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Electrolyte Values Laboratory test Normal Value Description

Na+ 136-145 mEq/L

Serum Osmolality 275-290 mOsm/kg Concentration of solutes (sodium) in ECF
Ca++ 8.6-10.2 mg/dL

K+ 3.5-5.0 mEq/L
Urine Osmolality 200-800 mOsm/kg Indicator of urine concentration. (Urea,
creatinine, uric acid)
Mg++ 1.3-2.1 mEq/L

Cl- 97-107 mEq/L Urine Specific Gravity 1.010-1.025 Measures kidney’s ability to conserve or
excrete H20
HPO4- 3.0-4.5 mEq/dL *inc. glucose/protein in urine can give a
falsely elevated specific gravity.
HCO3- 24-31 mEq/L BUN 10-20 mg/dL Inc: dec renal func, GI bleeding,
(3.6 to 7.2 mol.L) dehydration, inc. protein intake, fever,
sepsis
ABG Values Dec: liver dse, low protein diet,
starvation, expanded fluid vol.
(< Acidosis) (>Alkalosis)
pH 7.35 to 7.45 Creatinine 0.7-1.4 mg/dL Increases when renal function decreases
Higher H+ conc. Lower H+ conc. (62-124 mmol/L)
(<alkalosis) (>acidosis)
PaCO2 35 to 45 mmHg Hematocrit 42%-52% men Inc: dehydration, polycythemia
35%-47% women Dec: over hydration, anemia
(< Acidosis) (>Alkalosis)
HCO3 22 to 26 mEq/L Urine Sodium 75-200mEq/24hrs Inc Na+ intake, inc = inc. Na- excretion
Partially compensated: Uncompensated: (75-200 Dec in circulating fluid volume = Na+ is
• PaCO2 or HCO3 is out of normal • PaCO2 or HCO3 is normal mmol/24hrs) conserved
range • pH is not normal Urine output 1 ml/kg/hr for all age groups Dec U/O = dehydration, infection, or
• pH is not normal >30 cc per hr obstruction in urinary tract.
↑ pH ↓pH ↑ pH ↓pH
↓ PaCO2 ↑ PaCO2 ↑ HCO3- ↓HCO3-
Respiratory Respiratory Metabolic Metabolic
alkalosis acidosis alkalosis acidosis
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ISOTONIC SOL’N HYPOTONIC

Isotonic • Expands ECF
• Hypovolemic states
0.9% NaCl / NS • Resuscitative efforts
• Shock
Na+ 154 mEq/L • DKA
Cl- 154 mEq/L • Metabolic alkalosis
(Also available c dextrose 5% conc. • Hypercalcemia SOL’N
common) 308 mOsm/L • Mild Na+ deficit 0.45% NaCl (half strength saline) • Provides Na+, Cl, and free water
• Monitor for FVE & hyperchloremic acidosis • Aids in elimination of solute
in pts with: impaired renal func, HF, or edema. Na+ 77 mEq/L • Hypertonic dehydration
• Only solution to be given with Cl- 77 mEq/L • Na+ and Cl- depletion
blood products 154 mOsm/L • Gastric fluid loss
• Tonicity similar to plasma • Not indicated: 3rd spacing and inc. ICP
• Administer cautiously; may cause fluid
shifts from vascular system into cells,
resulting into CV collapse and inc. ICP
Lactated Ringer’s Solution • Contains multiple electrolytes in similar
conc. found in plasma HYPERTONIC SOL’N
• Hypovolemia
Na+ 130 mEq/L • Burns
K+ mEq/L • Fluid lost as bile or diarrhea 3% NaCl • Inc ECF
Ca++ 3 mEq/L • Acute blood loss replacement • Decrease cellular swelling
Cl- 109 mEq/L • Lactate metabolized as bicarbonate Na+ 513 mEq/L • Hyponatremia
• CI: lactic acidosis— lactate Cl- 513 mEq/L • Administer slowly and cautiously,
metabolism impaired 1,026 moSm/L • Monitor for intravascular volume
• pH >7.5 overload and pulmonary edema
• Kidney injury — risk for hyperkalemia 5% NaCl • Supplies no calories
Na+ 855 mEq/L
Cl- 855 mEq/L
1,710 moSm//L
5% Dextrose in Water (D5W) • Renal excretion of solutes
• Hypernatremia COLLOID SOL’N
• Fluid loss
No electrolytes • Caution during post op period (ADH sec
50g of dextrose inc DT stress reaction) Dextran in NS or D5W • Volume/plasma expander for
• May dilute plasma electrolyte conc. intravascular part of ECF
• CI: head injury — inc ICP • Decreases ability to clot
• Fluid resuscitation — hyperglycemia • Remains in circulation for 24h
• May cause: peripheral circulatory collapse, • Treats hypovolemia in shock: inc. pulse
anuria with Na deficiency, and inc. body
fluid loss.
• Monitor for water intoxication
• Monitor for hypokalemia
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FVD (Hypovolemia)
Nursing Interventions
Loss of ECF volume exceeded the intake of fluid
Monitor I&O
Monitor VS
Contributing Factors -weak rapid pulse
-orthostatic hypotension
- ↓ temp
Vomiting Decreased intake Daily weights

Diarrhea Anorexia Monitor skin turgor

-sternum
Fistulas Nausea -inner thigh
-forehead
Excess sweating Inability to gain access to fluid Monitor tongue turgor
-↑ longitudinal furrows
-smaller in size DT fluid loss
Burns Diabetes insipidus -dry mucous membranes
Monitor mental function
Blood loss Uncontrolled DM
-delirium
-cold extremities
GI suction Third spacing
Encourage/assist with oral hygiene

Manifestations Administer IV fluids

Weight loss Flattened neck veins

Poor skin turgor Weakness

Oliguria Thirst

Concentrated urine Confusion

>3 cap. Refill Sunken eyes

Low CVP Cool clammy skin

↑ HBG, HCT, serum & urine ↓ Urine sodium, CVP

osmolality, specific gravity,
BUN, creatinine
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FVE (Hypervolemia) Manifestations

Isotonic expansion of ECF caused by abnormal retention of Na+ Weight gain ↑ BP, bounding pulse, RR, UO
and H2O.
Peripheral (pitting) edema ↓ HGB, HCT, BUN, serum
and urine osmolality, urine
Contributing Factors sodium, and specific gravity
Ascites CXR: pulmonary congestion
Kidney injury Distended jugular veins SOB
Heart failure Crackles, cough Dyspnea
Cirrhosis

Excess admin. Of Na+ containing fluids Nursing Interventions

Aminister diuretics (loop, thiazide, K sparing)

Interstitial to plasma fluid shifts (hypertonic fluids, burns)
Restrict sodium intake
Corticosteroid therapy
Monitor RR, symmetry, and effort
Severe stress
Monitor edema, ascites, measure abdominal girth
Hyperaldosteronism
Weight daily

Strict I&O

Monitor VS

Reposition regularly

Semi-fowlers position if dyspnea occurs

Elevate swollen extremities

Limit fluid intake

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Hyponatremia Clinical Manifestations Nursing Interventions

Serum sodium <135 mEq/L Anorexia Confusion Monitor I&O

Most abundant in ECF N/V Muscle cramps /twitching Daily weights

Controls H2O distribution in body
Muscle contraction and nerve impulses Headache Weakness / fatigue, lethargy Monitor laboratory values: urine specific gravity, serum sodium
levels
Euvolemic hyponatremia: H2O inc but Na+ stays same. Na+
Lethargy Muscular twitching
diluted — SIADH, DI, Adrenal Insuff— Addisons dse. —-> Encourage food and fluids with high sodium content
restrict fluids, ADH antagonist, declomyacin (no food, dairy, or
antacids) Lithium— inc toxicity. Dizziness Seizures
Water restriction in pts with normal or excess fluid volume
Hypovolemic hyponatremia: Dec in Na, dec in H2O — Papilledema Weight gain
vomiting, diarrhea, NG suction, diuretic therapy, bruns, Administer fluids: Lactated ringers or 0.9 NaCl
excessive sweating —-> 3% saline hypertonic sol’n (central line) Dry skin Edema
SIADH: Furosemide + hypertonic sol’n + lithium (observe for
Hypervolemic hyponatremia: Inc Na+ and Inc H2O — total body toxicity)
Abdominal cramping Alt. Mental status, and coma
H2O dilutes Na+ — CHF, KF, Exc. infusion of saline sol, or LF.
—> restrict fluid intake, diuretics, dialysis Highly hypertonic sol’n should be given slowly and pt
↑ Pulse ↓ BP, serum and urine sodium, monitored closely because only small volumes are needed to
urine specific gravity and elevate the Na+ conc. From a low level
Contributing factors osmolality
Pt c CV dse: assess for signs of circulatory overload— cough
dyspnea, puffy eyelids, dependent edema, excess weight gain.
Diuretics Auscultate lungs for crackles
Mnemonics
GI fluid loss Monitor CNS changes: lethargy, confusion, muscle twitching
N- Na+ excretion inc with: S: seizures & stupor seizures
Renal dse renal problems, sweating, DI, A: abdominal cramping/
aldosterone sec. attitude changes
O- overload of fluids: CHF, L: lethargic
Adrenal insufficiency
hypotonic fluids, LF T: tendon reflexes diminished Serum sodium must not be increased by >12 mEq/L in 24
and trouble concentrating hrs to avoid neurologic damage due to demyelination
Gain of water: excess. Admin of D5W, & H2O supplement for pt N- Na+ intake low: NPO,
receiving hypotonic tube feedings elderly L: loss of urine and appetite
SIADH A- Antidiuretic O: orthostatic hypotension and
hormone, adrenal overactive bowel sounds
Medications that retain water (oxytocin, tranquilizers) insufficiency. S: shallow respirations
S: spasms of muscles
Psychogenic polydipsia
Bacon, butter, canned foods, cheese, hot dogs, lunch meat,
Hyperglycemia processed food, table salt.

HF
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Hypernatremia
Clinical Manifestations
Serum sodium >145 mEq/L
Thirst
↑ Body temp, pulse, BP
Contributing factors Swollen, dry tongue
Fluid deprivation in pt who cannot respond to thirst Sticky mucous membranes
Hypertonic tube feedings w/o water supplement Halucinations
Diabetes insipidus
Restlessness
Heat stroke Irritability
Hyperventilation ↑ serum Na+, urine specific
gravity, osmolality
Watery diarrhea
Burns
Mnemonics
Diaphoresis
H: hypercortisolism
Exc. Corticosteroid, sodium bicarbonate, sodium chloride (Cushing’s syndrome and
administration. hyperventilation)
I: increased Na+ intake (oral or
Salt water, near drowning victims IV routes)
G: GI feeding without adequate
supplement
H: hypertonic solutions
(3% saline)
S: Sodium excretion dec.
(corticosteroids)
A: aldosterone problems
L: loss of fluid (fever,
sweating, dehydration)
T: thirst impairment
Your Nursing Ate 6 of 20
Nursing Interventions
Pulmonary edema Obtain medication hx
Hyperreflexia Monitor I&O
Twitching Daily weights
N/V Monitor laboratory values: urine specific gravity, serum sodium
levels, serum osmolality
Anorexia
Administer hypotonic electrolyte solution or isotonic non saline
solution (D5W)
Lethargy
Restrict sodium intake
Partial/tonic-clonic seizures
Provide oral hydration at regular intervals
↓ urine sodium, CVP
Enteral feedings— sufficient water supplementation
Pts c DI— need adequate hydration
Monitor neurologic signs, symptoms should improve as the
serum sodium gradually reduces.
S/Sx
Monitor for signs of cerebral edema
F: fever, flushed skin
R: restlessness, really
agitated I: increased fluid
retention
E: edema, extremely confused Isotonic sol’n safer than D5W; reduced risk for CE.
D: decreased urine output,
dry mouth, skin Serum Na+ gradually reduced at rate no faster than 0.5 mEq/
L/hr to prevent risk for cerebral edema
*rapid reduction of serum Na+ renders the plasma to be
hypo-osmotic to the fluid in the brain tissue = movement of
fluid into brain cells = life threatening cerebral edema
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Clinical Manifestations Nursing Interventions

Hypokalemia
Lethargy, low and shallow respirations, lethal cardiac Encourage potassium intake through diet
Serum K+ < 3.5 mEq/L changes, loss of urine, leg cramps, limp muscles, low BP and
HR Monitor I&O
Major intracellular electrolyte
Skeletal and muscle activity Anorexia
Monitor ECG
Myocardial irritability and rhythm
N/V
Adequate urine output must be established before admin. K+ via
IV
Muscle weakness
Contributing factors K+ is never given by IV push or IM, to avoid replacing K+
Polyuria too quickly. IV K+ must be admin. Through infusion pump.
Diarrhea < 2.5 mEq/L
dec. bowel motility Watch for phlebitis or infiltrates
Vomiting
Monitor for worsening signs of hypokalemia or hyperkalemia,
Ventricular asystole or fibrillation
Gastric suction watch magnesium, glucose, sodium, and calcium levels
Paresthesias Admin KCl, potassium acetate, or potassium phosphate as
Corticosteroid admin. ordered.
Dysrhythmias
Hyperaldosteronism: increases renal K+ wasting Give oral K+ with 1/2 glass of fluid to avoid irritating gastric
Ileus, abdominal distension mucosa
Carbencillin
Oral K+ can produce small bowel lesions — monitor for
Hypoactive reflexes abdominal dissension, pain, or GI bleeding.
Amphotericin B
ECG: flattened T waves, prominent U waves, ST depression, Hold lasix, thiazide, or K wasting diuretics and hold digoxin
Bulimia prolonged PR interval
Sprinolactone, aldactone - K sparring diuretics.
Osmotic diuresis
Mnemonics
Alkalosis
D- drugs (laxatives, P- potatoes and Carrots, raisins,
diuretics, pork bananas
Starvation corticosteroids O- oranges
I- inadequate intake T-
Diuretics— thiazide and loop (NPO, tomatoes
anorexia, nausea A- avoados
Digoxin toxicity T- too much water S-
intake strawberries
Cushing’s syndrome— inc. cortisol = dec. K+ C- Cushing’s S- spinach
syndrome (too fIsh
much mUshrooms
aldosterone Musk melons
H - heavy fluid loss — cantaloupe
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Hyperkalemia Clinical Manifestations Nursing Interventions

Serum K+ > 5.0 mEq/L Muscle weakness Monitor I&O
Tachycardia → Bradycardia Monitor EKG— Bradycardia → stop IV infusion of K+
Contributing factors
Dysrhythmias Take apical pulse
Pseudohyperkalemia
Flaccid paralysis Monitor serum K+, BUN, creatinine, glucose and ABG
Kidney injury
Paresthesias Potassium restriction
K+ sparing diuretics
Intestinal colic IV calcium gluconate if serum K+ is dangerously elevated,
Metabolic acidosis monitor for hypotension.
Cramps
Addison dse / hypoaldosteronism — deficient adrenal Sodium bicarbonate in severe metabolic acidosis — monitor for
hormones lead to Na+ loss and K+ retention Abdominal distension s/sx of circulatory overload and hypernatremia.

Crush injury IV admin regular insulin + hypertonic dextrose sol’n to shift K+

Irritability back into cells
Burns Anxiety Caution pts to use salt substitutes sparingly

Stored blood bank transfusions ECG: tall tented T waves, prolonged PR interval and QRS Monitor solution concentration & rate of administration via
duration, absent P waves, ST depression, Shortened QT interval infusion pump.
Rapid IV admin of K+

ACE inhibitors C: cellular movement from intra-cell to extra cell

(burns, tissue damage)
NSAIDs A: adrenal K+ SUPPLEMENTS DANGEROUS IN PATIENTS WITH
insufficiency R: renal IMPAIRED RENAL FUNCTION
Cyclosporine
insufficiency E: Decreased ability to excrete potassium — risk for hyperkalemia
Excessive K+ intake Aged (stored blood) has inc. K+ because of RBC deterioration
D: Drugs (K+ sparing, Ace inhibitors, NSAID)

M: muscle weakness
U: urine production low/absent
R: respiratory failure (muscle weakness/seizures)
D: decreased cardiac contractility
E: early signs of muscle twitching — profound
weakness, flaccid
R: rhythm changes EKG
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Hypocalcemia Clinical Manifestations Nursing Interventions

Serum Ca- < 8.6 mEq/L Tetany Dilute IV Calcium in D5W and give as a slow bolus or via IV
infusion.
Transmitting nerve impulses Numbness
Regulate muscle contaction and relax (inc. cardiac muscle) Observe for signs of infiltration —extraversion results in
Blood coagulation cellulitis or necrosis
(+) Trosseau’s sign carpopedal spasm induced by inflating bp
cuff 20 mmHg over systolic BP Monitor BP during infusion — postural hypotension
Absorbed in GI, stored in bones, excreted in kidneys
(+) Chvostek’s sign contraction of facial muscles by tapping on
Seizure precautions
facial nerve in front of ear.
Contributing factors Seizures — CNS and PNS irritability Safety precautions as indicated

Hypoparathyroidism: PTH releases Ca stores from the GI tract, Irritability, depression, impaired memory, confusion, delirium, Educate pt about foods rich in Ca-
renal tubule, and bones. hallucinations.
Malabsorption Oral form of Ca- with Vit D supplement. After meal or at
Bronchospasm, dyspnea, laryngospasm bedtime with full glass of water
Pancreatitis — Anxiety
Ca+ ions bind with fatty acids, forming soaps
Pancreas releases glucagon which inc. calcitonin prod = dec Ca- Impaired clotting time, brittle hair and nails, hyperactive bowel
signs Mnemonics
Alkalosis
Diarrhea L-low PTH (removal, neck C-confusion
Vitamin D deficiency surgery) R- reflexes hyperactive
↓ BP, prothrombin time, Mg++ O- oral intake inadequate A- arrhythmias (prolong QT or
Massive subcutaneous infection (alcoholism, bulimia) ST interval)
ECG: prolonged QT interval, lengthened ST. W- wound drainage (GI M- muscle spasms/
Peritonitis system) seizures P- positive
trousseau and
Massive transfusion of citrated blood — citrate + ionized calcium C- celiac’s disease, chron’s dse S- sign of chvostek
removes Ca from the circulation. (malabsorption)
Calcium salts are dangerous for pts receding digitalis derived A- acute
Chronic diarrhea meds — risk for toxicity pancreatitis L- low
vit D intake
Diuretic phase of kidney injury: Hyperphosphatemia = drop in 0.9% NaCl with Ca- salts inc. renal calcium loss C- chronic kidney dse
Ca- levels I- increase phosphorus
Sol’n c bicarbonate & phospate + Ca- yield precipitates levels U- using medications
Burns
(Mg supplements, laxatives,
Ca gluconate: 4.5 mEq of Ca- , give slowly & monitor HR, loop diuretics)
Alcoholism watch for infiltration/ phlebitis M- mobility issues
Ca chloride: 13.6 mEq of Ca-
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Hypercalcemia Clinical Manifestations Nursing Interventions

Serum Ca- > 10.2 mEq/L Muscular weakness: ↑Ca = ↓act. At myoneural junction. Ca- restriction

Constapation / Diarrhea Administer fluids: 0.9% NaCl, IV phosphate, Calcitonin (skin

test before admin. Salmon calcitonin for reax)
Anorexia
Administer diuretics: furosemide
N/V
Contributing factors Increasing pt mobility, early ambulation
Polyuria
Hyperparathyroidism Encourage fluid intake, fluids containing Na+ unless CI
polydipsia
Malignant neoplastic dse Adequate fiber
dehydration
Prolonged immobilization: bone mineral is lost = ↑Ca- in BS Safety precautions when confusion is present
Hypoactive deep tendon reflexes
Calcium supp. Monitor for s/sx of digitalis toxicity
Lethargy, confusion, coma
Vit D excess Monitor vital signs esp cardiac rate & rhythm
Deep bone pain
Oliguric phase of renal failure Admin calcitonin per dr. order
Flank pain
Acidosis
Calcium stones, HTN Mnemonics
Corticosteroid therapy
ECG: shortened ST segment and QT interval, bradycardia, H- Y-yogurt
Thiazide diuretic use: potentiate action of PTH on kidneys = ↓ heart block
Ca- urinary excretion. hyperparathyroidism I- S-
increased intake sardines
Digoxin toxicity: ↑Ca aggravates D.T G- glucocorticoids C- cheese
H- hyperthyroidism S-spinach
Hypercalcemia crisis | Serum Ca- > 17 mEq/L C- collared
C- Ca excretion dec. c/ greens T- tofu
Severe thirst & polyuria, abdominal cramps, peptic ulcer thiazide A- adrenal R-
symptoms, bone pain, intractable nausea. *req prompt treatment insufficiency (Addisons dse) rhubarb
before cardiac arrest occurs L- lithium usage: phos inc. Ca M- milk
dec.
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Hypomagnesemia Clinical Manifestations
Serum Mg++ <1.3 mg/dL Neuromuscular irritability
(+) Trosseau’s sign carpopedal spasm induced by inflating bp
Neuromuscular irritability and contractility cuff 20 mmHg over systolic BP
Regulation of PTH which plays a role in Ca+ levels
Regulates BP (+) Chvostek’s sign contraction of facial muscles by tapping on
Metabolizes lipids, carbs, and proteins. facial nerve in front of ear.
Absorbed in small intestine.
insomnia
Contributing factors Mood changes
Chronic alcoholism anorexia
Hyperparathyroidism vomiting
Hyperaldosteronism Increased tendon reflexes
Kidney injury
↑BP
Malabsorption disorders ECG: PVCs, flat or inverted T waves, depressed ST segment,
prolonged PR interval, widened QRS
Diabetic ketoacidosis
Referring after starvation Mnemonics
Parenteral nutrition Causes:
laxatives, diarrhea L- limited intake Mg+
(Starvation)
Acute MI, HF O- other electrolyte issues
(hypokalemia,
hypokalemia & hypocalcemia hypocalcemia) W- wasting
Mg+ via kidneys
Pharmacologic agents
M- malabsorption issues
(churns, celiac, PPIs,)
A- alcohol (poor dietary intake,
stimulates magnesium exc.)
G- glycemic issues (DKA,
insulin)
Your Nursing Ate 11 of
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Nursing Interventions
Dietary sources of Mg
Administer magnesium salts as indicated
Monitor VS during mag su administration
Monitor urine output, refer if <100ml over 4 hours
Seizure precautions
Safety precautions
Screen for dysphagia
Magnesium sulfate given too rapidly can lead to heart block
or asystole. Monitor for changes in cardiac rate, rhythm, or
respiratory distress.
IV mag su must be given via infusion pump at a rate not
faster than 150 mg/min or 67 mEq over 8 hours.
T: trousseau’s sign
W: weak respirations
I: irritability
T: torsades de pointes, tetany
C: cardiac changes, chovstek
H: hypertension, hyperreflexia
I: involuntary movements
N: nausea
G: GI issues (dec bowel sounds
+ mobility)
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Clinical Manifestations Nursing Interventions
Hypermagnesemia
flushing Restrict Mg
Serum Mg++ >3.0 mg/dL
hypotension IV calcium gluconate and ventilation in respiratory depression or
defective cardiac conduction
Muscle wekness
Hemodialysis with a magnesium free dialysate
Contributing factors drowsiness
Loop diuretics and NaCl or LR in pts with adequate renal func
Kidney injury Hypoactive reflexes
Monitor VS
Note shallow respirations and hypotension
Adrenal isufficiency Depressed respirations
Assess DTR and changes in LOC
Excess IV magnesium admin: PIH or hypomagnesemia Cardiac arrest
Tell pt to consult with their provider before taking any OTC
Diabetic ketoacidosis: catabolism causes the release of cellular Diaphoresis meds (kidney injury/ compromised renal function)
magnesium that can’t be excreted bc of a profound fluid volume
depletion and resulting oliguria Coma
Hypothyroidism Tachycardia → bradycardia

ECG: Prolonged PR interval and QRS, peaked T waves

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Hypochloremia Clinical Manifestations
Nursing Management
Serum Cl < 97 mEq/L aggitation
Monitor I&O, ABG, serum electrolytes
Maintains acid-base balance Irritability
Buffer in exchange of O2 and CO2 in RBC Report changes in LOC, muscle strength, and movement
Proportionate to Na+ conc. promptly
Tremors
Inverse to HCO3- conc. V/S monitoring
Muscle cramps
Respiratory assessment
Contributing factors Hyperactive DTR
Educate about foods high in chloride content:
Addison’s dse hypertonicity
Tomato juice, bananas, dates, eggs, cheese, milk, salty broth,
Reduced intake/absorption tetany canned vegetables, processed meats

Diabetic ketoacidosis Slow, shallow respi

Chronic respiratory acidosis Seizures, coma

Excessive sweating Dysrhythmias

Vomiting & diarrhea ↑ serum HCO3, total CO2 ↓ serum Cl-, Na+, K+, urine
Cl-
NG suction, GI drainage, gastric surgery

Burns, fever
Medical Management
Na+ and K+ deficiency
Normal saline 0.9% NaCl
Metabolic alkalosis
Half strength saline 0.45% NaCl
Diuretics (loop, osmotic, thiazide)
D/c or change diuretic
IVF that lack Cl-
Ammonium chloride tx for metabolic alkalosis
HF, CF

Admin of aldosterone, corticosteroids, bicarbonate, or laxatives.

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Hypechloremia Clinical Manifestations (same as metabolic acidosis) Nursing Management

Serum Cl- > 108 mEq/L Tachypnea Monitor I&O, ABG, serum electrolytes

Lethargy Report changes in LOC, muscle strength, and movement

promptly
Contributing factors Weakness
V/S monitoring
Exc. NaCl infusions with waterloss Deep, rapid respirations
Respiratory assessment
Head injury (Na+ retention) Decline in cognitive status, coma
Educate about avoiding foods high in chloride content:
hypernatremia Dec cardiac output, HTN
Tomato juice, bananas, dates, eggs, cheese, milk, salty broth,
Kidney injury canned vegetables, processed meats
Dyspnea
corticosteroids Tachycardia
dehydration Hypervolemia, fluid retention — Pitting edema
Severe diarrhea (loss of bicarbonate) Dysrhythmias
Respiratory alkalosis ↑ serum Cl-, K+, Na+ urine Cl- ↓ serum HCO3, normal anion
gap
Diuretics

Overdose of salicylates, kayexalate, acetazolamide,

phenylbutazone, and ammonium chloride use
Medical Management
Hyperparathyroidism
Hypotonic IV sol’n
Metabolic acidosis
LR: converts lactate to HCO3 in the liver

IV NaHCO3 - increase bicarbonate levels, dec chloride levels

Diuretics

Na, Cl, and fluids restriction

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Hypophosphatemia Clinical Manifestations Nursing Management

Serum HPO4- < 2.5 mg/dL parenthesias Prevent infection

Formation of ATP Muscle weakness Monitor serum phosphorous levels

Facilitates release of O2 from HGB
Maintains ABG, NS,& metal. Of carbs, protein, fat. Bone pain Monitor for infiltration during IV phosphorus admin.
Structural support to bones and teeth
tenderness Foods rich in phosphorous:

Chest pain Milk and milk products, organ meats, nuts, fish, poultry, whole
Contributing factors grains
confusion
Refeeding after starvation
cardiomyopathy
Alcohol withdrawal
RF
DKA
seizures
R&M alkalosis
Tissue hypoxia
Dec Mg++, K+, and hyperparathyroidism
Susc. To infections
Acute volume expansion, osmotic diuresis, carbonic anhydrase
inhibitors Nystagmus — eyes make repetitive, uncontrolled movements
vomiting

diarrhea

hyperventilation Medical Management

Vitamin D def. assoc c malabsorptive disorders IV admin of sodium or potassium phosphate

Acid-base disorders, respiratory alkalosis Oral supplements

Parenteral nutrition

Burns, diuretic and antacid use.

Hepatic encephalopathy
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Hyperphosphatemia Clinical Manifestations Nursing Management

Serum HPO4- > 4.5 mg/dL tetany Low phosphorus diet: avoid

Reciprocal relationship with calcium: high phosphorous = low tachycardia Milk and milk products, organ meats, nuts, fish, poultry, whole
calcium grains, sardines, dried fruits/vegetables, cream
Anorexia
Avoid phosphorus containing laxatives and enemas
Contributing factors N/V
Educate about s/sx of impending hypocalcemia and monitoring
for changes in U/O
Kidney injury/dse Muscle weakness

Exc. intake of HPO4- S/sx of hypocalcemia: soft tissue calcifications in lungs, heart,
kidney, and cornea
Vitamin D excesss
Decreased urine output
Respiratory and metabolic acidosis
Impaired vision
Hypoparathyroidism
palpitations
Volume depletion

Leukemia, lymphoma treated with cytotoxic agents Medical Management

Inc tissue breakdown Treat underlying condition

Rhabdomyolysis: death of muscle fibers and release of their Vitamin D (calcitirol)

contents into the BS
Calcium binding antacids (calcium carbonate, calcium citrate)

Amphojel

Restrict dietary phosphate

Forced diuresis with loop diuretic

Volume replacement c saline

dialysis

Surgery to remove large Ca- deposits

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Metabolic Acidosis High anion gap Causes: Assessment

Low pH and low plasma bicarbonate concentration Results from excessive accumulation of organic acid

Anion gap = Na+ + K+ - (Cl- + HCO3-) ketoacidosis

Anion gap = Na+ - (Cl- + HCO3-)
Lactic acidosis and dx findings
Reduced or Normal High anion
negative anion gap gap pH < 7.35
Salicylate poisoning
anion gap
W/o K+ <8 8-12 mEq/L >12 uremia Serum HCO3- < 22 mEq/L — cardinal feature

With K+ <12 12-16 mEq/L >16 Methanol Hyperkalemia as K+ moves out of cell — dysrhythmias

hypoproteine Normal anion High anion Ethylene glycol toxicity Medical management
mia gap gap metabolic
metabolic acidosis ketoacidosis with starvation Tx directed at correcting the metabolic imbalance, fixing the
acidosis cause of metabolic acidosis
Bicarbonate admin.
Normal anion gap metabolic acidosis (hyperchloremic Clinical manifestations
acidosis) Causes: NaHCO3- admin during cardiac arrest may lead tot paradoxical
headache intracellular acidosis
Results from direct loss of bicarbonate
confusion Monitor serum K+ closely
diarrhea
drowsiness In chronic metabolic acidosis: treat serum Ca+ levels first to
Lower intestinal fistulas prevent tetany
Increased respiratory rate, depth
ureterostomies Alkalizing agents
N/V
Early renal insuff. Dialysis
Hypotension
Exc admin of chloride
Cold, clammy skin
Administration of parenteral nutrition without bicarbonate or
bicarbonate producing solutes
Dysrhythmias and shock
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Metabolic Alkalosis Assessment and Dx findings

High pH and high plasma bicarbonate concentration pH > 7.45 and serum HCO3- > 26 mEq/L

PaCO2 increases to compensate for excess bicarbonate by

retaining CO2.
Causes: hypoventilation
Vomiting Hypoxemia
Gastric suction Urine chloride levels <25 mEg/L
-metabolic alkalosis due to: vomiting, CF, nutritional repletion,
Pyloric stenosis diuretic therapy, hypovolemia and hypochloremia
Hypokalemia from diuretic therapy (thiazide, furosemide), Urine chloride > 40 mEq/L
ACTH secretion (Cushing’s syndrome, Addison’s disease) (-) signs of hypovolemia
Mineralocorticoid excess or alkali loading
1) kidneys conserve potassium —> H+ excretion increases (H+
> HCO3 = alkalosis) Urine chloride conc < 15 mEq/L when decreased chloride levels
2) Potassium shifts from inside the cell to outside, making H+ and hypovolemia occur.
ions enter the cell to maintain neutrality. Less H+ ions in
plasma = greater number of bicarbonate ions = alkalosis `
Villous adenoma, chronic ingestion of milk and calcium Medical management
carbonate.
Monitor I&O carefully

Administer sodium chloride fluids

Clinical manifestations
In patients with hypokalemia, KCl is given
Tingling of fingers and toes
Cimetidine (H+ receptor antagonists — reduce production of
dizziness gastric hydrogen chloride, dec. alkalosis caused by gastric
suctioning
Hypertonic muscles
Carbonic anhydride inhibitors— treat metabolic alkalosis in
Depressed respirations patients who can’t tolerate rapid vol expansion (HF)

Atrial tachycardia

Decreased motility and paralytic ileum

U-waves (premature ventricular contractions) on EKG

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Respiratory acidosis: carbonic acid excess Clinical manifestations Medical management

Low pH and high PaCO2 inc. PR, RR, BP Tx aimed at improving ventilation

Inadequate excretion of CO2 with inadequate ventilation, Mental cloudiness, dizziness, disorientation Bronchodilators
resulting in inc. levels of carbonic acid
Feeling of fullness in the head Antibiotics for infec

Causes: Dec LOC, drowsiness Thrombolytics or anticoagulants

Acute pulmonary edema Dysrhythmias, Ventricular fibrillation Pulomnary hygiene measures

aspiration Papilledema Adequate hydration

Foreign object vasodilation Mechanical ventilation

atelectasis Hyperkalemia, muscle weakness Semi-fowler’s position

Pneumothorax cyanosis

OD of sedatives Tachypnea — rapid, shallow respirations

Sleep apnea

ARDS Assessment and Dx findings

Muscular dystrophy pH < 7.35 and PaCO2 > 45 mm Hg

GBS Compensation: renal retention of bicarbonate

Mysanthenia gravis CXR— identify respi dse

ECG

Drug screen for OD

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Respiratory alkalosis Clinical manifestations Medical management

High pH low paCO2 Lightheadedness due to vasoconstriction Breathe into a paper bag

Inability to concentrate Treat underlying condition

Causes Numbness and tingling

hyperventilation Tinnitus

Extreme anxiety Loss of consciousness

hypoxemia
Salicylate intoxication
Gram-negative bacteremia
Inappropriate ventilator settings
Chronic hypocapnia
Chronic hepatic insufficiency
tachycardia
Thank you for downloading my fluid &
Ventricular and atrial dysrhythmias electrolytes cram sheets! I hope this helps
you in studying for your med surg exams.
N/V Please bear in mind that these are my
Seizures personal notes & as accurate as I try to be,
there may be missing/inaccurate
Deep rapid breathing information. That being said, I still highly
encourage you to read your textbooks.

Cerebral tumors Assessment and Dx findings Best of luck on your nursing journey!

pH > 7.45 and PaCO2 < 35 mm Hg Padayon, Future Nurse.

Normal bicarbonate level
- Dane (Your Nursing Ate)
Possible hypokalemia, hypocalcemia, or hypophosphatemia

Toxicology screen R/O salicylate poisoning