Module 4: Electrolytes & Fluids Flashcards by A Stoll

What are the aspects of water in the body?

60% of total body wt is water
Depends on: fat content (10-20% water), muscle (75% water), sex (males > muscle = >water), age dependent: infant - 80%; late teen/adult - 50-60%; elderly - 40-50% (45-55%)

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Where is the water found in the body?

2/3 of water is in cells (ICF) = 40% TBwt
1/3 extracellular (ECF) = 20% TBWt
- Interstitial fluid (3/4 = 15% TBWt)
- Blood plasma: (1/4 = ~5%TBWt)
  - 55% of blood plasma (mostly water also clotting factors, hormones, electrolytes), 45% cells (RBC, WBC, platelets)
- Transcellular (“third space” - often ignored)
Water in body generally represented in blood b/c moves freely between body compartments

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How does water move throughout various fluid compartments?

Microcirculation:
- Simple diffusion (small molecules & electrolytes down concentration gradient)
- Vesicular transport: larger molecules
- Osmosis: water - low to high concentration
Starling forces: hypothesis - water movement governed by colloid & hydrostatic pressure. Net: flow into interstitium returned by lymphatic drainage
- Hydrostatic pressure: BP - push water out (inc in HF)
- Oncotic pressure: osmolality (density of solute load) wants to keep fluid in (albumin & other proteins in plasma) (cirrhosis, nephrotic syndrome)
  (Leaky capillaries net move out)

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What tests are indicated for fluid/electrolyte disturbances?

Serum electrolytes (Na, K, Cl, bicarb, glucose)
BUN & Cr: kidney function & hydration status
Serum osmolality: assess concentration of solutes in the blood (275-295mOsm/kg - Na major contributor + BUN & glucose)
Urine electrolytes
Albumin & total protein: reflects oncotic pressure & potential fluid shifts (must correct albumin for Ca levels)

Ask self: intake, output, or distribution

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How does the body maintain homeostasis?

Solute/ion concentration remain relatively constant
- Cell membrane highly selective: minor alterations w/ action potentials
- Capillary membranes more permeable
Water freely permeable b/t compartments
- Allows for homeostasis b/t ICF & ECF
- Water content normally dependent on I&O
  - Highly regulated by kidneys
Primary EC
- cation: Na
- anion: Cl & HCO3-
Primary IC cation:
- Cation: K & some Mg
- Anion: PO4 & protein
Dec EC vol -> dec venous pressure -> dec venous return -> dec atrial pressure -> inhib ADH & dec CO -> dec arterial pressure -> INC Ang II (vasoconstrictor)
Inc Osmolarity -> inc ADH
Body will select maintaining volume over osmolality

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What are the aspects of fluid intake and output?

Intake: 2-3L
- Sensible: 1.5L & 0.5L in solid
- Insensible: 150-400mL from oxidation (3mL/kg)
Output (2300mL)
- Sensible: 1.5L in urine, 250mL in feces, 100mL in sweat
- Insensible: lungs =350mL, skin = 350mL
Insensible losses inc w/ fever, broken skin barrier, burns, hyperventilation, diarrhea,

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Common causes and expected lab findings for hypovolemia?

Causes/history: excessive fluid loss (vomiting, diarrhea, sweating), inadequate intake, third-spacing
- Thirst, dizziness (esp o. hypoTN), fatigue & weakness, wt loss, recent fluid loss, dec UO
Lab findings:
- Elevated BUN:Cr & Hct & serum Osmo, Na (if dehydrated), urine specific gravity (>1.020), serum lacttate
- BNP & CXR normal
- Echo: IVC small & collapses w/ inspiration
PE:
- Dry mucous membranes
- Dec skin turgor tachycardia
- Orthostatic hypotension
- Low BP & JVP, high HR, skin & mucosa cool, dry, poor turgot, cap refil delayed, peripheral edema absent, pulm: clear, Abd: normal

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Common causes and expected lab findings for hypervolemia?

Causes/hx: HF, kidney failure, excessive Na intake, inappropriate fluid admin
- Fatigue & weakness, SOB (orthopnea), edema, abd bloating/ascites, wt gain (UO - normal)
Lab findings:
- Dec BUN & hct
- Low serum osmolality
- Possible dilutional hyponatremia
- High BNP (<200pg/mL 95% sen, 63% specificity) NT-proBNP <200 (99% sen, spec 43%)
- Norm: Serum lactate
- CXR: pulm congestion, pleural effusion (88% sen, 90% spec)
- Echo: reduced cardiac function if HF present (79% sen, 82% spec)
  - Diffuse B lines pretty good sen (88%) not spec, + BNP 88% sen, 90% spec
PE: Edema, elevated jugular venous pressure, crackles, wt gain
- Inc BP, HR, JVP (>8cm - mod sens & good spec), warm skin + edema (bilateral leg edema 94% sen, low spec), crackles, rales (low sen, spec 90%), pleural effusion, ascites (Cap refill normal)

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What are the key concepts of sodium and water?

Assess Na & water Separately
- Na status: determines vol of ECF compartment
- Water status: determines Na
- Ask: Does my pt have a problem with Na, Water, or both
Body systems designed to keep
- EC Na in narrow range (135-145mEq/L)
- ECFV w/i reasonable limits

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Common causes and expected lab findings for hyponatremia?

Causes: excessive water intake, SIADH, HF, kidney dz, vomiting & diarrhea
Lab:
- Serum Na <135mEq/L,
- low serum osmolality
- Ur Na low (elevated in SIADH & diuretics)
S/S: Hypotension, tachycardia, dry mucous membrane, poor skin turgor

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Common causes and expected lab findings for hypernatremia?

Causes: water loss (DI, diarrhea, sweating) or excessive Na intake (not enough water intake - dementia)
Lab:
- SNa >145mEq/L
- inc S Osmolality
- Ur Osmolality >800 mOsm/kg (<300mOsm/kg in DI)
  (Isotonic (volume concern) then sift to D5W/Half Saline) - rapid correction dangerous b/c -> cerebral edema)

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What regulates Na amouints?

Juxtaglomerular receptors triggered by rec renal perfusion activates RAAS retains Na
Volume: atria/great veins triggered by small variation in atrial/venous filling. Inc atrial filling releases atrial natriuretic factor promotes renal Na excretion
Pressure: aorta/carotid sinus, dec in vol -> activate sympathetic nervous system, cause renal retention of Na
Key: as ECFV inc/dec, pathways activated to counteract

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What is an approach to the evaluation of hyponatremia?

Hx, PE, assessment ECF vol determine hyponatremia classification
- R/O hyperglycemia & other cause nonhypotonic hyponatremia to confirm hypotonic hyponatremia
Hypovolemia: measure UrNa concentration
- > 30mEq/L - kidney loss (Diuretics, glucosuria in uncontrolled diabetes)
- <30mEq/L - non-kidney losses (Diarrhea, hemorrhage)
Euvolemia: measure Ur Na, specific gravity, & osmolality
- > 30mEq/L, >1.003, >100mOsm/kg: SAIDH, glucocorticoid deficiency, severe hypothyroidism (SCLC puts of exogenous ADH)
- <30mEq/L, <1.003, <100mOsm/kg: excessive water intake, low solute intake,
Hypervolemia: Measure Ur Na concentration
- > 30mEq/L: AKI or CKD
- <30mEq/L: HF, Cirrhosis, Nephrotic syndrome
  (Diuretics & Fluid)

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What are more key concepts for Na and water?

Abnormal ECF vol: problem w/ Na control mechanisms
Abnormal ECF Na concentration: problem with water control mechanisms
Hypovolemia: loss of Na & water
Hypervolemia: due to Na & water retention
Hyponatremia: inc water cannot be excreted
Hypernatremia: loss of water that has not been replaced

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What are the aspects of potassium metabolism?

Mostly inside cell
Essential for function of excitable tissues (neuron, muscles)
Internal K balance:
- Into cell: insulin, epi, alkalosis,
- Out of cell: exercise, cell lysis, hyperosmolality, acidosis
External K balance
- Injection = excreted
- DCT & Collecting duct: ALD promotes K secretion

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Common causes and expected lab findings for hypokalemia?

Causes: diuretic use, vomiting, diarrhea, inadequate intake, renal tubular acidosis, hypomagnesemia, hyperALD, insulin & albuterol use, refeeding syndrome
Lab findings: Serum K <3.5mEq/L, ECG changes (flattened T), & Ur K <20mEq/L
(H+-K- ATPase pump in kidney work to correct alkalosis w/ excretion K & H+ -> hypokalemia)

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Common causes and expected lab findings for hyperkalemia?

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Causes: renal failure, K-sparing diuretics, tissue breakdown (rhabdo, tumor lysis syndrome, hemolysis), potassium supplements, hypoALD, metabolic acidosis
Lab findings:
- Serum K >5mEq/L
- ECG: peaked T, flat P, PRi prolongation, QRS widening -> possible cardiac arrest
- Ur K: >20mEq/L
  (Tx: IV Ca gluconate stabilize cardiac membrane, Insulin & B=-agonist K back into intracellular compartment)
Pseudohyperkalemia due to hemolysis in the blood draw tube

What are the aspects of Calcium metabolism?

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Thyroid glad releases calcitonin stim Ca deposit, dec Ca uptake from intestines & kidneys
PTH: stim Ca release from bone & inc uptake from intestines & kidneys
- Kidney activated vit D to inc Ca uptake in intestines

Common causes and expected lab findings for hypocalemia?

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Causes: hypoparathyroidism, vit D deficiency , renal failure
Lab: low S Ca <8.4mg/dL, prolonged QT, low ionized Ca
Clinical earl: must correct for low albumin levels. Use correction calculator or ionized Ca level (ABG)
- Measured total Ca (mg/dL) + 0.8 (4.0-serum albumin (g/dL))
Alkalosis lowers ionized Ca

Common causes and expected lab findings for hypercalcemia?

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Causes: hyperparathyroidism, malignancy (bone break down, or PTH-like hormones) excessive vit D intake
Lab findings:
- S Ca >10.5mg/dL, shortened QT & elongated PRi, & elevated ionizing Ca
Bones, Stones, Groans, and Moans
- Neurologic changes (lethargy, fatigue, memory loss, psychosis, depression), anorexia & nausea, constipation, kidneys stones, bone pain
  (Tx: Isotonic fluids, bisphosphonates, parathyroidectomy)
  Ca think QT
Acidosis raises ionized Ca

How is phosphate metabolized?

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Food (~20mg/kg/d)-> intestines -> feces (6mg/kg/d)
Formed into bones any left over release in urine through kidney
- PTH promotes renal tubular excretion

Common causes and expected lab findings for hypophosphatemia?

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Causes: refeeding syndrome (insulin drives phosphate into cells), hyperparathyroidism, chronic alcoholism
Lab findings: S phosphate <2/5mg/dL, muscle weakness, hemolysis
Clinical pearl: PTH aka “phosphate trashing hormone”

Common causes and expected lab findings for hyperphosphatemia?

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Causes: renal failure, excessive phosphate intake or hypoparathyroidism
Lab: serum phosphate >4/5mg/dL, calcifications, & pruritus

How is magnesium metabolized?

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Intake -> intestinal absorption -> fecal secretion
Resorption form skeleton (Mag storage ~60%)
Intracellular Mg ~40%
Renal reabsorption

Common causes and expected lab findings for hypomagnesemia?

- Causes: alcoholism (excess excretion d/t alcohol-induced tubular dysfunction + dietary deficiency, acute pancreatitis, diarrhea) malabsorption, diuretics - Symptoms: lethargy, anorexia, tetany of seizures, NV, inc DTR - Labs: S Mg <1.7 mg/dL, muscle cramps & ECG (Prolonged QT) (often cause hypokalemia d/t opening channels that dump it into the urine)

Common causes and expected lab findings for hypermagnesemia?

- Causes: renal failure, excessive Mg intake (antacids/laxatives) (UNCOMMON) - Lab: Serum Mg >2/6mg/dL, bradycardia, & resp depression - Exam: **diminished/absent DTR**

How do the kidneys regulate acid-base balance?

- Kidneys are slow - Retain Bicarb makes the blood alkaline - Release bicarb makes the blood acidic - HCO3- secreted into tubules then reabsorbed 1) H+ into lumen of tubule by exchange w/ Na 2) H+ combines w/ HCO3- forms H2CO3 disassociated to H2O + CO2 3) CO2 into cell then disassociated to HCO3- 4) HCO3- into blood by Na-HCO3- simporter (but Cl-HCO3- transporter in TAL, DCT) - Kidney also produces additional HCO3-

How do the lungs regulate acid-base

- Lungs are fast - Blow off CO2: blood becomes alkaline - Retain CO2: blood becomes acidic - Acidosis/alkalosis stimulates receptors: peripheral (Carotid & aorta), central: medulla oblongata (CSF) - Stimulates respiration rate to increase or decrease

What is acidosis vs alkalosis by pH level?

- Acidosis: <7.35 - Alkalosis: >7.45

What is the anion gap? & explain its meaning

Anion Gap = [Na+] - ([Cl-]+[HCO3-])

What is the delta gap and what does it mean?

- Delta ratio = (AG -12) / (24 - bicarb) - Way to figure out if there is a mixed acid-base disorder - Delta Ratio <1: combined metabolic acidosis & non-anion gap metabolic acidosis (HAGMA + NAGMA ie diarrhea + lactic acidosis or in renal failure) - Delta Ratio 1-2: pure high anion gap metabolic acidosis (Uncomplicated cases; lactic acidosis often; DKA) - Delta Ratio >2: combined high anion gap metabolic acidosis & metabolic alkalosis (vomiting + alcoholic ketoacidosis or COPD w/ lactic acidosis)

What are the common causes of increased anion gap metabolic acidosis?

"CAT-MUDPILERS" - Cyanide & CO poisoning - Arsenic - Toluene - Methanol, Metformin - Uremia - DKA/alcoholic KA - Paraldehyde, Propylene glycol, - Isonazid/infxn/inhalants, Iron, INH - **Lactic acidosis (MC)** - Ethylene glycol, ethanol - Rhabdo/Renal failure - Salicylates, solvents, starvation

What are the common causes of normal anion gap acidosis?

"HARDUPS" - Hyperalimentation (IV feeding - excessice cloride, NaCl admin, Ca Cl, TPN). Hypoaldosteronism (addison's disease), - Acetazolamide (CAI), - **Renal tubular acidosis** - **Diarrhea** - Uretero-Pelvic shunt (utereoenterostomy) - Post-hypocapnia/ pancratic enterostomies - Spironolactone/Small bowel fistula

What are the common causes of metabolic alkalosis?

- "CLEVER PD": - Contraction, - Licorice, - Endo (Conn's, Cushing's), primary hyperparathyrodiism (M. alk -> hypoCa -> primary hyperparathyroidism for correction, primary hyperparathyroidism leads to NAGMA) - **Vomiting (loose H+)/**NG tube suctioning - Excess Alki - Refeeding Alkalosis, (addition of HCO3 - hyperalimentation therapy) - Post-hypercapnia, - Diuretics (Loop & Thiazide) - Disproportionate loss of CL (Cl diarrhea) - Chloride & K depletion secondary to excessive corticoseroids - ABCDE-HS: antacids, baking soda, certain laxatives/CF, dehydration, diuretics, electrolyte imbalances/emesis-recurrent (or prolonged NG decompression), hyperaldosteronism/hypochloremia, steroids - Little acid or too much bicarb

What are the common causes of respiratory acidosis?

- Hypoventilation: "CHAMPP" - **CNS depression** (severe brainstem injury, opioids, benzo ETOH, ketamine, Ecstasy (gamma-hydroxybutyrate) or other depressants) - Hemo/pneumothorax - Airway obstruction - Myopathy - Pneumonia - Pulmonary edema (**COPD, asthma, pulmonary fibrosis, PE, severe pneumonia)

What are the common causes of respiratory alkalosis?

- Hyperventilation: "CHAMPS" - CNS dz - **Hypoxia** - **Anxiety (MC)**- Mech ventilators - Progesterone - **Salicylate** (effects medullary center -> hyperventilation)/Sepsis (G-) Intrathoracic disorders (PE, pneumonia, asthma, pulmonary edema) Liver insufficiency, pregnancy (shallower breaths)

How is an adjusted anion gap calculated? Why?

(**Hypo**albuminemia): AAG = AG + (2.5 x (normal albumin (4.0) - measured albumin)) "Why adjust for **hypo**albuminemia - Albumin = neg changed protein (anion) in plasma, contributing ~10-15mEq/L to un measured anions at normal levels (3.5-5.0g/dL) - In conditions like (**Liver dz, nephrotic syndrome, or severe inflammation where albumin levels drop**) failing to adjust for **hypo**albuminemia might **underrepresent the severity** of metabolic acidosis - If albumin levels drop p(**hypo**albuminemia), fluid may shift out of blood vessels into tissues (causing edema)

What are the acid-base steps?

1) Check pH (tells primary direction) 2) Respiratory vs metabolic (look at PaCO2, look at HCO3-) 3) Assess compensation - Respiratory primary: uncompensated, partially, fully - Acidosis primary: appropriate, resp alk, resp acid 4) If metabolic acidosis: calculate anion gap & check albumin 5) if High anion gap, calculate delta ratio

What are the aspects of compensation of respiratory acidosis?

- Compensation - Expected compensation: kidneys retain HCO3- & dec H+ offset pH dec (hrs-days) - Fully compensated: pH return to normal despite abnormal PaCO2 & HCO3- - Uncompensated: body hasn't started fixing problem: HCO3- still normal - Partially Compensated: pH remains abnormal (<7.35), but HCO3- adjusts toward compensation. (above normal)

What are the aspects of compensation of metabolic acidosis?

- Actual PaCO2 lower than range: concurrent respiratory alkalosis (Salicylate toxicity) - Actual PaCO2 higher than this rage suggests concurrent respiratory acidosis

Module 4: Electrolytes & Fluids Flashcards

(40 cards)