Acis-base, fluid, and electrolyte disorders- Pt. 1

normal serum Na

• sodium and water lost in roughly similar proportions

• Na concentration remains normal

• ex. proportional GI fluid losse

hypoNa

• na loss with relatively greater water retention

• Na becomes diluted

• ex> GI loss + ADH + hypotonic fluid intake

hyperNa

• eater loss exceeds Na loss

• Na becomes concentrated

• ex> sweating + inadequate water replacement

hypovolemic

• reduced extracellular volume

• orthostaissm tachym dry mucosa, decreased urien putput

• GI losses, diuretics, hemorrhage

• may have reduced renal perfusion

hypervolemic

• increased total extracellular volume

• edema, JVD, crackles, weight gain

• HF, cirrhosis, kidney failure

• effective arterial volume may still be reduced

when is ADH repleased

in response to:

• increased plasma osmolality

• decreased effective circulating volume

• nonosmotic stimuli such as nausea, pain, adn stress

effects of ADH

• increases water reabsorption

• more ADH→ more concentrated urine/lower urine volume and high blood volume

• less ADH→ more dilute urine/higher urine volue and low blood volume

serum osmolality

• tital concentration of dissolved partile sin blood

• classify hypoNA; eval osmolar disturbances

urine osmolality

• how concentrated or dilute the urine is

• assess renal water conservation/excretion

urine sodium

• urine sodium concentration- assess renal na conservation

• help assess renal Na handling and causes of hypoNa

urine potassium

• helps assess renal potassium loss

• help dist renal from extrarenal K loss

urine chloride

• renal chloride excretion

• particularily useful in eval metabolic alkosis

tonicity

• effect of solutes on water mvmt across cell membranes

hypotonic

• water moves into cells→ swelling

hypertonic

• water moves out of cells→ shrinking

hypoNa- assessment

• Na <135

• first step: determine if hypotonic

• low serum osmolality→ TRUE hypotinic hypoNa

• normal serum osmolality→ consider pseudohypoNa, severe hyperlipidemia, severe hyperproteinemia

• high serum osmolality→ another osmole is pulling water extracellularly, hyperglycemia sodium correction calc, mannitol

hypoNa dx- first step

• assess neuro sx adn clinical stability

  • seizures, marked impairment od consciousness, or severe neurologic deterioration attributable to hypoNa

  • initiate emergency tx with 3% hyperotnic saline while diagnostic eval proceeds

hypoNA dx- if clinically stable

• check serum osmolality adn glucose

• if hypotonic, check urine osmolality

  • is kidney acreting dilute urine, or is water excretion imapired

• interpret urien Na alongside volume status

• ID cause and choose tc

true hypoNa

• Urine osm ≤100; very dilute urine; ADH effect appropriately suppressed

  • primary polydipsia

  • low solute intake

• urien osm >100: urine not maximally dilute; ADH effect id present or watrer excretion is impaired

  • hypovolemia

  • SIADH

  • adrenal insuff

if ADH is active, assess volume- hypovol

• GI losses

• diuretics

• hemorrhage

• renal salt wasting

• primary adrenal insuff

if ADH active, assess volume- apparently euvolemic

• SIADH

• secondary adrenal insuff

• severe hypothyrpidism

if ADH is active, assess volume- hypervolemic

• HF

• cirrhosis

• advanced kidney dz

• nephrotic syndrome

urine sodium- ≤30

• kideny often conserving Na

• consider low effective circulating volume

• GI loseesm HF, cirrhosis

urine Na- >30

• kidney not strongly conserving sodium

• diuretics

• adrenal insuff

• renal salt wasting

• SIADH

• caution: diuretics, CKD, recent IV fluids, and certain other conditions affect interpretation

hypovolemic hypoNa- kidney conserving Na

• low urine Na

• think extrarenal loss

• vom

• diarrhea

• heme

hypovolemic hypoNa- kidney wasting Na

• high urine Na

• think renal loss

• diuretics

• adrenal insuff

• salt wasting renal dz

iatrogenic hypoNa

• thizides

• antidepressants- SSRIsSNRIs

• antiseizure meds

• desmopressin

• hypotonic IV flkuids/excess free water

• potop setting

acute hypoNa

• rapid decrease serum osmolality (within 48hrs) → water moves into brain cells→ cerebral edema

acute hypoNa sx

• HA

• n/v

• confusion

• lethargy

• seizures

• coma

  • severe = emergency

when to use 3% saline (NaCl) in severe hypoNa

• severe neuro sx= emergency

• seizures

• comba/obtundation

• severe encephalopathy

• sig neuro deterioration attributable to hyponaturemia

treating with 3% NaCl

• 100mL IV over 10 minutes, reassess

• initial goal= increase Na approx 4-6mEq/L

• do NOT attempt to normalize Na immediately

  • raising extracellular tonicity modestly draws water out of swollen brain cells, reducing cerebral edema

danger of correctign Na

• osmotic demyelination syndrome (ODS)

• concernign in chronic or unknown duration hypoNa

• risk increases with excessive correction

higher ridk pts of ODS

• very low initial Na

• hypoK

• etoh use disorder

• advanced liver dz

• prevention

conservative correction limit of hypoNa in high risk pts

• ≤8 in 24 hrs

hypovolemic hypoNa tx

• isotoninc crystalloid (0.9% saine)

• restores circulating volume and suppresses nonosmotic ADH

SIADH tx

• fluid restriction; address cause and offending meds

• reduces retained free water

hypervolemic hypoNa tx

• treat heart/liver/kidney dz; fludi restriction when appropriate; selected loop duiretics

• addresses excess water and underlying dz

hyperNa causes

• too little water relative to solute

• Na>145

• water losses: GI, skin, rena;

• inadequate intake/access: i,paired thirst, inability to obtain water

• renal losses: osmotic diuresis, diabetes insupidus

• less common

  • excess Na admin

low urine vol + concentrated urine

• appropriate renal water conservation; consider inadequate intake or extrarenal losses

high urine vol + inapprop dilute urine

• diabetes insipidus (AVP def or resistance)

high urine vol + substantial urinary osmoles

• osmotic diuresis (glucose, urea, mannitol)

why does HyperNa affect the brain

• increased. extracellular tonicity→ water moves out of brain cells

• brain cells shrink

• sx:

  • thirst, irritability

  • weakness, lethargy

  • confusion

  • seizures/coma in severe cases

• chronic adaptation can make sx less dramatic

• memory: hypertonic extracellular fluid pulls water OUT

step 1 of treating hyperNa- assess circulation

• shock or sig hypovol→ restore perfusion with isotonic crystalloid

step 2 of treating hyperNa- replace water deficit

• oral/enteral free water when feasible

• IV D5W when appropriate

• selected hypotonic crystalloid depending on volume/electrolyte needs

step 3 of treating hyperNa- treat the cause

• central diabetes insipidus→ desmopressin

• osmotic diuresis→ address glucose/solute losses

• inadequate water intake→ ensure reliable water access

step 4 of treating hyperNa- monitor

• serial Na, urine output, fluid balance

• individualize correction based on duration, severitym ongoing losses, adn clinical setting

results of K abnormalities

• skeletal muscle

• GI smooth muscle

• respiratory muscle

• cardiac conduction

mech of hyperK- cells

• redistribution: K shifts out of intact cells

• insulin def

• certain types of acidosis

• cell destruction: K released from damaged cells

• rhabdomyolysis

• tumor lysis syndrome

mech of hyperK- kidneys

• reduced renal K excretion

• AKI/CKD

• hypoaldosteronism

mech of hyperK- meds

• ACEi/ARBd

• spirinolactone/epleronone

• amiloride

• NSAIDs

• trimethorim

• K supp

hyperK on ECG

• peaked Twaves→ PR prolongation/P wave flattenign→ QRS widening→ SINE wave → VF/asystole

• severity does not correlate with serum K

hyperK emergency

• ECG changes

• sig weakness/paralysis

• rapidly raising K

• severe elevation/impaired elimination

hyperK emergency- tx priorities/approach

• stabilize: protect cardiac membrane

• shift: temp move K into cells

• eliminate: remove excess K from body

hyperK tx- stabilize: protect the heart

• IV calcium gluconate

• IV calcium chloride

• rapidly stabilizes cardiac conduction

• does nOT lower serum K

• repeat according to ECG repsonse and clinical protocol

hyperK tx- shift K

• temp lower serum K

• regular insulin IV + dextrose: drives. into cells

  • monitor glucose after insulin

• nebulized albuterol: beta2 stimulation promotes cellular K uptake

• sodium bicarb: consider selectively in sig metabolic acidosis

hyperK tx- eliminate

• loop diuretics: furosemide when appropriate renal function and urine output are present