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ELECTROLYTES TiKi TaKa _____________________

NOTES: ====== . Human blood PH is maintained at 7.35-7.45 by many mechanisms, . the most important are the regulation of CO2, bicarbonate and H atoms by lungs and kidney. . PH < 7.35 = acidosis while PH > 7.45 = alkalosis. . PaCO2 & HCO3 can differentiate between respiratory and metabolic acid base disturbance. . Sometimes mixed acid-base disorders present with PH within normal range. . Normal HCO3 = 24 mEq/L and normal PaCO2 = 40 mmHg. . Metabolic acid-base disturbance is due to primary change in HCO3 concentration. . Respiratory acid-base disturbance is due to primary change in PaCO2. . Primary rise in PaCO2 (respiratory acidosis) and drop of plasma HCO3 (metabolic acidosis). . Primary drop in PaCO3 (respiratory alkalosis) and rise in plasma HCO3 (metabolic alkalosis). .. HCO3 primary change (metabolic) while PaCO2 primary change (Respiratory). .. Primary = the main change is in Paco2 or HCO3. .. Compensatory = slight change in the other item. .. i.e.: PaCO2 = 45 & HCO3 = 35 --> metabolic.... PaCO2 = 26 & HCO3 = 28 --> respiratory .. if great change in both PaCO2 & HCO3 --> think of mixed acid-base imbalance (Fix the formula & calculate PaCO2 and compare it with that of the case).

. METABOLIC ACIDOSIS: ______________________ . Decreased blood PH < 7.35. . Decreased blood HCO3 < 24 mEq/L (1ry). . Decreased PaCO2 (Compensatory respiratory alkalosis), . PaCO2s in metabolic acidosis is calculated by winter's formula: PaCO2 = 1.5 (HCO3) + 8 . Causes: See below N.B: . Hyperventilation (tachypnea) is the mode of respiratory compensation for metabolic acidosis (to wash CO2). . Calculating the plasma anion gap is the best next step in diagnosis of patient's acid-base status, . due to it narrow the differential diagnosis in case of metabolic acidosis e.g. A) Some of the most common cause of anion gap metabolic acidosis: - Lactic acidosis: Hypoxia, poor tissue perfusion, mitochondrial dysfunction. - Ketoacidosis: Type 1 D.M, starvation & alcoholism. - Methanol ingestion: Formic acid accumulation. - Ethylene glycol ingestion: glycolic and oxalic acid accumulation. - Salicylates poisoning: causes mixed metabolic acidosis and respiratory alkalosis. - Uremia: Failure to excrete (H) as NH4. B) Most common causes of normal anion gap metabolic acidosis: - RTA (renal tubular acidosis) --> has +ve urine anion gap (UAG). - Diarrhea --> has -ve urine anion gap (UAG).

. METABOLIC ALKALOSIS: ____________________ . Increased blood PH > 7.45. . Increased blood HCO3 > 24 mEq/L (1ry). . Increased PaCO2 (compensatory respiratory acidosis). . PaCO2 in metabolic alkalosis is calculated by the formula: PaCO2 = (0.9 HCO3) + 16 +,- 2. . Causes; - Vomiting, diuretic --> Volume depletion --> + Renin-aldosterone system. - Exogenous alkali intake. - mineralocorticoids excess --> bicarbonate retention, H & K loss --> metabolic alkalosis. . Metabolic alkalosis is divided into: ------------------------------------------------1- Saline responsive condition (with urine chloride < 20 mEq/L) and volume depletion, ------------------------------------------------------------------------------------------------------------------ due to GIT proton (H) loss (vomiting), volume contraction or diuretics, - treated by normal saline. 2- Saline resistant condition (with urine chloride > 20 mEq/L) and volume expansion, ---------------------------------------------------------------------------------------------------------------- Hyperaldosteronism, Barrter syndrome, Gitelman syndrome and excessive, black liquorice ingestion. - Not treated by normal saline. . Hyperemesis gravidarum causes volume depletion --> metabolic alkalosis with respiratory compensation. . RESPIRATORY ACIDOSIS: ________________________ . Increased blood paCO2 > 40 mmHg (1ry). . Increased blood HCO3 (Compensatory). . Decreased minute ventilation. (Minute ventilation = Respiratory rate Tidal volume. . Caused by alveolar hypoventilation as: - Chest disease: COPD, Obstructive sleep apnea, silicosis, obesity. - Neuromuscular disease: Myasthenia gravis, lambert-eaton, polymeilitis, G. barre.$ - CNS disease: Stroke, infection, brain stem lesion. - Drug induced: anesthesia, Narcotics and sedatives. . RESPIRATORY ALKALOSIS: ________________________ . Decreased blood PaCO2 < 40 mm Hg. . Decreased blood HCO3 (compensatory). . Increased minute ventilation (washing co2). . Caused by alveolar hyperventilation due to: pneumonia, high altitude, anemia, anxiety, pain, . Fever, pulmonary embolism, pleural effusion, atelectasis & Salicylate intoxication. . MIXED ACID-BASE DISORDERS (Metabolic acidosis and respiratory alkalosis) _________________________________________________________________________ . It may cause inappropriately normal laboratory values. . Calculate the expected change in PaCO2 & HCO3 and compare it with the patient measured values in the case, . To determine if a mixed disorder exists or a normal physiologic compensation has occurred, . PaCO2s in metabolic acidosis is calculated by winter's formula: PaCO2 = 1.5 (HCO3) + 8. . Salicylates intoxications --> + Respiratory center --> Tachypnea and respiratory alkalosis, . Also causes anion gap metabolic acidosis due to increased production and decreased renal elimination of organic acids as lactic and ketoacids.

. ADRENAL INSUFFICIENCY (Addison's disease): _______________________________________ . Non specific manifestations: Anorexia, fatigue, GIT complains, weight loss and hypotension. . The most common electrolyte abnormality is HYPONATREMIA. . Also HYPERKALEMIA is common; due to decreased activation of aldosterone receptors (with mild hyperchloremic acidosis). . DIURETIC ABUSE: _______________ . Causes increased excretion of water and electrolytes by the kidney. . Dehydration, weight loss, orthostatic hypotension. . Hypokalemia and hyponatremia due to increased urinary excretion of Na & K --> increased urine Na & K. . Eating disorders may cause the patient abuse diuretics. . CAUSES OF ORTHOSTATIC HYPOTENSION: ----------------------------------. Decreased intravascular volume: Decreased fluid intake, polyuria and diarrhea. . Decreased vascular tone: autonomic neuropathy or medications as (antihypertensive and antipsychotics). . DIABETES INSIPIDUS: _______________________ . Causes euvolemic hypernatremia. . present with severe polyuria and mild hypernatremia. . Based on urine osmolality DI is of 2 types: ----------------------------------------------------------- Complete D.I: urine osmolality < 300 mosml/kg (Normally < 100 mosm/kg). - Incomplete D.I: urine osmolality 300-400 mosm/kg. . Based on etiology D.I is of 2 types: ------------------------------------------------- Central D.I: decreased ADH release due to: CNS; trauma, hge, infection or tumor. - Nephrogenic D.I: due resistance to ADH: common causes; hypercalcemia, severe hypokalemia, tubulointerstial renal disease, - medications as: Lithium(ttt of bipolar disorder), demeclocycline, foscarnet, amphotricine and cidofovir. . N.B:- Divalporic acid is used in bipolar disorder but doesn't cause D.I. - Dehydration --> HYPOVOLEMIC hypernatremia + increased urine osmolality. . PSYCHOGENIC POLYDIPSIAL: __________________________ . Excessive free water intake --> hyponatremia. . Patient with psychiatric illness. . Like D.I euvolemic polyuria but psychogenic polydipsia (hyponatremia), whereas D.I (hyppernatremia).

. HYPONATREMIA: _______________ . Serum sodium < 130 mEq/L. . Causes According to:
============================================================================================= - Serum osmolarity - Extracellular volume - Urine findings - Causes of hyponatremia =============================================================================================== 1) Normal ------. hyperproteinemia. . hyperlipidemia. =============================================================================================== 2) High - hyperglycemia. - Exogenous solutes (mannitol & radiocontrast). =============================================================================================== - Non renal salt loss: . Dehydration. - U Na < 10 . Vomiting. - HYPOVOLEMIC mEq/L . Diarrhea. ================================================================================================ - Renal salt loss: . Diuretics. . ACEIs. . Mineralocorticoids deficiency. ================================================================================================ 3) Low (< 280 m0sm/kg) - U Na > 20 mEq/L Uosm < 300 - psychogenic polydipsia. - Beer potomania. - U Na > 20 mEq/L (> 295 m0sm/kg) --------

- EUVOLEMIC ================================================================================================ - UNa >20 mEq/L - SIADH Uosm > 300 ================================================================================================ - CHF. - HYPERVOLEMIC -------- Hepatic failure. - Nephrotic syndrome. =============================================================================================

... Hypovolemic hyponatremia is usually due to volume depletion -> decreased effective arterial volume to the kidney --> -> Increase Aldosterone, Renin and ADH. . SIADH: ________ . Euvolemic hyponatremia. . Decreased serum osmolarity & increased urine osmolarity. . Increased urine sodium concentration. . Failure to correct with normal saline infusion.

. DIAGNOSTIC CRITERIA OF SIADH: ------------------------------1- S.osm. < 270. 2- U.osm > S.osm. 3- U.Na > 20 mEq/L. 4- No hypovolemia. 5- Normal renal, adrenal & thyroid function. 6- No other known causes of hyponatremia. 7- No obvious stimulus (surgical, traumatic or painful) known to activate ADH release. . RENAL TUBULAR ACIDOSIS TYPE 4 (RTA TYPE 4): _________________________________________ . Caused by Aldosterone deficiency or renal insensitivity to aldosterone. . Lack of aldosterone effect --> failure to secrete acids as NH4 and retention of potassium. . Causes NON ANION GAP METABOLIC ACIDOSIS (i.e normal anion gap). . Hyperkalemia and renal insufficiency. . Occur in diabetic nephropathy and worsened by drugs that inhibit Renin-aldosterone system as: ACEIs & ARBs. .N.B: - Serum anion gap = S. Na - ( S. CL + S. HCO3)... Normally (6-12) anion gap if > 12. - Urine anion gap = U. Na - U. CL. . Both DIARRHEA & RTA are associated with (normal anion gap metabolic acidosis). . Both are differentiated by Urine anion gap (UAG). . Acid excreted by the kidney is buffered by NH4CL, so the more acid excreted; the more chloride found in urine. . In RTA --> decreased acid secretion --> decreased Chloride in urine --> positive UAG. . In Diarrhea --> intact kidney ability to excrete acids & diarrhea is associated with acidosis --> increased renal acid excretion -> increased urine chloride --> Negative UAG. . CHRONIC RENAL FAILURE --> decreased acid (NH4) secretion & accumulation of organic anions --> hypochloremic (anion gap) metabolic acidosis. . Furosemide --> volume depletion --> contraction metabolic alkalosis (increased serum HCO3). . ADDISON DISEASE: __________________ . Caused by T.B., hemorrhage.... . Decreased; cortisone, adrenal sex hormones and aldosterone secretion. . Normally; aldosterone acts on renal distal tubules to reabsorb Na in exchange with K & H ions. . Aldosterone deficiency --> loss of Na (hyponatremia) and retaining of K & H ( hyperkalemic metabolic acidosis). . i.e. Normal anion gap hyperkalemic, Hyponatremic metabolic acidosis. . DRUGS CAUSING HYPERKALEMIA: _____________________________ . Non selective beta blockers -> interfere with beta2 mediated intracellular K uptake --> increase extracellular K. . ACEIs, ARBs & K sparing diuretics --> inhibition of aldosterone or the ENaC channel (epithelial Na channel in the collecting tubules). . Cyclosporine --> blocks aldosterone activity. . Heparin --> blocks aldosterone activity. . Digitalis --> inhibit Na-ATPase pump. . NSAIDs --> decrease renal perfusion --> decrease K delivered to collecting ducts. . Succinylcholine --> causes extracellular leakage of K through acetylcholine receptors. . Trimethoprim --> block ENaC channel (Like K sparing diuretics). . Also trimethoprim causes competitive inhibition of renal tubular creatinine secretion --> artificial rise in serum creatinine without change in GFR.

. In case of hyperkalemic patient with multiple drug therapy the best next step after control hyperkalemia . by K binding resin as (sodium polystyeren sulfonate) is review all his current medications (As one of these drugs maybe the cause of hyperkalemia). . POSTICTAL ANION GAP METABOLIC ACIDOSIS: ____________________________________ . Due to lactic acidosis from ++ production of lactic acid by the muscles & reduced hepatic uptake of lactate. . Usually transient & resolve 60-90 minutes after seizures. . So, the best management in this patient is observation for 2 hours then repeat lab. examination. . if not resolved after 2 hours --> look for other potential causes of metabolic acidosis.

.N.B.: IN ANY PATIENT with acid base imbalance: the PH & PaCO2 are the 2 lab.values that provide the best picture about acid-base status, as the bicarbonate can be calculated from these 2 values using the henderson-hasselbalch equation. CORRECTION OF HYPONATREMIA: ___________________________ 1- Asymptomatic or mildly symptomatic hyponatremia --> Normal saline. 2- Severe symptomatic hyponatremia --> rapid ++ in serum Na concentration by hypertonic saline (3% saline). - Acute symptomatic hypernatremia is a medical emergency require rapid increase in serum Na concentration. - Chronic hyponatremia require slow correction of serum Na concentration because the brain cells had adjusted to the hyponatremic state, So, rapid ++ in serum Na can cause osmotic central pontine demyelination syndrome, so correction is done. by very slowly increase in serum Na (not more than 0.5 mEq/L/h. SALYSIALATE TOXICITY: ____________________ . Suspected in patient with triad of: fever, tinnitus and tachypnea (after drug intoxication). . Causes mixed Respiratory alkalosis and anion gap metabolic acidosis. . Explanation: - Aspirin stimulates respiratory center causing tachypnea --> respiratory alkalosis (CO2 wash). - Aspirin causes anion gap metabolic acidosis by: . Uncoupling of Oxidative phosphorylation --> increasing O2 consumption by tissues & also hyperpyrexia. . -- enzymes involved in carbohydrate and lipid metabolism -> accum. of organic acids (pyruvate, lactate). . Impair renal function --> accumulation of organic acids. .N.B: - Normal acid-base status --> PH 7.39-7.41, PaCO2 35-40 and HCO3 24. - Respiratory acidosis without compensation --> PH < 7.39, primary decrease in PaCO2 and normal HCO3. - Respiratory acidosis with compensation --> PH < 7.39, primary -- in PaCO2 and compensatory ++ in HCO3. - Respiratory alkalosis with compensation --> PH > 7.41, primary -- in PaCO2 and compensatory -- in HCO3. - Respiratory alkalosis without compensation --> PH > 7.41, primary -- in PaCO2 and near normal HCO3 - Metabolic acidosis without compensation --> PH < 7.39, primary -- in HCO3 and near normal PaCO2. - Metabolic acidosis with compensation --> PH < 7.39, primary -- in HCO3 and compensatory -- in PaCO2. - Metabolic alkalosis with compensation --> PH > 7.41, primary ++ in HCO3 and compensatory ++ in PaCO2. - Metabolic alkalosis without compensation --> PH > 7.41, primary increase in HCO3 and near normal PaCO2. .. HCO3 primary change (metabolic) while PaCO2 primary change (Respiratory). .. Primary = the main change is in Paco2 or HCO3. .. Compensatory = slight change in the other item. .. If great change in both PaCO2 & HCO3 --> think of mixed acid-base imbalance (Fix the formula & calculate PaCO2 and compare it with that of the case).

. PREGNANCY causes --> normal physiological chronic compensated respiratory alkalosis -> due to high progesterone level --> stimulate respiratory center --> Tachypnea -> consequent chronic mild respiratory alkalosis with metabolic compensation. . It is common in late pregnancy due to increase of progesterone with the increase of gestational age. . FAMILIAL HPOCALCURIC HYPERCALCEMIA: ----------------------------------------------------------. Increased serum calcium and increased/inappropriately normal PTH level are suspecious for either: . PRIMARY HYPERPARATHYROIDISM -->normal or increased urinary calcium excretion. . FAMILAR HYPOCALCURIC HYPERCALCEMIA --> decreased urinary calcium excretion. . Ethylene glycol, Ethanol and Methanol: ------------------------------------------------------. All of them cause metabolic acidosis with an anion gap and an osmolar gap. . But Ethylene glycol --> calcium oxalate (rectangular, envelope shaped crystals) in urine. .N.B: how to calculate osmolar gap?? -------------------------------------------------- 1st calculate serum osmolarity = {2Na + Glu/18 + BUN/2.8}. - Then calculate osmolar gap = observed osmolarity (case) - calculated osmolarity.... (Normally < 10). . HYPOKALEMIC HYPOCHLOREMIC METABOLIC ALKALOSIS after vomiting: --------------------------------------------------------------------------------------------------. Mechanism: 2 phases; - Generation phase: Vomiting --> loss of gastric fluid containing HCL , NaCL and water. - the loss of H ions as HCL -> unbalanced retention of HCO3 (because of the loss of gastric acidity -> no stimulus for HCO3 release by the pancreas), - HCO3 is instead retained in the blood --> metabolic alkalosis. - Maintenance phase: Vomiting -> volume loss & -- ECV -> -- renal perfusion -> activation of renin-angiotensin-aldosterone system. - Aldosterone --> retain water and excrete H & K in urine --> hypokalemia and contraction metabolic alkalosis. . the 1st step in management is to restore the ECF Volume by iv normal saline & K. . this will decrease activation of renin-aldosterone system by restoring proper renal perfusion. . i.e. the step in management of volume contraction metabolic alkalosis --> normal saline and k. . DIABETIC KETOACIDOSIS (DKA): -------------------------------------------. Causes anion gap metabolic acidosis. . Common in type I DM ( blood gluc. > 250-600 mg/dl) less common in type II. . Polyuria, polydipsia, abdominal pain, nausea and vomiting mimic surgical abdomen. . PRIMARY POLYDIPSIA: -------------------------------. Problem of excessive water intake common in schizophrenic patients. . Normal functioning kidney --> excrete diluted urine (of low specific gravity < 1.003) i.e. low osmolarity. . Dx: withholding water intake --> increased urine osmolarity & specific gravity --> confirm diagnosis. . Administration of phenothiazine to schizophrenia -> ++ thirst sensation -> worse 1ry polydipsia & hyponatremia.

N.B.: - Nephrogenic diabetes insipidus (DI) due to lithium (ADH resistance) -> loss water -> hypernatremia & maximally diluted. - Central DI --> loss water --> hypernatremia & maximally diluted. - To distinguish between central and nephrogenic DI --> exogenous ADH --> if corrected = central DI, if not corrected = Nephrogenic DI. - SIADH --> excessive free water retention --> hyponatremia & concentrated urine. - Carbamazepine intensifies kidney response to ADH --> free water retention & hyponatremia --> as SIADH. . ALCOHOLICs refractory hypokalemia: ---------------------------------------------------. Chronic alcoholics --> multiple electrolyte imbalance --> hypokalemia, hypomagnesemia, hyponatremia. . Mg is important cofactor for K uptake and maintenance of intracellular K level. . So refractory hypokalemia is due to hypomagnesemia, . So correction of hypomagnesemia is essential to correct hypokalemia. . BOWEL ISCHEMIA AND METABOLIC ACIDOSIS: ---------------------------------------------------------------. common in patients with astherosclerosis and peripheral vascular disease. . Acute abdomenal pain, nausea, vomiting, hypoactive bowel sounds and abdomenal tenderness. . Mechanism: bowel ischemia --> accumulation of lactic acid from anaerobic metabolism --> lactic acidosis --> metabolic acidosis with anion gap. . N.B.: DKA --> blood glucose > 250 - 600 mg/dl. . HYPERNATREMIA: -------------------------. The most common cause is hypovolemia. . Mild cases can be treated by 5% Dextrose in 0.45% saline. . Severe cases --> initially treated with IV normal saline 0.9% then switch to half normal saline 0.45%, . when the volume deficit has been restored in order to better replace the free fluid loss. . GASTRIC OUTLET OBSTRUCTION: --------------------------------------------. Due to prepyloric peptic ulcer --> scaring & fibrosis --> obstruction. . Causes severe vomiting --> volume contraction --> hypokalemic, hypocholeremic, metabolic alkalosis. . Emergent ttt is NAOGASTRIC suction to decompress the stomach, then hydration with NaCl & K replacement. . MANGEMENT OF HYPERKALEMIA: 3 steps ---------------------------------------------------------1- Membrane stabilization (normalize cells electrical activity) with calcium gluconate. 2- Drive K intracellular: Insulin/glucose administration is the most rapid way to decrease serum K level, also B2 agonist (Albuterol) shift K intracellular. 3- Remove K from the body: Sodium polysteren sulfonate (Kalyexalate) bind K in GIT, FUROSEMIDE loop diuretic leads to loss of K in urine, RENAL Dialysis is the most definitive way to remove K from the body in Renal failure. . Shifting K intracellularly is more rapid than removing it from the body. . Insulin/glucose is more rapid than any other method.

. HYPOCALCEMIA: -----------------------. May occur during or immediately following major surgery due to repeated blood transfusion. . Due to volume expansion and hypoalbuminemia, so usually asymptomatic because the ionized Ca is normal. . When ionized calcium is decreased (due to binding with citrate of repeated transfusion) --> symptoms appears. . Hyperactive tendon reflexes, muscle cramps and rarely convulsions. . N.B.: - hypomagnesemia mimic hypocalcemia because it -- PTH secretion and -- peripheral response to PTH. - Hypokalemia --> muscle weakness, cramps may be flaccid paralysis if severe hypokalemia. -> EKG shows U wave in severe hypokalemia. - Hyperkalemia --> muscle weakness, flaccid paralysis if severe hyperkalemia --> EKG changes, maybe a systole. - Hyponatremia --> a symptomatic, but if prolonged --> weakness, lethargy, delirium and seizures. - Hypermagnesemia --> if mild --> decreased deep tendon reflexes, if severe --> lost deep tendon reflexes, muscle paralysis & may cardiac arrest. . CARBON MONOXIDE POISONING: ----------------------------------------------. After exposure to fire (house ....). . CO --> decrease delivery of O2 to tissue by 2 mechanisms: - binds to hemoglobin 260 times than O2 --> displace o2 from Hb --> -- O2 carrying by the blood. - causes shift of the oxy-hemoglobin dissociation curve to the left --> -- unloading of O2 from Hb in the tissue. . this increase the anaerobic metabolism --> increase lactic acid production --> anion gap metabolic acidosis. . this type of lactic acidosis due to decrease O2 delivery to tissue is calle type A lactic acidosis. . It occurs in CO poisoning and circulatory failure. . LOOP DIURETICS: -----------------------. Frequently used in cirrhotic patients with volume overload and ascites. . Potential side effects are --> Hypokalemia, metabolic alkalosis, pre-renal renal failure . HYPERCALCEMIA: ------------------------. Manifested by nonspecific symptoms --> abd. pain, constipation, polyuria and neuropsychiatric illness. . TTT: 1st IV normal saline 0.9% --> ++ renal excretion of Ca by -- ca reabsorption at the proximal tubules. . Then LOOP diuretics --> inhibit Ca reabsorption at loop of Henle. . treatment of the cause of hypercalcemia. . SUCCINYLCHOLINE: --------------------------. Is a depolarizing neuromuscular blocker that can cause life threating hyperkalemia. . It should not be used in patient with or at high risk of hyperkalemia such as (burn, crush injury patient & patient with demyelinating syndromes. . Non depolarizing agents as vecuronium and rocuronium are better used.

CALCIUM LEVEL IN HYPOALBUMINEMIA: -----------------------------------------------------. Only 45% of circulating ca is free and physiologically active (ionized ca). . the remainder is bound to albumin with a ration 0.8 mg/dl Ca per 1 gm albumin. . thus every reduction in serum albumin 1 gm/dl leads to reduction in serum Ca by 0.8 mg/dl though the ionized Ca level doesn't changed. . For patient with abnormal serum albumin concentration (as liver disease) acorrect ca level is calculated by:

Corrected Ca = 0.8 (normal albumin - measured albumin) + measured ca.

. Normal albumin = 4 gm/dl. . CUCHING'S SYNDROME: ---------------------------------. Caused by excess corticosteroids intake as in BA or endogenous adrenal hyper-secretion of cortisone. . Manifested by: truncal obesity, weight gain, easy bruising, proximal muscle weakness, hypertension, . Hyperglycemia, acne, Osteopenia, osteoporosis, cataract. . HYPERNATREMIA AND HYPOKALEMIA (common). SEPTIC SHOCK: ------------------. History of sepsis with hypotension, fever, oliguria and acidosis. . due to hypotension & hypo perfusion --> anaerobic metabolism --> lactic acidosis. . IV normal saline 0.9 % is the 1st step in treatment metabolic acidosis of septic shock. . with or without vasopressor for hypotension & antibiotics for infection.

Dr. HISHAM ELKILANY. __________________