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

(> 295 m0sm/kg) ----- ---- - hyperglycemia.- Exogenous solutes (mannitol & radiocontrast).

===============================================================================================

- Non renal salt loss: . Dehydration.

- U Na < 10 . Vomiting. - HYPOVOLEMIC mEq/L . Diarrhea.

================================================================================================ - U Na > 20 - Renal salt loss: mEq/L . Diuretics.

. ACEIs. . Mineralocorticoids deficiency.

================================================================================================3) Low

(< 280 m0sm/kg) - U Na > 20 - psychogenic polydipsia. mEq/L - Beer potomania.

Uosm < 300- EUVOLEMIC

================================================================================================- UNa >20 mEq/L - SIADHUosm > 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. . ALCOHOLIC’s 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.__________________