq/L Revised N value AG = 8 +/- 4 mEq/L Changes in methods of measurement of Na, Cl & HCO3 and resultant shift of Cl value to higher range.
Slide 62 : Limiting factors for AG LABORATORY VARIATIONS – Variations in normal reference range of components of AG to be taken into consideration. Each institution should assign a normal range for AG based on these values. INHERENT ERRORS IN CALCULATION – All limits of components valid for 95% of N population. Probability of false +ve determination for each variable (Na/Cl/HCO3) = 0.05 Probability of false +ve determination for AG = 3 x 0.05 = 0.15
Slide 63 : HYPOALBUMINEMIA - Pts with low albumin can have high AG acidosis, but measured AG may be N because albumin has many -ve surface charges & accounts for a significant proportion of AG. Severe hypoalbuminemia may exhibit N AG as low as 4. Therefore in severe hypoalbuminemia if AG is normal, one must suspect an additional metabolic cause for increased AG ALKALOSIS-Alkalemic patients with pH > 7.5, AG may be ? due to met alkalosis per se & not because of additional met acidosis. Reasons proposed for the same include:
Slide 64 : Surface charges on albumin become more -ve in alkalemic conditions (due to loss of protons) --> ? unmeasured anions Assoc vol contraction --> hyperproteinemia Induction of glycolysis and resultant hyperlactatemia HYPERCALCEMIA - Fall in AG as expected (? UC) except in paraneoplastic hypercalcemia for unknown reasons Oster et al. Nephron 1990; 55:164-169. DRUGS - Lithium and polymyxin cause fall in AG (? UC) while carbenicillin cause ? in AG (act as UA)
Slide 65 : CLEARANCE OF ANIONS - Pts with expected ? AG acidosis may have N AG because of clearance of added anions e.g. DKA pts in early stage with adequate clearance of ketones may have a normal AG as also those in recovery phase ? AG - ? HCO3- RELATIONSHIP - used to assess mixed acid-base disorders in setting of high AG Met Acidosis: ? AG/? HCO3- = 1 ? Pure High AG Met Acidosis ? AG/? HCO3- > 1 ? Assoc Metabolic Alkalosis ? AG/? HCO3- < 1 ? Assoc N AG Met Acidosis Based on assumption that for each 1 mEq/L increase in AG, HCO3 will fall by 1 mEq/L
Slide 66 : However: Non HCO3 buffers esp intracellular buffers also contribute to buffering response on addition of H+. Becomes more pronounced as duration of acidosis increases. Hence ? AG/? HCO3- > 1 even in absence of Met Alkalosis All added anions may not stay in EC comp and those that diffuse inside cells could lead to a lesser rise in AG than expected Hence ? AG/? HCO3- < 1 even in states expected to have high AG Met Acidosis Salem et al, Arch Int Med 1992; 152: 1625-1629
Slide 67 : Strict use of AG to classify met acidosis & of ?AG/?HCO3 to detect mixed/occult met acid-base disorders can be assoc with errors because of the possibility of change of AG by factors other than metabolic acid-base disturbances. Use of sequential AG determinations and observation of temporal profile of AG more imp than single value.
Slide 68 : Modifications/Alternatives for AG ? AG/? HCO3- = 1-2 ? Pure High AG Met Acidosis ? AG/? HCO3- > 2 ? Assoc Met Alkalosis ? AG/? HCO3- < 1 ? Assoc N AG Met Acidosis Black RM. Intensive Care Medicine 2003; 852-864 Use of Corrected AG Corrected AG = Calculated AG + 2(Albumin gm/dL) + 0.5 (PO43- mg/dL) Kellum JA et al. Chest 1996; 110: 18S
Slide 69 : METABOLIC ACIDOSIS
Slide 70 : 1. HCO3 loss a. Renal b. GIT Decreased renal acid secretion – Increased production of non-volatile acids a. Ketoacids b. Lactate c. Poisons d. Exogenous acids Pathophysiology
Slide 71 : Causes of High AG Met Acidosis Ketoacidosis: Diabetic Alcoholic Starvation Lactic Acidosis: Type A (Inadequate O2 Delivery to Cells) Type B (Inability of Cells to utilise O2) Type D (Abn bowel anatomy) Toxicity: Salicylates Paraldehyde Methanol Toluene Ethylene Glycol
Slide 72 : Renal Failure Rhabdomyolsis Causes of N AG Met Acidosis HCO3 loss: GIT Diarrhoea Pancreatic or biliary drainage Urinary diversions (ureterosigmoidostomy) Renal Proximal (type 2) RTA Ketoacidosis (during therapy) Post-chronic hypocapnia
Slide 73 : Impaired renal acid excretion: Distal (type 1) RTA Hyperkalemia (type 4) RTA Hypoaldosteronism Renal Failure Misc: Acid Administration (NH4Cl) Hyper alimentation (HCl containing AA sol) Cholestyramine Cl HCl therapy (Rx of severe met alkalosis) Black RM. Intensive Care Medicine 2003; 852-864
Slide 74 : Manifestations of Met Acidosis Cardiovascular Impaired cardiac contractility Arteriolar dilatation, venoconstriction, and centralization of blood volume Increased pul vascular resistance Fall in C.O., ABP & hepatic and renal BF Sensitization to reentrant arrhythmias & reduction in threshold of VFib Attenuation of cardiovascular responsiveness to catecholamines Adrogue et al, NEJM 1998; 338(1): 26-34
Slide 75 : Respiratory Hyperventilation ? strength of respiratory muscles & muscle fatigue Dyspnea Metabolic Increased metabolic demands Insulin resistance Inhibition of anaerobic glycolysis Reduction in ATP synthesis Hyperkalemia (secondary to cellular shifts) Increased protein degradation Cerebral Inhibition of metabolism and cell vol regulation Mental status changes (somnolence, obtundation & coma) Adrogue et al, NEJM 1998; 338(1): 26-34
Slide 76 : SERUM AG URINARY AG Total Urine Cations = Total Urine Anions Na + K + (NH4 and other UC) = Cl + UA (Na + K) + UC = Cl + UA (Na + K) – Cl = UA – UC (Na + K) – Cl = AG Helps to distinguish GI from renal causes of loss of HCO3 by estimating Urinary NH4+ (elevated in GI HCO3 loss but low in distal RTA). Hence a -ve UAG (av -20 meq/L) seen in former while +ve value (av +23 mEq/L) seen in latter. Evaluation of Met Acidosis Kaehny WD. Manual of Nephrology 2000; 48-62
Slide 77 : PLASMA OSMOLAL GAP – Calc P Osm = 2[Na+] + [Gluc]/18 + [BUN]/2.8 N Meas P Osm > Calc P Osm (upto 10 mOsm/kg) Meas P Osm - Calc P Osm > 15-20 mOsm/kg ? presence of abn osmotically active substances (usually an alcohol) URINE OSMOLAL GAP - similar to P. Osm gap Calc U Osm = 2[(Na+u ) + (K+u)] + [Gluc u]/18 + [UUN]/2.8 Meas P Osm > Calc P Osm ? excretion of NH4+ with non Cl- anion (e.g. hippurate) [NH4+ u] usually ? 50% of osmolal gap
Slide 78 : Met Acidosis N AG ? AG Ketones +ve Serum Lactate ? P Osm Gap ?(OH) B/AA = 5:1 ?(OH) B/AA = 3:1 +ve UAG - ve UAG Lactic Acidosis Intoxications DKA Alcoholic GIT RTA Ketoacidosis < 5.5 Urine pH ? K ? K > 5.5 Type 1 Type 2 Type 4 U Osm Gap Iatrogenic Acid Gain ? N
Slide 79 : Treatment of Met Acidosis Severe acidemia ? Effect on Cardiac function most imp factor for pt survival since rarely lethal in absence of cardiac dysfunction. Contractile force of LV ? as pH ? from 7.4 to 7.2 However when pH < 7.2, profound reduction in cardiac function occurs and LV pressure falls by 15-30% Most recommendations favor use of base when pH < 7.15-7.2 or HCO3 < 8-10 mEq/L. When to treat?
Slide 80 : How to treat? Rx Underlying Cause HCO3- Therapy Aim to bring up pH to ?7.2 & HCO3- ? 10 mEq/L Qty of HCO3 admn calculated: 0.5 x LBW (kg) x HCO3 Deficiency (mEq/L) Vd of HCO3 ?50% in N adults. However in severe met acidosis can ? to 70-80% in view of intracellular shift of H+ and buffering of H+ by bone and cellular buffers.
Slide 81 : Why not to treat? Considered cornerstone of therapy of severe acidemia for >100 yrs Based on assumption that HCO3- admn would normalize ECF & ICF pH and reverse deleterious effects of acidemia on organ function However later studies contradicted above observations and showed little or no benefit from rapid and complete/over correction of acidemia with HCO3.
Slide 82 : Adverse Effects of HCO3- Therapy ? CO2 production from HCO3 decomposition ? Hypercarbia (V>A) esp when pul ventilation impaired Myocardial Hypercarbia ? Myocardial acidosis Impaired myocardial contractility & ? C.O. ? SVR and Cor A perfusion pressure ? Myocardial Ischemia esp in pts with HF Hypernatremia & Hyperosmolarity ? Vol expansion ? Fluid overload esp in pts with HF Intracellular (paradoxical) acidosis esp in liver & CNS (? CSF CO2)
Slide 83 : ? gut lactate production, ? hepatic lactate extraction and thus ? S. lactate ? ionized Ca ? VO2, ? PaO2, ? P50O2 CORRECTION OF ACIDEMIA WITH OTHER BUFFERS: Carbicarb - not been studied extensively in humans - used in Rx of met acidosis after cardiac arrest and during surgery - data on efficacy limited
Slide 84 : THAM THAM (Trometamol/Tris-(OH)-CH3-NH2-CH3) - biologically inert amino alcohol of low toxicity. Capacity to buffer CO2 & acids in vivo as well as in vitro pK at 37 C = 7.8 (HCO3 has pK of 6.1) More effective buffer in physiological range of blood pH Accepts H+/CO2 and generates HCO3/? PaCO2 R-NH2 + H2O + CO2 ? R-NH3+ + HCO3- R-NH2 + H+ + La- ? R-NH3+ + La-
Slide 85 : Rapidly distributed in ECF except RBCs & liver cells --> excreted by kidneys in the protonated form (NH3+) Effective as buffer in closed or semi closed system (unlike HCO3- which req an open system to eliminate CO2) Effective in states of hypothermia Side Effects: 1. Tissue irritation and venous thrombosis if admn through peripheral vein - seen withTHAM base (pH = 10.4) THAM acetate (pH = 8.6) well tolerated - does not cause tissue or venous irritation
Slide 86 : 2. Large doses can cause resp depression 3. Hypoglycemia Initial loading dose of THAM acetate (0.3 ml/L sol) calculated: Lean BW (kg) x Base Deficit (mEq/L) Max daily dose ~15 mmol/kg Use in severe acidemia (pH < 7.2): 1. Resp failure: a) Induced Acute Hypercapnia - Apnoeic oxygenation during bronchoscopy and organ collection from organ donors b) ARDS with permissive hypercapnia
Slide 87 : c) Acute Severe Asthma with severe respiratory acidosis 2. DKA 3. Renal failure 4. Salicylate or Barbiturate intoxication 5. Raised ICT due to cerebral trauma 6 Cardioplegia during Open heart surgery 7. CPR (after restoration of cardiac function) 8. During liver transplantation 7. Chemolysis of renal calculi 8. Severe burns Nahas et al, Drugs 1998; 55(2):191-224
Slide 88 : METABOLIC ALKALOSIS
Slide 89 : Introduction Met alkalosis common (up to 50% of all disorders) Severe met alkalosis assoc with significant mortality Arterial Blood pH of 7.55 ? Mortality rate of 45% Arterial Blood pH of 7.65 ? Mortality rate of 80% (Anderson et al. South Med J 80: 729–733, 1987) Metabolic alkalosis has been classified by the response to therapy or underlying pathophysiology
Slide 90 : 1. INITIATING EVENT a. HCO3- gain b. H+ loss 1) Renal 2) GIT c. H+ shift d. Contraction/chloride depletion Pathophysiology
Slide 91 : 2. MAINTENANCE Alkaline loads generally excreted quickly and easily by the kidney. Significant metabolic alkalosis can thus only occur in the setting of impaired HCO3- excretion Causes of impaired HCO3- excretion 1) Decreased GFR – volume depletion 2) Increased reabsorption –  volume/chloride depletion hyperaldosteronism
Slide 92 : Pathophysiological Classification of Causes of Metabolic Alkalosis H+ loss: GIT Chloride Losing Diarrhoeal Diseases Removal of Gastric Secretions (Vomiting, NG suction) Renal Diuretics (Loop/Thiazide) Mineralocorticoid excess Post-chronic hypercapnia Hypercalcemia High dose i/v penicillin Bartter’s syndrome Black RM. Intensive Care Medicine 2003; 852-864
Slide 93 : HCO3- Retention: Massive Blood Transfusion Ingestion (Milk-Alkali Syndrome) Admn of large amounts of HCO3- Contraction alkalosis Diuretics Loss of high Cl-/low HCO3- GI secretions (vomiting and some diarrheal states) H+ movement into cells Hypokalemia Refeeding Black RM. Intensive Care Medicine 2003; 852-864
Slide 94 : Classification of Causes of Metabolic Alkalosis acc to response to therapy VOLUME/SALINE RESPONIVE (Vol/Cl- Depletion) Gastric losses: vomiting, mechanical drainage, bulimia, gastrocystoplasty Chloruretic diuretics: bumetanide, chlorothiazide, metolazone etc. Diarrheal states: villous adenoma, congenital chloridorrhea Posthypercapneic state Dietary chloride deprivation with base loading: chloride deficient infant formulas Cystic fibrosis (high sweat chloride) Gall JH. J Am Soc Nephrol 2000; 11: 369–375.
Slide 95 : VOLUME REPLETE/SALINE UNRESPONIVE K+ DEPLETION/MINERALOCORTICOID EXCESS Primary aldosteronism: Adenoma Renin-responsive Idiopathic Glucocorticoid-suppressible Hyperplasia Carcinoma Apparent mineralocorticoid excess: Primary deoxycorticosterone excess: 11 ?- & 17 ?- hydroxylase deficiencies Drugs: licorice (glycyrrhizic acid) as a confection or flavoring, carbenoxolone Liddle syndrome Gall JH. J Am Soc Nephrol 2000; 11: 369–375.
Slide 96 : Secondary aldosteronism Adrenal corticosteroid excess: Severe hypertension: malignant/accelerated renovascular Hemangiopericytoma, nephroblastoma, RCC Bartter and Gittleman syndromes and their variants Laxative Abuse, Clay Ingestion HYPERCALCEMIC STATES (? HCO3- reabsorption) Hypercalcemia of malignancy primary secondary exogenous Gall JH. J Am Soc Nephrol 2000; 11: 369–375.
Slide 97 : Ac or Ch milk-alkali syndrome (both HCO3- & Ca ingested ? additional mechanisms for alkalosis incl vomiting & ? GFR MISC Carbenicillin/ampicillin/penicillin. HCO3- ingestion: massive or with renal insufficiency Recovery from starvation Hypoalbuminemia (Alkalosis usually mild and due to diminution of -ve charge normally contributed by albumin towards AG & shift in buffering curve for plasma). Gall JH. J Am Soc Nephrol 2000; 11: 369–375.
Slide 98 : Manifestations of Met Alkalosis Symp of met alkalosis per se difficult to separate from those of Cl-/K+/Vol depletion ? latter usually more apparent than those directly attributable to alkalosis. Cardiovascular Arteriolar constriction Reduction in Coronary BF/Anginal threshold Predisposition to refractory SV & V arrhythmias (esp if pH > 7.6) Respiratory - Hypoventilation (Compensatory) ? Hypercapnia/Hypoxemia Adrogue et al, NEJM 1998; 338(2): 107-111
Slide 99 : Metabolic Stimulation of anaerobic glycolysis & organic acid production Reduction plasma ionized Calcium conc. Hypokalemia (secondary to cellular shifts) Hypomagnesaemia & Hypophosphatemia Cerebral Reduction in Cerebral BF ? mental status changes (stupor, lethargy & delirium) N-M irritability (related to low ionized plasma Ca) ? Tetany, Hyperreflexia, Seizures Adrogue et al, NEJM 1998; 338(2): 107-111
Slide 100 : Urinary Cl- & K+ measurements before therapy useful diagnostically. Low urinary chloride (<10 mEq/L) seen in alkalotic states where Cl- depletion predominates (except cause is use of chloruretic diuretic) ? Remains low until Cl- repletion nearly complete. Urinary K+ conc of >30 mEq/L with ? S. K+ suggests renal K+ wasting due to: Intrinsic renal defect Diuretics High circulating aldosterone Urinary K+ conc of <20 mEq/L with ? S. K+ suggests extra renal K+ loss. Evaluation of Met Alkalosis
Slide 101 : Treatment of Metabolic Alkalosis Although relationship between alkalemia and mortality not proven to be causal, severe alkalosis should be viewed with concern, and correction by the appropriate intervention should be undertaken when the arterial blood pH exceeds 7.55 Imm goal of therapy is moderation & not full correction of the alkalemia. Reducing plasma HCO3- to <40 mEq/L short-term goal, since the corresponding pH ? 7.55 or lower. Most severe metabolic alkalosis is of Cl- responsive type
Slide 102 : Treatment of Vol Depleted/Saline Responsive Metabolic Alkalosis Rx underlying cause resp for vol/Cl- depletion While replacing Cl- deficit, selection of accompanying cation (Na/K/H) dependent on: Assessment of ECF vol status Presence & degree of associated K depletion, Presence, degree & reversibility of ? of GFR. Pts with vol depletion usually require replacement of both NaCl & KCl.
Slide 103 : DEPLETION OF BOTH CL- & ECF VOL (most common): Isotonic NaCl appropriate therapy ? simultaneously corrects both deficits. In patients with overt signs of vol contraction, admn of min of 3 - 5 L of 150 mEq/L NaCl usually reqd to correct vol deficits & metabolic alkalosis. When ECF vol is assessed as normal, total body Cl- deficit can be estimated as: 0.2 x BW (kg) x Desired [Cl-] – Measured [Cl-] (mEq/L) Replace continuing losses of fluid & electrolytes Correction of Na, K & Cl deficits & assoc prerenal azotemia promotes HCO3 excretion and alkaline diuresis with a ? in plasma HCO3 towards normal.
Slide 104 : DEPLETION OF CL- & ? ECF VOL Admn of NaCl is inadvisable for obvious reasons. Chloride should be repleted as KCl unless hyperkalemia present or concomitant ? GFR where ability to excrete K+ load is hampered. Administration of acetazolamide accelerates bicarbonaturia esp: If natriuresis with a high Na excretion rate req simultaneously If high serum K+ present Monitoring needed to detect associated kaliuresis and phosphaturia. GFR must be adequate (C/I if S. creat >4 mg/dl)
Slide 105 : CL- DEPLETION with ? ECF VOL & HYPERKALEMIA (Use of NaCl/KCl C/I) Hydrochloric Acid I/v HCl indicated if correction reqd imm Amount of HCl given as 0.1 or 0.2 M sol needed to correct alkalosis estimated as: 0.5 x BW (kg) x Desired [Cl-] – Measured [Cl-] (mEq/L) Continuing losses must also be replaced. Use of 50% of BW as Vd of infused protons done so that infused protons act to correct alkalosis in both ICF and ECF & restore buffers at both sites ½ correction given since imm goal of therapy is correction of severe & not full correction of alkalemia.
Slide 106 : HCl has sclerosing properties ? must be admn through a central venous catheter (placement confirmed radiologically to prevent leakage of HCl ? sloughing of perivascular tissue) Infusion rates N < 0.2 mmol/kg BW/hr with max rate of 25 mEq/h. HCl can also be infused after adding it to AA sol, fat emulsion or dextrose sol containing electrolytes & vit without causing adverse chemical RX - can also be admn through a peripheral vein Req frequent measurement of ABG and electrolytes. Ammonium Chloride Can be given into a peripheral vein Rate of infusion should not exceed 300 mEq/24 h. C/I in presence of renal or hepatic insufficiency (worsening of azotemia & ppt of acute ammonia intoxication with coma respectively).
Slide 107 : Dialysis In presence of renal failure or severe fluid overload state in CHF, dialysis +/- UF may be reqd to exchange HCO3 for Cl & correct metabolic alkalosis. Usual dialysates for both HD/PD contain high [HCO3-] or its metabolic precursors & their conc must be reduced. In pts with unstable hemodynamics, CAVH/CVVH using NaCl as replacement sol can be done. Adjunct Therapy PPI can be admn to ? gastric acid production in cases of Cl-depletion met alkalosis resulting from loss of gastric H+/Cl- (e.g. pernicious vomiting, req for continual removal of gastric secretions, gastrocystoplasty Met alkalosis likely to persist & replacement of preexisting deficits hampered by ongoing losses
Slide 108 : Treatment of Vol Replete/Saline Unresponsive Metabolic Alkalosis MINERALOCORTICOID EXCESS Therapy should be directed at either removal of the source or its blockade. K-sparing diuretics, esp spironolactone helpful in reversing adverse effects of mineralocorticoid excess on Na, K and HCO3excretion. Restriction of Na and addition of K to diet also helpful both in Rx of alkalosis as well as HTN. Correction of K deficit reverses alkalinizing effects but elimination of aldosterone excess essential to achieve permanent correction.
Slide 109 : MILK-ALKALI SYNDROME & OTHER HYPERCALCEMIC STATES Cessation of alkali ingestion & Ca sources (often milk and calcium carbonate) Treatment of underlying cause of hypercalcemia Cl- and Vol repletion for commonly associated vomiting
Slide 110 : SERIAL ABGs CLINICAL PROFILE SUPPORTING LAB DATA/ INVESTIGATIONAL TOOLS CLINICIAN’S JUDGEMENT CORRECT INTERPRETATION SIMPLE DISORDER (DEG OF COMPENSATION) MIXED DISORDER (ORDER OF PRIMARY & SUBSEQUENT DISORDERS) SUMMARY OXYGENATION /VENTILATORY STATUS
Slide 111 : THANK YOU

 


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