Objectives. Objectives

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1 Diagnosis & Management of Electrolyte & Acid Base Disturbances In the Acute Care Sophia Chu Rodgers, FNP, ACNP, FAANP, FCCM University of New Mexico Sandoval Regional Medical Center Albuquerque, New Mexico Objectives List the principles of electrolyte disturbances, functions of electrolytes & osmolality Outline the emergent management of hypo-, hypernatremia, hypo- hyperkalemia Objectives Recognize the manifestations and explain the treatment for syndrome of inappropriate antiduretic hormone (SIADH), and diabetes insipidous (DI) Differentiate between metabolic and respiratory acidosis and alkalosis 1

2 80-year-old woman with hypertension and heart failure Confusion, lethargy, poor oral intake, and weakness for 3 days BP 108/70 mm Hg, HR 110 beats/min, respiration 18 breaths/min Nonsustained ventricular tachycardia on monitor What electrolyte disorders might contribute to her presentation? What risk factors does this patient have for electrolyte disturbances? Principles of Electrolyte Disturbances Implies an underlying disease process Treat the electrolyte change, but seek the cause Clinical manifestations are not specific to a particular electrolyte change & may be due to multiple abnormalities Principles of Electrolyte Disturbances Urgency of treatment are determined by clinical manifestations, not lab values Speed & magnitude of correction dependent on clinical circumstances Frequent reassessment of electrolytes Monitored by EKG 2

3 Functions of Electrolytes Regulate water distribution Govern acid base balance Transmit nerve impulse Contribute to energy generation Assist in blood clotting Activate muscle cells Major Intracellular & Extracellular Electrolytes PO4 - Mg + Ca + PO4 - Cl - Ca + K + Mg + Na + Cl - Na + K + Osmolality Defined as number of osmoles per liter of solution Useful as a measure of water balance 3

4 Osmolality 1 T Salt in 1 L water Normal 2 T Salt in 1 L water Hyper- Osmolality 1 T Salt in 2 L water Hypo- Osmolality Calculate Osmolality Serum osmolality (mosm/l) = 2(Na) + ( glucose ) + ( BUN ) Example: 2(140) + (4.9) + (6.4) = 291 Normal Calculated 290 mosm/kg H 2 O Normal Measured mosm/kg H 2 O Hypo-Osmolality < 275 mosm/kg H 2 O Hyper-Osmolality >300 mosm/kg H 2 O Sodium Main ECF cation Governs normal ECF osmolality Maintains acid base balance Activates nerve & muscle cells Influences water distribution with chloride Normal meq/l 4

5 Diagnosis of Hyponatremia Laboratory Serum sodium < 135 meq/l Physical Examination Symptoms depend on how quickly sodium level dropped Headaches, nausea, abdominal cramps, muscle twitching, tremors, weakness Changes in mental status shortened attention span to lethargy or confusion If < 110 meq/l can develop stupor, coma, seizures Diagnosis of Hyponatremia Assess patient volume status Hypovolemia Euvolemia Hypervolemia Fluid status fairly = Poor skin turgor Dry, cracked mucous membranes UOP Weak, rapid pulse Hypotension Orthostatic hypotension CVP &/or PAWP Edema Distended neck veins Hypertension Weight gain Rapid bounding pulse CVP &/or PAWP Hyponatremia Measure plasma osmolality (P OSM ) >295 mosm *Hyperglycemia *Mannitol *Glycerol <280 mosm mosm Assess Volume Status *Hyperlipidemia *Hyperproteinemia >10g/dl Hypovolemic NA Euvolemic (no change) TBW (more) Hypervolemic NA + (more) TBW NA + TBW(more) *Hemorrhage *Vomiting *Diarrhea *Third spacing *Diuretics * Mineral- Corticoid *Osmotic diuresis (glucose, mannitol) *Proximal RTA *Sodium losing nephritis *SIADH Uosm > Posm *Adrenal Insufficiency (Glucocorticioid deficiency) *Drugs *SSRI, Haloperidol, Morphine, *Elavil, nicotine, MAOI *Hypothyroidism *CHF *Nephrotic Syndrome *Cirrhosis *Acute renal *Chronic renal failure 5

6 Syndrome of Inappropriate Antidiuretic Hormone Pathophysiology Release of ADH (arginine vasopressin or AVP) is not inhibited by a reduction in plasma osmolality Primarily a condition that results in abnormal water retention & not a problem with solute (sodium) loss Consequently, this leads to dilutional hyponatremia Does not cause ECF volume expansion, edema, or hypertension Regulation of Sodium and water Na Level (water excess) Serum osmolality < 280 mosm/kg Thirst diminishes, leading to water intake ADH release is suppressed Renal water Excretion Serum Osmolality Normalizes 6

7 Syndrome of Inappropriate Antidiuretic Hormone Diagnosis Laboratory: Euvolemic hyponatremia <134 meq/l Posm <275 mosm/kg Urine osmolality >100 mosm/kg of water Urine sodium >40 meq/l with normal dietary salt intake Syndrome of Inappropriate Antidiuretic Hormone Diagnosis Other findings: Clinical euvolemia without edema or ascites Low blood nitrogen urea (BUN) Normal serum creatinine Low uric acid Normal acid base Normal adrenal, thyroid function Syndrome of Inappropriate Antidiuretic Hormone Etiology Meningitis Head injury Subarachnoid hemorrhage Cancer Lung (especially small cell lung as well as other small cell malignancies of other organs) Infections Brain abscess Pneumonia Lung abscess 7

8 Syndrome of Inappropriate Antidiuretic Hormone Etiology Drugs Phenothiazine Carbamazepine Chlorpropamide SSRI (fluoxetine, sertraline, paroxetine) Methylenedioxymethamphetamine (MDMA -Ectasy) Oxytocin Vincristine Morphine Amitriptyline Syndrome of Inappropriate Antidiuretic Hormone Etiology Guillain Barre Sarcoidosis Hypothyroidism Adrenal Insufficiency Syndrome of Inappropriate Antidiuretic Hormone Treatment Treatment the underlying cause Long term fluid restriction of 1.2 to 1.8 liter/day Severe (severe confusion, convulsion, coma): use hypertonic saline 3% 1-2 ml/kg IV in 3-4 hours 8

9 Syndrome of Inappropriate Antidiuretic Hormone Treatment Demeclocycline (Declomycin) can be used in chronic situations when fluid restrictions are difficult to maintain Potent inhibitor of ADH Has a 2-3 day delay in onset Extensive side effects Syndrome of Inappropriate Antidiuretic Hormone Treatment Urea Shown favorable long term results with protective effects in myelinosis & brain damage Contraindicated in liver cirrhosis Syndrome of Inappropriate Antidiuretic Hormone Treatment Conivaptan (Vaprisol) In the setting of hypothyroidism, adrenal insufficiency, pulmonary disorders Tolvaptan (Samsca) Raises the serum sodium in patients with euvolemic or hypervolemic hyponatremia Given in hospitalized patients 9

10 Syndrome of Inappropriate Antidiuretic Hormone Caution Too rapid rise in sodium can cause osmotic demyelination syndrome Avoid correction by >12 meq/l/day in a 24 h and / or 18 meq/l in 48 h. Target 8 meq/l esp. in liver or renal disease, severe hypokalemia, or malnutrition Adrogue HJ, Madias, NE: Hyponatrermia. NEJM 342: , 2000 Mohmand, HK, Issa D, Ahmed Z et al. Hypertonic saline for hyponatremia: the inadvertent Overcorrection. Clin J Am Soc Nephrol 2: , Treatment of Hyponatremia Treat the underlying cause Hypovolemic hyponatremia Loss of sodium & TBW but sodium loss is greater Give normal saline Hypervolemic hyponatremia Accumulation of sodium & TBW but water is greater free water loss with diuretics Treatment of Hyponatremia Euvolemic hyponatremia Increase in TBW & sodium is unchanged Restrict free water free water loss with diuretic Infuse normal saline cautiously 10

11 Treatment of Hyponatremia Correct slowly to prevent osmotic demyelination syndrome Speed of correction depends on severity of symptoms Which solution should we use Sodium Chloride 0.9% 154 meq/l 0.45% 77 meq/l 3% 513 meq/l Lactated Ringer Sodium 130 meq/l Potassium 4 meq/l Calcium 3 meq/l Chloride 109 meq/l Lactate 28 meq/l Treatment of Hyponatremia (Desired change in Na) X total body water x kg [TBW= 0.6 for men; 0.5 for women] -For example: Na from 106 to 112 meq/l in 70 kg male (112mEq/L-106mEq/L) x (0.6L x 70 kg)=252 meq 1.5 liter of 0.9% normal saline or- Give 0.5 liter of 3% normal saline 11

12 Mr. Quintana is an 86 y.o. resident of a nursing home. He was transported to the ED with signs of restlessness, agitation, confusion, weakness, flushed skin, dried mucous membrane and skin turgor. His family reports that he had stopped eating and drinking several days ago. Which electrolyte disturbance would most likely be seen? A. Hypokalemia B. Hyperkalemia C. Hypernatremia D. Hyponatremia Mr. Quintana is an 86 y.o. resident of a nursing home. He was transported to the ED with signs of restlessness, agitation, confusion, weakness, flushed skin, dried mucous membrane and skin turgor. His family reports that he had stopped eating and drinking several days ago. Which electrolyte disturbance would most likely be seen? A. Hypokalemia B. Hyperkalemia C. Hypernatremia D. Hyponatremia Hypernatremia Definition: Indicates intracellular volume depletion with a loss of free water which exceeds sodium loss Serum sodium >145 meq/l 12

13 Etiology of Hypernatremia Salt Intake H 2 O Intake Salt tablets Altered thirst NaHCO 3 Impaired access Hypertonic saline H 2 O loss Diarrhea Vomiting Excessive sweating Diuresis Diabetes Insipidus Diabetes Insipidus (DI) Definition: Condition characterized by excessive thirst & excretion of large amounts of severely diluted urine Regulation of Sodium and water Na Level (water deficit) Serum osmolality > 300 mosm/kg Thirst increases, leading to water intake ADH release is increased Renal water Excretion Serum Osmolality Normalizes 13

14 Diabetes Insipidus (DI) Types: Central DI Caused by a deficiency of arginine vasopressin (AVP) or antidiuretic hormone (ADH) Head injury Infection Ischemia to the hypothalamus or pituitary gland Surgery Tumor Familial (autosomal dominant disease) Diabetes Insipidus (DI) Types: Nephrogenic Kidneys resistant to the effects of the ADH Certain drugs: Lithium, Amphotericin B, Demeclocycline Hypercalcemia Kidney disease (polycystic) Diabetes Insipidus (DI) Types: Psychogenic polydipsia Characterized by a primary increase in water intake Seen in anxious middle age women Psychiatric illness 14

15 Diabetes Insipidus (DI) Signs and Symptoms Excessive urination Abrupt in central DI Gradual in nephrogenic DI Extreme thirst (craving for cold or ice water or ice) Dehydration Electrolyte disturbance Nocturia (new onset) Diabetes Insipidus (DI) Diagnosis Plasma sodium & urine osmolality Type of DI Plasma sodium Urine osmolality Primary polydipsia < 137 meq/l < one half plasma osmolality DI > 142 meq/l < plasma osmolality Excludes DI Normal > 600 mosmol/kg Urine output measurement MRI Head Diabetes Insipidus (DI) Diagnosis Water restriction test Do not give desmopressin (vasopressin) before the test Have patient stop drinking for 2 to 3 hours Measure urine volume & osmolality every hour Measure plasma sodium & osmolality every 2 hours 15

16 Diabetes Insipidus (DI) Diagnosis Water restriction test Continue test until one of the following end points is reached: Urine osmolality reaches a normal value (>600 mosmol/kg) Urine osmolality is stable on two or three successive hourly measurements despite a rising plasma osmolality Plasma osmolality exceeds 295 to 300 mosmol/kg or the plasma sodium is 145 meq/l or higher Diabetes Insipidus (DI) Diagnosis: Give Desmopressin 10 mcg nasal or 4 mcg subcut. or IV in the last 2 settings Monitor urine volume & osmolality every 30 min over next 2 hours Diabetes Insipidus (DI) Interpretation: Central DI (complete)- Desmopressin will lead to a rise in urine osmolality & significant drop in UOP Central DI (partial) Rise of urine osmolality by 15-50% 16

17 Diabetes Insipidus (DI) Interpretation: Nephrogenic DI (complete) no elevation in urine osmolality Nephrogenic DI (partial) up to 45% increase in urine osmolality Primary polydipsia rise in urine osmolality (>500 mosmol/kg) & no response to ADH Diabetes Insipidus (DI) Treatment: Treat the underlying cause Central DI Desmopressin Intranasal 5-40 mcg/day or divided q8-12h Oral, initial 0.05 mg q12h; effective range mg divided q8-12h, observe fluid restriction IV/SC 2-4 mcg/day divided q 12h Diabetes Insipidus (DI) Treatment: Nephrogenic DI Desmopressin will be ineffective Hydrochlorathiazide. Can be used with amiloride to prevent hypokalemia Stop offending drugs especially lithium 17

18 Clinical Manifestations Skin flushed Agitation, restlessness Low grade fever Thirst Hypernatremia Hypernatremia Treatment Treat the underlying cause Diabetes Insipidus, use Vasopressin, stop hypertonic saline Treat water deficit (0.6 x wt [kg]) x ( obs Na+ - 1) 0.6 x 70 x x.17 = 7.19 L 24 =.299 x 1000 = 299ml / h =150ml/h over 24 h Hypernatremia Treatment Solution D5W Hypotonic 0.45% normal saline Enteral and IV fluid 18

19 Mr. Sanchez is a 57 y.o. male admitted to the hospital with 5 day history of abdominal pain, severe diarrhea, nausea and vomiting. Which electrolyte disturbance would he most likely have? A. Hypernatremia B. Hyponatremia C. Hypokalemia D. Hyperkalemia Mr. Sanchez is a 57 y.o. male admitted to the hospital with 5 day history of abdominal pain, severe diarrhea, nausea and vomiting. Which electrolyte disturbance would he most likely have? A. Hypernatremia B. Hyponatremia C. Hypokalemia D. Hyperkalemia Potassium Major cation in the ICF Functions Maintain cells electrical neutrality & osmolality Aid neuromuscular transmission of nerve impulses Assist skeletal & cardiac muscle contraction & electrical conductivity Affect acid base balance in relationship to the hydrogen ion 19

20 Potassium s role in acid-base balance Normal Acidosis Hyperkalemia Alkalosis Hypokalemia Hypokalemia Diagnosis Serum level is <3.5 meq/l (normal 3.5 to 5 meq/l) Elevated ph and bicarbonate level Slightly elevated serum glucose level Characteristic ECG changes Widened QRS ST T wave flatten U wave Hypokalemia Etiology GI losses, i.e., suction, lavage, prolonged vomiting, diarrhea, fistulas, Diuresis, magnesium depletion, Cushings, renal tubular acidosis Drugs: diuretics, corticosteroids, insulin, cisplatin, certain antibiotics, epinephrine, albuterol Diseases: hepatic, hyperaldosteronism, acute alcoholism, CHF, malabsorption syndrome, nephritis 20

21 S&S of Hypokalemia S&S of Hypokalemia Skeletal muscle weakness U wave ECG change Constipation, ileus Toxicity of digoxin (from hypokalemia) Irregular, weak pulse Orthostatic hypotension Numbness (paresthesia) Treatment of Hypokalemia Correct underlying cause Discontinue offending drugs Correct hypomagnesemia, alkalosis & other electrolyte disturbances 21

22 Treatment of Hypokalemia Hypokalemia (K<3.5 meq/l) K 2.5 meq/l (<3 meq/l if on digoxin) K<3.5 but >2.5 meq/l and no symptoms Life-threatening symptoms Non-life threatening or no symptoms Enteral replacement KCl meq every 4-6 h IV KCL meq/h via central catheter Enteral replacement KCl meq every 2-4 h and/or IV KCL 10 meq/h 53 y.o. male with history of renal failure, admitted with dizziness and syncope. This is his 12 lead ECG: What electrolyte disorder might contribute to this ECG? Hyperkalemia Serum level > 5 meq/l Etiology Renal dysfunction Acidemia Hypoaldosteronism Drugs, ie., potassium sparing diuretics, ACEI, succinycholine Cell Death Rhabdomyolysis Tumor lysis Burns Hemolysis Excessive Intake 22

23 Clinical Manifestations of Hyperkalemia Musculoskeletal Muscle weakness Paralysis Parasthesis Hypoactive reflexes Treatment of Hyperkalemia If significant ECG abnormalities are present, administer calcium chloride, 5 to 10 ml of a 10% solution. 23

24 Treatment of Hyperkalemia Redistribution of Potassium Administer 10 units of regular insulin with 50g of 50% dextrose over 5 to 10 minutes NaHCO 3 1 meq/kg over 5 to 10 minutes Inhaled B 2 agonist in high doses (Albuterol 10 to 20 mg) Treatment of Hyperkalemia Removal from body Increase urine output with a loop diuretic Increase GI loss with sodium polystrene sulfonate 25 to 50 g in sorbitol, enterally or by enema Initiate Dialysis Jennifer is a 23 y.o. type 1 diabetic admitted with a blood sugar of 720, ketonuria, and basic metabolic panel as follow: sodium 126, potassium 5.4, Cl 92, CO 2 9. Blood gases was drawn and result: ph 7.2 PCO 2 20 PaO 2 98 What type of acid base disturbance does she have? A. Respiratory Alkalosis B. Metabolic Alkalosis C. Respiratory Acidosis D. Metabolic Acidosis 24

25 Jennifer is a 23 y.o. type 1 diabetic admitted with a blood sugar of 720, ketonuria, and basic metabolic panel as follow: sodium 126, potassium 5.4, Cl 92, CO 2 9. Blood gases was drawn and result: ph 7.2 PCO 2 20 PaO 2 98 What type of acid base disturbance does she have? A. Respiratory Alkalosis B. Metabolic Alkalosis C. Respiratory Acidosis D. Metabolic Acidosis Acid-Base Acid-Base 25

26 Acid-Base 3 Regulators of Acid Base Method 1- Buffers Bicarbonate, phosphate, protein Act by binding with acids and bases to neutralize Method 2 Respiratory System Chemoreceptors in the medulla of the brain sense ph changes and vary the rate and depth of breathing to compensate Responds to ph changes within minutes Method 3 Kidneys Maintain ph by reasorb or excrete acids and bases into the urine Can take hours to days Arterial Blood Gas (ABG) Overview ph is a measure of hydrogen ion concentration PCO 2 measures partial pressure of carbon dioxide & indicates effectiveness of ventilation PCO 2 levels move in the opposite direction as ph HCO 3 represents the metabolic component, and moves in the same direction as ph 26

27 Steps in interpreting ABG Step 1:check the ph ( ) <7.35 acidosis >7.45 alkalosis Steps in interpreting ABG Step 2: What is the PCO 2 (35-45 mm Hg) <35 mm Hg) alkalosis >45 mm Hg) acidosis Steps in interpreting ABG Step 3: Look at the bicarbonate (22-26 meq/l) <22 meq/l acidosis >26 meq/l alkalosis 27

28 Steps in interpreting ABG Step 4 Match the PCO 2 or HCO 3 with the ph ph is acidotic, PCO 2 is acidotic, the disturbance is caused by the respiratory system respiratory acidosis ph is alkalotic, HCO 3 is alkalotic, the disturbance is caused the metabolic (renal) system metabolic alkalosis Steps in interpreting ABG Step 5 Does the PCO 2 or HCO 3 go in the opposite direction of the ph? If so, there is compensation by that system ph acidotic PCO 2 acidotic HCO 3 alkalotic, compensation by the metabolic (renal) system ph 7.27 acidosis PCO 2 27 mmhg alkalosis HCO 3 10 meq/l acidosis (respiratory) (metabolic) Primary: metabolic acidosis Compensation: yes, from respiratory 28

29 Steps in interpreting ABG ph 7.3 acidosis PCO 2 58 mmhg (respiratory) acidosis HCO 3 26 meq/l (metabolic) normal Primary: respiratory acidosis Compensation: no Steps in interpreting ABG ph 7.22 acidosis PCO 2 22 mmhg (respiratory) alkalosis HCO 3 10 meq/l (metabolic) acidosis Primary: metabolic acidosis Compensation: yes Steps in interpreting ABG ph 7.58 alkalosis PCO 2 40 mmhg (respiratory) normal HCO 3 38 meq/l (metabolic) alkalosis Primary: metabolic alkalosis Compensation: no 29

30 Steps in interpreting ABG ph 7.38 normal PCO 2 54 mmhg (respiratory) acidosis HCO 3 32 meq/l (metabolic) alkalosis Primary: respiratory acidosis or metabolic alkalosis Compensation: yes Steps in interpreting ABG ph 7.26 acidosis PCO 2 48 mmhg (respiratory) acidosis HCO 3 18 meq/l (metabolic) acidosis Primary: respiratory & metabolic acidosis Compensation: no Winter s Formula To calculate for metabolic acidosis compensation Expected PCO 2 = 1.5 x HCO /- 2 ph 7.24 acidosis PCO 2 24 mmhg alkalosis (respiratory) HCO 3 10 meq/l acidosis (metabolic) 1.5 x =23 +/- 2 (21-25) 30

31 Steps in interpreting ABG Step 6: What s the PaO 2 & SaO 2? Give information regarding the oxygenation status High >100 mm Hg Low < 80 mm Hg SaO 2 95% Gas in car to groomers $4.50 Cat car carrier $32.99 Grooming Fee $ Getting the look of one pissed off cat 31

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