Electrolyte Electrolyte DisturbancesDisturbances

Hypercalcemia, Hyponatremia, Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia Hypernatremia, Hyperkalemia

HypercalcemiaHypercalcemia

EtiologyEtiology

Hypercalcemia results when the Hypercalcemia results when the entry of calcium into the circulation entry of calcium into the circulation exceeds the excretion of calcium into exceeds the excretion of calcium into the urine or deposition in bone. the urine or deposition in bone.

Sources of calcium are most Sources of calcium are most commonly the bone or the commonly the bone or the gastrointestinal tract gastrointestinal tract

EtiologyEtiology

Hypercalcemia is a relatively common Hypercalcemia is a relatively common clinical problem. clinical problem.

Elevation in the physiologically Elevation in the physiologically important ionized (or free) calcium important ionized (or free) calcium concentration. concentration.

However, However, 40 to 45 percent of the 40 to 45 percent of the calcium in serum is bound to calcium in serum is bound to proteinprotein, principally albumin; , , principally albumin; , increased protein binding causes increased protein binding causes elevation in the serum total calcium. elevation in the serum total calcium.

Increased Increased bonebone resorption resorption

Primary and secondary Primary and secondary hyperparathyroidism hyperparathyroidism

Malignancy Malignancy Hyperthyroidism Hyperthyroidism Other - Paget's disease, estrogens or Other - Paget's disease, estrogens or

antiestrogens in metastatic breast antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic cancer, hypervitaminosis A, retinoic acid acid

Increased Increased intestinalintestinal calcium calcium absorptionabsorption

Increased calcium intake Increased calcium intake Renal failure (often with vitamin D Renal failure (often with vitamin D

supplementation) supplementation) Milk-alkali syndrome Milk-alkali syndrome Hypervitaminosis D Hypervitaminosis D Enhanced intake of vitamin D or Enhanced intake of vitamin D or

metabolites metabolites Chronic granulomatous diseases (eg, Chronic granulomatous diseases (eg,

sarcoidosis) sarcoidosis) Malignant lymphoma Malignant lymphoma Acromegaly Acromegaly

EtiologyEtiology

Hyperalbuminemia Hyperalbuminemia 1) severe dehydration 1) severe dehydration

2) multiple myeloma who have a 2) multiple myeloma who have a calcium-binding paraprotein. calcium-binding paraprotein.

This phenomenon is called This phenomenon is called pseudohypercalcemia (or factitious pseudohypercalcemia (or factitious hypercalcemia)hypercalcemia)

Other causesOther causes

Chronic lithium intake Chronic lithium intake Thiazide diuretics Thiazide diuretics Pheochromocytoma Pheochromocytoma Adrenal insufficiency Adrenal insufficiency Rhabdomyolysis and acute renal failure Rhabdomyolysis and acute renal failure Theophylline toxicity Theophylline toxicity Familial hypocalciuric hypercalcemia Familial hypocalciuric hypercalcemia Immobilization Immobilization Total parenteral nutritionTotal parenteral nutrition

Primary Primary hyperparathyroidismhyperparathyroidism

Activation of osteoclasts leading to Activation of osteoclasts leading to increased bone resorption in primary increased bone resorption in primary hyperparathyroidism (also cancer).hyperparathyroidism (also cancer).

Adenoma (80%)Adenoma (80%) Hyperplasia (15-20%)Hyperplasia (15-20%) Carcinoma (<1%)Carcinoma (<1%)

Secondary Secondary hyperparathyroidismhyperparathyroidism

Due to increased PTH in response to Due to increased PTH in response to decreased calciumdecreased calcium

ESRDESRD

Tertiary Tertiary hyperparathyroidismhyperparathyroidism

An autonomous nodule develops An autonomous nodule develops after longstanding secondary after longstanding secondary hyperparathyroidism hyperparathyroidism

Familial hypocalciuric Familial hypocalciuric hypercalcemia (FHH)hypercalcemia (FHH)

Mutation in the Ca-sensing receptor Mutation in the Ca-sensing receptor in parathyroid and kidney which in parathyroid and kidney which increases the Ca set pointincreases the Ca set point

May also increase the PTH May also increase the PTH ( parathyroid isn’t sensing Calcium)( parathyroid isn’t sensing Calcium)

MalignancyMalignancy

PTHrP- PTH related peptide PTHrP- PTH related peptide (squamous cell lung cancer, renal, (squamous cell lung cancer, renal, breast, bladder)breast, bladder)

Cytokines (TNF, INTERLEUKIN-1)Cytokines (TNF, INTERLEUKIN-1) OAF: Local osteolysis (breast cancer, OAF: Local osteolysis (breast cancer,

multiple myeloma)multiple myeloma) Tumoral effect (Hogkins / NHL)Tumoral effect (Hogkins / NHL)

Vitamin D ExcessVitamin D Excess

Granulomas (sarcoid, TB, histo)Granulomas (sarcoid, TB, histo) Vitamin D IntoxicationVitamin D Intoxication

Increased bone turnoverIncreased bone turnover

HyperthyroidismHyperthyroidism ImmobilizationImmobilization Paget’s diseasePaget’s disease Vitamin AVitamin A

MiscellaneousMiscellaneous

Thiazides (increase resorption in Thiazides (increase resorption in kidney)kidney)

Ca-based antacids (Milk-Alkali Ca-based antacids (Milk-Alkali Syndrome)Syndrome)

Adrenal insufficiencyAdrenal insufficiency

Clinical ManifestationsClinical Manifestations

BonesBones

stonesstones

abdominal groansabdominal groans

psychic moanspsychic moans

BonesBones

OsteopeniaOsteopenia Osteitis fibrosa cystica (seen in Osteitis fibrosa cystica (seen in

severe hyperparathyroidism only)severe hyperparathyroidism only)

Osteitis Fibrosa Cystica

Cysts, fibrous nodules, salt and pepper appearance on X-ray

StonesStones

NephrolithiasisNephrolithiasis NephrocalcinosisNephrocalcinosis Nephrogenic Diabetes InsipidusNephrogenic Diabetes Insipidus

Abdominal GroansAbdominal Groans

AnorexiaAnorexia NauseaNausea VomitingVomiting ConstipationConstipation PancreatitisPancreatitis Peptic ulcer diseasePeptic ulcer disease

Psychic MoansPsychic Moans

FatigueFatigue

DepressionDepression

ConfusionConfusion

LabsLabs

Free Calcium Measured or Free Calcium Measured or Calculated( Measured Ca+(0.8x(4.0-Calculated( Measured Ca+(0.8x(4.0-

alb) or use med-math?alb) or use med-math? PTH (irma assay)PTH (irma assay) PTH rpPTH rp VIT D , VIT AVIT D , VIT A PO4PO4 URINE CALCIUM- 24 HRSURINE CALCIUM- 24 HRS

TreatmentTreatment

Normal Saline (4-6L per day)Normal Saline (4-6L per day)

FILL THE TANKFILL THE TANK Furosemide-CALCIURESIS Furosemide-CALCIURESIS

Start after patient is intravascularly repletedStart after patient is intravascularly repleted Bisphosphonates- Inhibits osteoclast Bisphosphonates- Inhibits osteoclast

activity(reducing bone resorption and activity(reducing bone resorption and turnover) malignancy and ?Immobilizationturnover) malignancy and ?Immobilization

28 hrs half-life( zolendronate, pamidronate)28 hrs half-life( zolendronate, pamidronate)

TreatmentTreatment

SQ/IM( not nasal spray)Calcitonin 4 SQ/IM( not nasal spray)Calcitonin 4 u/kg q12 hrsu/kg q12 hrs

increase to 8 units q 12 hrsincrease to 8 units q 12 hrs

Onset 6-8 hours,duration 2-3 daysOnset 6-8 hours,duration 2-3 days

Steroids( targets OAF, 5-A Steroids( targets OAF, 5-A Hydroxylase)Hydroxylase)

Onset 24-48 hrs daysOnset 24-48 hrs days

Primary Hyperparathyroid

Surgery (JCEM 2009)Age <50 yrs, GFR <60ml/min, Cal 1

mg/dl above normal, DEXA <-2.5

MedicalBisphonates,Calcitonin,estrogen,sermEarly DEXA scans

Hypercalcemia QuizHypercalcemia Quiz

PTH IncreasedPTH Increased Cal IncreasedCal Increased PO4 decreasedPO4 decreased

What do I have?What do I have?

quizquiz

PTH DECREASEDPTH DECREASED CAL INCREASEDCAL INCREASED PO4 DECREASED/ INCREASED- PO4 DECREASED/ INCREASED-

EITHEREITHER

WHAT IS IT?WHAT IS IT?

QUIZQUIZ

PTH DECREASEDPTH DECREASED CAL INCREASEDCAL INCREASED PO4 INCREASEDPO4 INCREASED

WHAT IS IT?WHAT IS IT?

QUIZQUIZ

PTH NORMALPTH NORMAL CAL INCREASEDCAL INCREASED PO4 DECREASEDPO4 DECREASED

QUIZQUIZ

PTH INCREASEDPTH INCREASED CAL DECREASEDCAL DECREASED PO4 INCREASEDPO4 INCREASED

QUIZQUIZ

PTH INCREASEDPTH INCREASED CAL DECREASEDCAL DECREASED PO4 DECREASEDPO4 DECREASED

HyponatremiaHyponatremia

Santosh Reddy MDSantosh Reddy MD

DEFINITIONDEFINITION

Defined as Serum Sodium less than Defined as Serum Sodium less than 136 meq/lt136 meq/lt

4 % of hospitalized patients4 % of hospitalized patients

NEJM 2000:342:1581-NEJM 2000:342:1581-9( Adrogue,Madias)9( Adrogue,Madias)

HyponatremiaHyponatremia

Disorders of sodium are generally Disorders of sodium are generally due to changes in total body water, due to changes in total body water, not sodiumnot sodium

Hyper- or Hypo- osmolality Hyper- or Hypo- osmolality watershifts watershifts

changes in brain cell volumechanges in brain cell volume changes in mental status, seizureschanges in mental status, seizures

Hyponatremia: Hyponatremia: pathophysiologypathophysiology

Excess water compared to sodium, Excess water compared to sodium, almost always due to almost always due to increased increased ADHADH

The increased ADH may be:The increased ADH may be: Appropriate (e.g. hypovolemia or Appropriate (e.g. hypovolemia or

hypervolemia with too little effective hypervolemia with too little effective arterial volume)EAV.arterial volume)EAV.

Inappropriate (e.g. SIADH)Inappropriate (e.g. SIADH)

WorkupWorkup

Measure Measure plasma osmolality plasma osmolality to to determine if hypo, hyper, or isotonic determine if hypo, hyper, or isotonic hyponatremiahyponatremia

Urine OsmolalityUrine Osmolality Serum NASerum NA Urine NAUrine NA

Hypertonic HyponatremiaHypertonic Hyponatremia

Excess of another effective osmoles, Excess of another effective osmoles, such as mannitol, glucosesuch as mannitol, glucose

Each 100mg/dL of glucose above 100 Each 100mg/dL of glucose above 100 causes a decrease in Na by 1.8 causes a decrease in Na by 1.8 mEq/LmEq/L

Isotonic HyponatremiaIsotonic Hyponatremia

Lab artifact from Lab artifact from hyperlipidemia hyperlipidemia

or hyperproteinemiaor hyperproteinemia

Hypotonic HyponatremiaHypotonic Hyponatremia

Most common scenarioMost common scenario True excess of water compared to NaTrue excess of water compared to Na

Hypotonic HyponatremiaHypotonic Hyponatremia

hypovolemichypovolemic euvolemiceuvolemichypervolemichypervolemic

UNa>20 UNa<10

FeNa>1% FeNa<1%

Pt’s clinical history

Uosm>100 Uosm<100 Uosm var.

UNa<10 UNa>20FeNa<1% FeNa>1%

SIADH,

adrenal insuff,

hypothyroidism

Primary polydipsia,

low solute

Reset osmostat

Renal losses

Extrarenal losses

CHF, cirrhosis, nephrosis

Renal failure

Hypovolemic Hypotonic Hypovolemic Hypotonic HyponatremiaHyponatremia

Renal losses: Thiazides or other Renal losses: Thiazides or other diuretics, salt-wasting nephropathy, diuretics, salt-wasting nephropathy, adrenal insufficiencyadrenal insufficiency

Extra-renal losses: GI losses Extra-renal losses: GI losses (diarrhea), third-spacing (pancreatitis), (diarrhea), third-spacing (pancreatitis), inadequate intake, insensible lossesinadequate intake, insensible losses

Euvolemic Hypotonic Euvolemic Hypotonic HyponatremiaHyponatremia

SIADHSIADH

pulmonarypulmonary-pneumonia, asthma, COPD, PTX, -pneumonia, asthma, COPD, PTX, +pressure ventilation, small cell lung cancer+pressure ventilation, small cell lung cancerintracranialintracranial-trauma, stroke, hemorrhage, -trauma, stroke, hemorrhage, tumors, infection, hydrocephalustumors, infection, hydrocephalusdrugs-drugs-antipsychotics, antidepressants, thaizidesantipsychotics, antidepressants, thaizidesmisc-misc-pain, nausea, post-op statepain, nausea, post-op state

EndocrinopathiesEndocrinopathies (adrenal insuff, (adrenal insuff, hypothyroidism)hypothyroidism)

Reset osmostat ( exercise, seizures)Reset osmostat ( exercise, seizures)

Low soluteLow solute

““tea & toast”, “beer potomania” – tea & toast”, “beer potomania” – increased free water intake with increased free water intake with greatly decreased solute loadgreatly decreased solute load

Maximum rate of water excretion on Maximum rate of water excretion on a normal diet is 10-12 L per day – a normal diet is 10-12 L per day – more than this you overwhelm the more than this you overwhelm the excretory capacity of the kidneyexcretory capacity of the kidney

Hypervolemic Hypotonic Hypervolemic Hypotonic HyponatremiaHyponatremia

CHF: CHF: low effective arterial volume (EAV) low effective arterial volume (EAV) ADH ADH

Cirrhosis: Cirrhosis: ascites causes low EAVascites causes low EAV ADH ADH

Nephrotic syndrome: Nephrotic syndrome: hypoalbuminemia hypoalbuminemia causes low EAV causes low EAV ADH ADH

Advanced renal failureAdvanced renal failure

Methods to increase NaMethods to increase Na

Restrict free water range 800-1.2 lt Restrict free water range 800-1.2 lt per dayper day

Remove stimulus for ADH Remove stimulus for ADH (volume (volume replete, increase EAV, treat pulmonary replete, increase EAV, treat pulmonary pathology, etc)pathology, etc)

DemeclocyclineDemeclocycline (ADH antagonist) (ADH antagonist) 300MG BID TO QID300MG BID TO QID

Normal salineNormal saline after NA deficit is after NA deficit is calculatedcalculated

TreatmentTreatment

NA deficitNA deficit: HYPOTONIC EUVOLEMIA: HYPOTONIC EUVOLEMIA

TBW ( 60 % MEN : 50% WOMEN) x TBW ( 60 % MEN : 50% WOMEN) x

(DESIRED NA----MEASURED NA )(DESIRED NA----MEASURED NA ) Ex: 100 kg Man, MEASURED NA 120Ex: 100 kg Man, MEASURED NA 120

TBW 60 MEQ x 12( D--- M sodium)TBW 60 MEQ x 12( D--- M sodium)

720 MEQ PER 24 HOURS720 MEQ PER 24 HOURS

TreatmentTreatment

0.9 % : 154 meq/ LT0.9 % : 154 meq/ LT 3% : 514 meq / LT3% : 514 meq / LT

GIVE : 4. 6 LT OF 0.9 % NACLGIVE : 4. 6 LT OF 0.9 % NACL

1.4 LT OF 3 % NACL1.4 LT OF 3 % NACL

Treatment of Euvolemic Treatment of Euvolemic HyponatremiaHyponatremia

Asymptomatic: Asymptomatic: correct at rate of correct at rate of < < 0.5 0.5 mEq/L/hrmEq/L/hr

Symptomatic:Symptomatic: initital initital rapid correction of Na rapid correction of Na (2 mEq/L/hr) until symptoms resolve(2 mEq/L/hr) until symptoms resolve

Rate of correction should NOT exceed 12mEq in a Rate of correction should NOT exceed 12mEq in a 24 hour period, or 18mEq in a 48 hour period to 24 hour period, or 18mEq in a 48 hour period to avoid avoid Central pontine myelinosis Central pontine myelinosis (CNS (CNS demyelination demyelination changes in mental status, changes in mental status, paralysis, pseudobulbar palsy)paralysis, pseudobulbar palsy)

NEPHROLOGY 1994;4:1522-30NEPHROLOGY 1994;4:1522-30

TreatmentTreatment

Conivaptan( vaprisol): Conivaptan( vaprisol): AquaresisAquaresis:blocks :blocks the activity of AVP ,free water the activity of AVP ,free water excretion,without losses of NA/Kexcretion,without losses of NA/K

EVEREST trial for CHFEVEREST trial for CHF

Tolvaptan( Salt 1 and 2 trials) V2 Tolvaptan( Salt 1 and 2 trials) V2 receptor antagonist( hypervolemic or receptor antagonist( hypervolemic or Euvolemic)Euvolemic)

HypernatremiaHypernatremia

Santosh ReddySantosh Reddy

DefinitionDefinition

Increase in the serum sodium Increase in the serum sodium concentration greater than 145 concentration greater than 145 meq /L meq /L

HypernatremiaHypernatremia

Usually loss of hypotonic fluid, can Usually loss of hypotonic fluid, can also be infusion of too much also be infusion of too much hypertonic fluidhypertonic fluid

Hypernatremia is a strong thirst Hypernatremia is a strong thirst stimulus, so usually only affects pts stimulus, so usually only affects pts w/o access to water (intubated, w/o access to water (intubated, altered mental status,insensible altered mental status,insensible losses nursing home patient)losses nursing home patient)

HypernatremiaHypernatremia

By definition, all pts are hypertonicBy definition, all pts are hypertonic Can be HypovolemicCan be Hypovolemic

HypervolemicHypervolemic

EuvolemicEuvolemic

Workup: HypernatremiaWorkup: Hypernatremia

Check volume status Check volume status (vitals, orthostatics, (vitals, orthostatics, JVP, skin turgor, mucous membranes, BUN, Cr)JVP, skin turgor, mucous membranes, BUN, Cr)

If hypovolemic, check UIf hypovolemic, check Uosmosm and U and UNaNa to to determine whether free water loss is determine whether free water loss is renal or extra-renalrenal or extra-renal

If euvolemic, check UIf euvolemic, check Uosm osm to evaluate to evaluate for complete or partial DIfor complete or partial DI

HypernatremiaHypernatremia

hypovolemichypovolemic euvolemiceuvolemichypervolemichypervolemic

UOsm300-600 UOsm>600

UNa>20 UNa<20

Uosm<300 Uosm 300-600 Uosm >600

Complete DI Partial DI, reset osmostat

Intracellular osmole

generation

Renal losses

Extrarenal losses

Exogenous hypertonic saline, Mineralocorticoid excess

Hypovolemic HypernatremiaHypovolemic Hypernatremia

Renal water losses: osmotic diuresis Renal water losses: osmotic diuresis from glucose/mannitolfrom glucose/mannitol

Extra-renal water losses: diarrhea, Extra-renal water losses: diarrhea, insensible (fever, exercise)insensible (fever, exercise)

Euvolemic HypernatremiaEuvolemic Hypernatremia

Diabetes Insipidus: central or Diabetes Insipidus: central or nephrogenicnephrogenic

Seizures, exercise: intracellular Seizures, exercise: intracellular osmole generation osmole generation water shifts water shifts transient increase in Natransient increase in Na

Reset osmostat( I,I,I)Reset osmostat( I,I,I)

Hypervolemic Hypervolemic hypernatremiahypernatremia

Hypertonic saline administrationHypertonic saline administration

Mineralocorticoid excess: causes Mineralocorticoid excess: causes ADH suppressionADH suppression

TreatmentTreatment

Replete free water deficitReplete free water deficit

Free water deficit = TBW x (Free water deficit = TBW x (SerumSerumNaNa--140140))

140140 D5 W replacementD5 W replacement Restore access to waterRestore access to water Correct volume status Correct volume status

TreatmentTreatment

Must replete free water deficit via IVF Must replete free water deficit via IVF or enteral feedsor enteral feeds

Correct at rate < 0.5 mEq/L/hr to Correct at rate < 0.5 mEq/L/hr to avoid cerebral edemaavoid cerebral edema

Must consume > 1L HMust consume > 1L H22O/dayO/day

TreatmentTreatment

For hypovolemia hypernatremia For hypovolemia hypernatremia – Correct with ¼ or ½ NSCorrect with ¼ or ½ NS

For Hypervolemic hypernatremiaFor Hypervolemic hypernatremia– Correct with DCorrect with D55W and a loop diureticW and a loop diuretic

TreatmentTreatment

DI: Central: desmopressin DI: Central: desmopressin

Nephrogenic : Salt restriction + Nephrogenic : Salt restriction + Thiazides Amiloride, Nsaids.Thiazides Amiloride, Nsaids.

V 1 A AND V2 receptor blockage V 1 A AND V2 receptor blockage trialstrials

HyperkalemiaHyperkalemia

HyperkalemiaHyperkalemia

Transcellular shiftsTranscellular shifts

Decreased excretion by kidneysDecreased excretion by kidneys

Normal GFR Normal GFR

a)Normal aldosterone (CHF,Cirrhosis)a)Normal aldosterone (CHF,Cirrhosis)

b)Hypoaldosterone(Diabetes etc)b)Hypoaldosterone(Diabetes etc)

Hyperkalemia: Transcellular Hyperkalemia: Transcellular shiftsshifts

Acidosis, Acidosis, Beta-blockersBeta-blockers insulin deficiencyinsulin deficiency dig intoxicationdig intoxication massive cellular necrosismassive cellular necrosis hyperkalemic periodic paralysishyperkalemic periodic paralysis

Hyperkalemia: decreased Hyperkalemia: decreased excretionexcretion

Decreased GFR (AKI)Decreased GFR (AKI)

Hypoaldosteronism with a normal Hypoaldosteronism with a normal GFR (due to low renin, low GFR (due to low renin, low aldosterone, or decreased response aldosterone, or decreased response to aldosterone)to aldosterone)

Hyperkalemia: symptomsHyperkalemia: symptoms

WeaknessWeakness ParesthesiasParesthesias PalpitationsPalpitations Peaked T waves on EKG Peaked T waves on EKG (look like they (look like they

might hurt to sit on)might hurt to sit on)

Other EKG findings: Other EKG findings: increased PR interval, increased PR interval, widened QRS, sine wave pattern, PEAwidened QRS, sine wave pattern, PEA

Peaked T wavesPeaked T waves

Sine wave

WorkupWorkup

Rule out pseudohyperkalemia (IVF + Rule out pseudohyperkalemia (IVF + KCl, hemolysis due to venipuncture, KCl, hemolysis due to venipuncture, increased plt or WBC)increased plt or WBC)

Rule out transcellular shiftRule out transcellular shift Assess GFRAssess GFR If normal GFR, calculate TTKGIf normal GFR, calculate TTKG

TTKG: TTKG: Trans-Tubular Potassium Trans-Tubular Potassium GradientGradient

(Urine(UrineKK/Plasma/PlasmaKK)/(Urine)/(UrineOsmOsm/Plasma/PlasmaOsmOsm)) TTKG tells you how well aldosterone TTKG tells you how well aldosterone

is workingis working TTKG<7 TTKG<7 decreased effective decreased effective

aldosterone functionaldosterone function TTKG>7 TTKG>7 normal aldosterone normal aldosterone

functionfunction

TreatmentTreatment Calcium Gluconate/Calcium Chloride: Calcium Gluconate/Calcium Chloride:

stabilizes cell membranesstabilizes cell membranes 1-2 amps I.V 1-2 amps I.V 1-3 mins onset lasts 20-30mins1-3 mins onset lasts 20-30mins Insulin:drives K into cells Insulin:drives K into cells regular Insulin 10 units IV with 1-2 regular Insulin 10 units IV with 1-2

amps of D50amps of D50 Beta-2 agonists: Beta-2 agonists: drives K into cells;drives K into cells;Albuterol 10-20mcg inh or IV 0.5mg Albuterol 10-20mcg inh or IV 0.5mg Onset 30-60 minsOnset 30-60 mins

Treatment

Bicarbonate: Bicarbonate: drives K into cells in exchange for Hdrives K into cells in exchange for H

1-3 amps 1-3 amps

Onset 15-30 mins last 60 minsOnset 15-30 mins last 60 mins

Kayexalate: Kayexalate: exchanges Na for K in gutexchanges Na for K in gut

30-90 mg PO/PR 30-90 mg PO/PR

Onset 1-2 hrsOnset 1-2 hrs

Diuretics;decreases total body K; IV Diuretics;decreases total body K; IV lasixlasix

hemodialysis: hemodialysis: decreases total body K decreases total body K