Soda bicabonate

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Soda Bicarbonate - Indications:

Soda Bicarbonate - Indications By Dr Shashidhar Patil

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Sodium bicarbonate  or  sodium hydrogen carbonate  is the  chemical compound  with the formula  Na HCO 3 . Sodium bicarbonate is a white solid that is  crystalline  but often appears as a fine powder . the  salt  has many related names such as  baking soda ,  bread soda ,  cooking soda , and  bicarbonate of soda

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.... Sodium bicarbonate: first commercially produced in the late 1950’s Acidosis is thought to have adverse physiological effects and generally is associated with increased mortality. Consequently, therapy to correct acidosis, usually with sodium bicarbonate is been widely used. In recent years, however, this approach is changing. Disease process Add acid Loose alkali acidosis Is it a compensatory Mechanism…? Does it do any good ? Any Harm ? At what level to intervene ? Impaired acid excretion

Hypertonicity… Hyperosmolality:

Hypertonicity … Hyperosmolality 7.5% , 8.4%, 4.2% Na = HCO 3 = 0.9 mEq/ml Osmolality = 1800 pH = ? 1ml produces 22 ml CO 2 Medical Chemistry of NaHCO 3 Normal serum osmolality is around ….290 1800 / 6 = 300 , that’s why ideal dilution of Soda-Bi- Carb should be 6 times 8

Causes of severe metabolic acidosis:

Causes of severe metabolic acidosis General Mechanism Specific Clinical Examples True HCO 3  deficit     kidney Renal tubular acidosis     gastrointestinal Diarrhea H +  gain     exogenous acid NH 4 Cl administration, toxins     abnormal lipid metabolism Diabetic ketoacidosis a     abnormal carbohydrate metabolism Lactic acid     normal protein metabolism Uremic acidosis

Sodium Bicarbonate :

6 Sodium Bicarbonate Type Isotonic sodium bicarbonate 1.26% Hypertonic sodium bicarbonate (1mmol/ml) 8.4% Uses Correction of metabolic acidosis Alkalinisation of urine Routes IV

Ion content of sodium bacarbonate (mmol/L):

7 Ion content of sodium bacarbonate (mmol/L) Na + K+ HCO 3 C1 Ca 2 1.26% sodium 150 150 Bacarbonate 8.4% sodium 1000 1000 bacarbonate

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Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base which, given time, can be converted back to bicarbonate

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1. What are the deleterious effects of acidemia and when are they manifest? 2. When is acidemia severe enough to warrant therapy? In considering acute bicarbonate replacement four questions should be considered

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3. How much bicarbonate should be given and how is that amount calculated? 4. What are the deleterious effects of bicarbonate therapy?

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Decreased myocardial contractility Fall in cardiac output Fall in BP Pulmonary venoconstriction Deleterious effects of acidemia

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Decreased binding of norepinephrine to its receptors Acidemia may adversely affect cell functions such as enzymatic reactions, ATP generation, fatty acid biosynthesis, and bone formation/ resorption Deleterious effects of acidemia

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Drugs which are salts of weak acids are more active during acidemia More receptor binding More entry to cells Best example is ASA Deleterious effects of acidemia

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tolbutamide methotrexate phenobarbital phenytoin

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Optimal extracelluar pH 7.4 Optimal intracellular pH 7.1 Deviations from normal pH will obviously decrease the efficiency of all reactions

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Acidemia protects the central nervous system against seizures, it sensitizes the myocardium to arrhythmias Extracellular pH is a surrogate for intracellular pH

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Acidemia of Metabolic Acidosis Suppresses Cardiac Contractility Releases Catecholamine Ionotrophic Effect >7.2 <7.2 NaHCO3 Depressed myocardial contractility Decreased catecholamine efficacy Arrhythmias Pulmonary vasoconstriction Hypotension Depressed Myocardial Function

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Most authorities in acid-base physiology would give bicarbonate to a patient with an arterial pH < 7.1 Not a hard and fast rule More on this later When is acidemia severe enough to warrant therapy?

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The volume of distribution of bicarbonate is approximately that of total body water In patients with metabolic acidosis it is said to vary from 50% to greater than 100%, depending on the severity of the acidemia How much bicarbonate should be given and how is that amount calculated ?

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Any calculated amount is approximate Fernandez et al have derived a formula for calculating the bicarbonate space (KI 36:747-752, 1989) (0.4 + 2.6 / pHCO3) (body weight) How much bicarbonate should be given and how is that amount calculated?

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At a pCO 2 of 13 mm Hg and HCO 3 of 4 mEq/l, the arterial pH is 7.1 Raise the HCO 3 to only to 8 mEq/L the blood pH will increase to 7.4 This assumes the pCO 2 doesn’t change How much bicarbonate should be given and how is that amount calculated?

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If the bicarbonate concentration rises only 1 mEq/L the pH would be above 7.2 Arterial pCO 2 typically however does not remain the same after bicarbonate infusion In severely acidotic patients it rises 6.7 ± 1.8 mm Hg when an infusion of sodium bicarbonate is given (1.5 mmol/kg over 5min) How much bicarbonate should be given and how is that amount calculated?

Soda-Bi-Carb……:

Soda-Bi- Carb …… .…Adverse-Effects

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Bicarbonate therapy is associated with an increase in mortality True in humans and experimental animals under a variety of acidemic conditions Fall in blood pressure and cardiac output What are the deleterious effects of bicarbonate therapy?

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Shifts in ionized calcium In strong acid acidosis potassium also shifts out of the cell Sensitizes the heart to abnormal electrical activity and subsequent arrhythmias What are the deleterious effects of bicarbonate therapy?

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“Paradoxical” intracellular acidosis – CO 2 shifts into cells Both volume expansion and hypernatremia can occur Fulminate congestive heart failure with flash pulmonary edema may result What are the deleterious effects of bicarbonate therapy?

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Intracellular acidosis…. 1 ml NaHCO 3 Gives 22 ml CO 2 NaHCO 3 = Na + HCO 3 H + + HCO 3 H 2 O + CO 2

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In vitro studies show that intracellular alkalinization hastens cell death following anoxia Stimulates superoxide formation, increases pro-inflammatory cytokine release, and enhances apoptosis Relationship to human disorders unknown What are the deleterious effects of bicarbonate therapy?

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Rebound alkalemia – especially with low arterial pCO 2 Blood lactate and ketone bodies increase This “potential” bicarbonate will be converted back to actual bicarbonate unless it lost in the urine What are the deleterious effects of bicarbonate therapy?

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Deleterious effects…

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PaO 2 …60 mmHg 90 % 7.4 7.8 7.0 Impaired tissue oxygenation with correction of acidemia …... Hb . Sat.% RT. LT. 100% 80%

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Oxygen delivery 24 to 48 hrs Low 2-3 DPG levels Secondary to reduced glycolysis Direct effect of pH on Hb  affinity of O2 ACIDOSIS……………. OXYGEN DELIVERY Acute acidemia facilitates oxygen delivery chronic acidemia hampers oxygen delivery Correcting acute acidemia could be more dangerous..!!

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How do I give soda bicarb …..? × Indication : if pH is less than 7.10 in DKA ( less than 7.1 and not improving ) HCO 3 required = half of BW × ( 15 – HCO 3 ) Dilute 4 to 6 times give over 2 hours Diluent : water for injection / 5%dextrose Ensure adequate ventilation

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Acetoacetate and beta- hydroxybutyrate are lost in the urine before the patient arrives at the hospital The patient is truly bicarbonate deficient More urinary loss of ketone bodies occurs following fluid administration and volume repletion DKA

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Hyperchloremic metabolic acidosis the day after insulin therapy Almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired Bicarbonate therapy markedly increases blood acetoacetate and beta-hydroxybutyrate levels DKA

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Bicarbonate therapy delays the removal of ketone bodies from the blood Bicarbonate therapy markedly increases blood acetoacetate and beta- hydroxybutyrate levels DKA

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Mortality greater than 80% Outcome depends on the treatment of its cause Cardiogenic or hemorrhagic shock Exogenous toxins such as cyanide or metformin Lactic Acidosis

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During /Post resuscitation ..role of NaHCO3 ? I don’t have ABG facility and the patient is in shock Should I give S.B. ? Child with diarrhoea and shock I would like to add S.B. to normal saline bolus , comment….. If the child admitted with me has received large dose of S.B. what should I monitor ? How do I dilute S.B., Rate of infusion….? Role of S.B. in wide anion gap acidosis….? Intratracheal administration for treatment of metabolic A Can S.B. be used for treatment of hyponatremia ? ( equivalent to 6 % saline,7.5 % contains 0.9 mEq ./ml) FAQ,S …………? .. CO & BP fell sooner when NaHCO3 was used to treat lactic acidosis (Graf 1985 Science) .. NaHCO3 corrected arterial metabolic acidosis, but led to a decrease in intramyocardial pH, and reduced the likelihood of successful resuscitation ( Kette 1990 Circulation) .. Hypertonic solutions adversely affect cardiac resuscitation efforts by reducing CPP ( Kette 1991 JAMA)

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OVERDOSAGE: Should alkalosis result, the bicarbonate should be stopped and the patient managed according to the degree of alkalosis. NORMAL SALINE may be given. Potassium chloride is indicated if there is hypokalemia. Severe alkalosis may be accompanied by hyperirritability or tetany and these symptoms may be controlled by calcium gluconate .

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CASE #1: A 20 year-old man with a five-year history of type 1 diabetes mellitus was admitted for the ninth time in diabetic ketoacidosis. He was poorly responsive and had Kussmaul respirations. Before any therapy he had a plasma Na of 140 mEq/L, K 4 mEq/L, Cl 109 mEq/L, CO 2 3 mEq/L, and his creatinine was 1 mg/dL. The arterial pH was 6.95, pCO 2 14 mm Hg, and the calculated HCO3 was 3 mEq/L.

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Urine and blood ketones were strongly positive. He was treated with insulin and appropriate fluid and electrolyte replacement. He was not given bicarbonate. The next day he was fully oriented. His plasma Na was 142, K 4, Cl 114 and his CO 2 was 18 mEq/L. The remainder of his clinical course was unremarkable.

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CASE #2: An 80 year old man was admitted with severe congestive heart failure. He was hypotensive and oliguric. He had both pulmonary and peripheral edema. His baseline creatinine was known to be 1.6 mg/dL. On arrival at the emergency room his plasma Na was 135 mEq/L, K 4 mEq/L, Cl 97 mEq/L, CO 2 7 mEq/L, and his creatinine was 2.5 mg/dl. His arterial pH was 7.1, pCO 2 20 mm Hg, and the calculated HCO 3 was 6 mEq/l. The blood lactate level was 20 mmol/L .

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The patient was intubated and placed on a respirator keeping his pCO 2 at 20 mmHg. CVVHD was begun with a bath containing 14 mEq /L of bicarbonate. He was given an infusion of 300 mEq of bicarbonate over two hours; with a total body water of 43 liters, one would aim for a HCO 3 of 14 mEq /L: (7 mEq /L X 43 L = 301 mEq ). At the end of that time his pH was 7.2 and the HCO 3 was 13 mEq /L. Five days later he was transferred out of the intensive care unit, his lactic acidosis resolved.

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Case #1 got no bicarbonate even though his pH was < 7.0 Case #2 received bicarbonate though he had a higher pH Bicarbonate therapy must be individualized

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Desired HCO 3 – observed HCO 3 Use total body water Assume pCO 2 will not change Give that amount which will raise the pH to 7.2

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Reevaluate in two hours Make new plan based on the new data Correct the underlying cause(s)

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Case 3………………… 16 yrs old boy with diarrhea and LRI is in shock His ABG is ……. pH ……7.01 P co 2 …36 HCO 3 …5.5 ACIDOSIS LOW BICARB BUT CO 2 IS HIGH ? WOULD BICARB BE INDICATED ? NO

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Case 4…… 15 yr …Girl Diarrhoea , Jr resident noted that the she is moderately Dehydrated and had R/R of 68 / min. A Bolus of N-saline was given followed by a dose of bicarb , thinking that the girl may be acidotic. After about 4 hours she has seizures . Sugar normal and so was calcium , seizure were controlled but recurred Again ………………. Though the serum calcium was “normal ” These were hypocalcaemic seizures . Ionic calcium low

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CASE 5…………. DKA WITH RT LOWER LOBE CONSOLIDATION AND HYPOXIA pH….7.016 CO 2 ……6 BICARB..6 PO 2 …..58 Severe metabolic acidosis with mild hypoxia Sugar 689 , ketones ++++ , COMA Received Bicarb with other standard protocol for DKA……………sugar 326 mg % pH ……7.36 CO 2 …. 34 BICARB…18 PO 2 …..63 ABG LOOKS BETTER , MILD HYPOTENSION , ON SUPPORT SUGAR IS OK Patient deteriorates soon for no obvious reason , his sugar is OK , ABG = Acidosis Anion gap still wide , ketones not very high pH ….7.16 CO 2 …14 BICARB..9 PO 2 …..45 5 HOURS AFTER …………………LACTIC ACIDOSIS

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Rapid correction of acidosis shifts curve to left……..tissue hypoxia Mild hypotension Diabetics have low 2.3. DPG Soda bicarb . promotes lactic acidosis What can Happen with Mr Soda-Bi- Carb ? In severe DKA, bicarb therapy is not supported by the literature. In fact, at least 2 human studies have shown possible deleterious effects of bicarbonate administration even in patients with pH < 7.0 . Thus the administration of sodium bicarbonate to patients with diabetic ketoacidosis cannot be recommended at any pH ( class 1 )

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Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base which, given time, can be converted back to bicarbonate

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Severe Metabolic Acidosis with adequate ventilatory Support Hyperkalemia Hypermagnesaemia Tricyclic antidepressant drug poisoning Sodium channel blocker poisoning Indications as per A.H.A…………. Sodium bicarbonate indicated ….. In the treatment of certain drug intoxications… Barbiturates (where dissociation of the barbiturate-protein complex is desired) , Poisoning by salicylates or methyl alcohol . In hemolytic reactions (requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products.) In Nutshell….. Role is doubtful AND not justified in all Wide anion Gap Metabolic Acidosis (ORGANIC ACIDOSIS) e.g. Lactic Acidosis, DKA, Uremic Acidosis, Alcoholic KA. But …… Well justified in Non Gap Metabolic Acidosis (INORGANIC ACIDOSIS.. True HCO 3 deficit) e.g. Severe Diarrhoea, RTA, CRF.

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Reference: Sandra Sabatini and Neil A. Kurtzman : Bicarbonate Therapy in Severe Metabolic Acidosis, JASN in press. . Published on March 5, 2008 as doi : 10.1681/ASN.2007121329

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