Disruptions in Homeostasis (Electrolytes, Fluids, Acid-Base)

med/surge exam 2

Fluid compartments distribution

2/3 intracellular (ICF), 1/3 extracellular (ECF)

Diffusion

Movement of solutes from high concentration to low concentration

Osmosis

Movement of water from low solute concentration to high solute concentration

Filtration

Movement of fluid due to hydrostatic pressure overcoming osmotic pressure → fluid goes from intravascular to interstitial

Fluid volume deficit (FVD) pathophysiology

Loss of water + sodium → ↓ circulating volume → ↓ tissue perfusion → ADH + RAAS activated

Fluid volume deficit clinical manifestations

Hypotension,

tachycardia

weak + thready pulse,

dry mucous membranes,

decreased skin turgor

flat neck veins

decreased urine output,

dizziness

Fluid volume deficit priority interventions

Isotonic IV fluids (NS) or oral hydration if possible,

monitor I&O,

daily weights,

fall precautions

Fluid volume excess (FVE) pathophysiology

Retention of sodium + water → ↑ ECF volume → fluid shifts into tissues → edema

caused by CHF, liver disease, kidney disease, COPD

Fluid volume excess clinical manifestations

Edema,

crackles,

dyspnea,

JVD,

bounding pulse

weight gain,

hypertension

Fluid volume excess priority interventions

Fluid restriction,

sodium restriction,

diuretics,

high Fowler’s,

monitor lungs

Normal sodium level

135-145 mEq/L

Hypernatremia pathophysiology

Water loss > sodium loss → ↑ osmolality → water leaves cells → cell shrinkage

Hypernatremia clinical manifestations

Thirst,

dry mucous membranes,

confusion,

seizures (less common)

restlessness

irritability

Hypernatremia priority interventions

NaCl or Hypotonic fluids,

oral hydration,

correct slowly

Hyponatremia pathophysiology

Excess water dilutes sodium → ↓ osmolality → water enters cells → cerebral edema

Hyponatremia clinical manifestations

Confusion,

headache,

seizures (MOST COMMON)

decreased LOC

Hyponatremia priority interventions

Fluid restriction,

salt tablets

hypertonic saline (severe),

seizure precautions

Normal potassium level

3.5-5.0 mEq/L

Hypokalemia pathophysiology

Loss of potassium via GI/renal or shift into cells → ↓ muscle and cardiac function

caused by diarrhea

Hypokalemia clinical manifestations

Weakness,

cramps,

numbness

ileus,

tachycardia

increased urine output

dysrhythmias,

flattened T waves

Hypokalemia priority interventions

Oral/IV potassium (never IV push),

monitor ECG,

monitor urine output

Hyperkalemia pathophysiology

Potassium shifts out of cells or decreased excretion → ↑ cardiac excitability

Hyperkalemia clinical manifestations

Peaked T waves,

dysrhythmias,

muscle weakness

bradycardia

decreased urine output

Hyperkalemia priority interventions

Calcium gluconate → for dysrhythmias ,

Kayaxelate

insulin + glucose,

diuretics (furosemide),

dialysis

Normal magnesium level

1.3-2.1 mEq/L

Hypomagnesemia pathophysiology

Decreased intake or increased loss → ↑ neuromuscular excitability

Hypomagnesemia clinical manifestations

Tremors,

tetany,

seizures,

torsades de pointes

Hypomagnesemia priority interventions

Magnesium replacement (oral/IV),

cardiac monitoring

Hypermagnesemia pathophysiology

Excess magnesium (usually renal failure) → ↓ neuromuscular and cardiac activity

Hypermagnesemia clinical manifestations

Hyporeflexia,

bradycardia,

hypotension,

respiratory depression

Hypermagnesemia priority interventions

Calcium gluconate (IV),

IV fluids (NaCl),

loop diuretics (furosemide),

Normal calcium level

9.0-10.5 mg/dL

Hypocalcemia pathophysiology

↓ calcium → ↑ neuromuscular excitability

caused by decreased parathyroid hormone or decreased vit D

Hypocalcemia clinical manifestations

Tetany,

Chvostek sign,

Trousseau sign,

seizures,

prolonged QT

Hypocalcemia priority interventions

IV calcium gluconate,

Vit D

seizure precautions,

cardiac monitoring

Hypercalcemia pathophysiology

↑ calcium → ↓ neuromuscular excitability

Hypercalcemia clinical manifestations

Bone pain,

kidney stones,

constipation,

confusion,

shortened QT

Hypercalcemia priority interventions

IV fluids,

diuretics,

encourage mobility,

hydration

Normal pH

7.35-7.45

Normal PaCO2

35-45 mmHg

Normal HCO3

22-26 mEq/L

Metabolic acidosis pathophysiology

decreased pH + decreased HCO3 (CO2 will decrease to compensate)

Metabolic acidosis clinical manifestations

Kussmaul respirations,

confusion,

hypotension

Metabolic acidosis priority interventions

Treat cause (DKA → insulin),

IV fluids,

sodium bicarbonate if severe

Metabolic alkalosis pathophysiology

↑ bicarbonate + ↑ pH (CO2 will increase to compensate)

Metabolic alkalosis clinical manifestations

Confusion,

muscle weakness,

dysrhythmias

Metabolic alkalosis priority interventions

Treat cause,

IV fluids,

electrolyte replacement

Respiratory acidosis pathophysiology

Hypoventilation → CO2 retention → ↓ pH

(↓ pH + ↑ CO2) → bicarbonate will increase to compensate

Respiratory acidosis clinical manifestations

Slow respirations,

confusion,

drowsiness,

cyanosis

Respiratory acidosis priority interventions

Improve ventilation,

oxygen,

bronchodilators,

naloxone if opioid

Respiratory alkalosis pathophysiology

Hyperventilation → CO2 loss → ↑ pH

(↑ pH + ↓ CO2) → bicarbonate will decrease to compensate

Respiratory alkalosis clinical manifestations

Dizziness,

paresthesia,

anxiety,

caused by tachypnea

Respiratory alkalosis priority interventions

Treat cause,

slow breathing,

paper bag (anxiety),

adjust ventilator

ROME method

Respiratory Opposite (pH and CO2 opposite),

Metabolic Equal (pH and HCO3 same direction)