nursing 347 - fluid and electrolytes

normal adult fluids

• tbw: 60% of body weight

• 2/3 = intracellular fluid

• 1/3 = extracellular fluid

pediatric fluids

• 75-85% of body weight

• susceptible to significant changes in body fluid = dehydration in newborns

geriatric fluids

• low percent of tbw

• high adipose + low muscle

• thirst gone

obesity body fluids

• low percent of tbw

• high risk of dehydration

sodium and chloride balance

• raas system

• aldosterone = sodium + water reabsorption → excretes potassium

• sodium + water excretes

osmoreceptors

• hypothalamus detects blood too concentrated → dehydration

• response: triggers thirst

antidiuretic hormone

• keeps water in body

• makes kidney reabsorb water

volume/baroreceptors

• detects: low blood volume/low bp

• response: increases adh + thirst

isotonic alterations

• water + electrolyte issue = volume problem

• not concentration problem

hypernatremia

dehydration + high sodium

manifestations of hypernatremia

• high bp and brain cells shrink

• altered membrane potentials

• hyperchloremia often occurs

hyponatremia

low sodium + high water

hyponatremia manifestations

• cell swelling = cerebral edema

• altered action potentials

• increase intracranial pressure

potassium roles in body

• glycogen + glucose deposition

• normal cardiac rhythms

• skeletal and smooth muscle contraction

what affects serum potassium levels?

• aldosterone

• insulin

• epinephrine

what is the most efficient regulator for potassium?

the kidney is the most efficient regulator

hypokalemia causes

• low potassium intake

• high entry of potassium into cells

• high loss of potassium

hypokalemia manifestations

• low neuromuscular excitability

• skeletal muscle weakness

• smooth muscle atony

more hypokalemia manifestations

• cardiac dysrhythmias

• glucose intolerance

• unconcentrated (watery) urine

hyperkalemia

rare due to efficient renal excretion, therefore, can be caused by low renal secretion

causes of hyperkalemia

• high potassium intake

• shift from icf to ecf + cell truma

• low insulin

hyperkalemia - mild attack manifestations

• high neuromuscular irritability

• restlessness

• diarrhea + intestinal cramping

hyperkalemia - severe attack manifestations

• low resting membrane potential

• muscle weakness → paralysis

• low muscle tone

hospital monitoring of electrolyte imbalance

• daily monitoring

• nurses should look at labs for pt every day

• adjustment in treatment based on lab values

edema

fluid accumulation in interstitial spaces

what causes edema?

• high capillary hydrostatic pressure

• low plasma oncotic pressure

• high capillary permeability

• lymph channel obstruction

edema - high capillary hydrostatic pressure #1

• high vascular volume

• caused by:

  • chf, kidney disease

  • premenstrual sodium retention

  • pregnancy

edema - high capillary hydrostatic pressure #2

• venous obstruction

• caused by:

  • liver disease, portal vein obstruction

  • pulmonary edema

  • dvt

edema - low plasma oncotic pressure #1

• high loss of plasma protein

• caused by:

  • burns

  • glomerular disease

edema - low plasma oncotic pressure #2

• low production of plasma

• caused by:

  • liver disease → ascites

  • starvation, malnutrition

edema - high capillary permeability

caused by:

• inflammation

• allergic reactions

• tissue injury (trauma)

• burns

clinical manifestation of edema #1

• local: one area

  • sprained ankle, hives

• generalized: all over

  • chf - congestive heart failure

clinical manifestation of edema #2

• brain edema: high intracranial pressure

• laryngeal edema: block airway

• pulmonary edema: impaired gas exchange

clinical manifestation of edema #3

• high distance for diffusion of nutrients + oxygen

• tissues susceptible to injury + hypoxia

clinical manifestation of edema #4

• impaired circulation = compressed blood vessels

• ischemia + necrosis occur

diuretics

• block sodium and chloride reabsorption

• site of action: pct

types of diuretics

• loop (potassium wasting)

• thiazide

• potassium sparing

• osmotic

adverse reactions of diuretics

• hypovolemia

• acid-base imbalance

• electrolyte imbalance

loop diuretic

• medication: furosemide (lasix)

• mechanism: acts on ascending loop of henle to block reabsorption

• rapid onset

loop diuretic indications

• edema

• hypertension

• pulmonary edema

loop diuretic adverse effects

• hypokalemia, hyponatremia, hypochloremia

• dehydration + hypotension

• ototoxicity

• hyperglycemia

thiazide diuretics and loop diuretics comparison

• maximum diuresis lower than with loop diuretics

• not effective when urine flow is scant (unlike loop diuretics)

thiazide diuretics

• hydrochlorothiazide

• high renal excretion of sodium, chloride, potassium, water

• high levels of uric acid and glucose

thiazide diuretics important facts

• mechanism: early segment of dct

• peaks in 4-6 hours

therapeutic uses of thiazide diuretics

• essential hypertension

• edema

• diabetes insipidus

adverse effects of thiazide diuretics

• hyponatremia, hypochloremia, hypokalemia, dehydration

• hyperglycemia + hyperuricemia

• use in pregnancy + lactation

more adverse effects of thiazide diuretics

impacts on lipids, calcium, and magnesium

potassium-sparing diuretics

• small increase in urine

• high decrease in potassium excretion

• rarely used alone for therapy

potassium-sparing diuretics antagonists

• aldosterone antagonist: spironolactone

• non-aldosterone antagonist: triamterene + amiloride

spironolactone mechanisms

• other name: aldactone

• blocks aldosterone in distal nephron

• retention of potassium + high excretion of sodium

spironolactone therapeutic uses

• hypertension, edema, heart failure

• primary hyperaldosteronism

• premenstrual syndrome + pcos

• acne in young women

spironolactone adverse effects

• hyperkalemia

• benign and malignant tumors

• endocrine effects

spironolactone drug effects

• thiazide and loop diuretics

• agents that raise potassium levels

osmotic diuretic

• name: mannitol (osmitrol)

• pharmacokinetics: given parenterally

therapeutic uses of osmotic diuretic

• prophylaxis of renal failure

• reduction of intracranial pressure

• reduction of intraocular pressure

adverse effects of osmotic diuretic

• edema

• headache, nausea, vomiting

• fluid and electrolyte imbalance

normal values of pH

• 7.35-7.45

• lower = acidosis

• higher = alkalosis

normal values of PaCO2

• acid

• 35-45

normal values of HCO3-

• base

• 22-26

pH - acids

• substance that donates H+

• volatile = eliminated as CO2 gas

• nonvolatile = H+, eliminated only by kidneys

pH - base

• substance that accepts H+

• bicarbonate (HCO3-)

disruptions in acid base balance

• usually blood sample taken from artery

• called arterial blood gas

acidosis

• pH <7.35

• respiratory acidosis = too much carbonic acid

• metabolic acidosis = kidneys excrete metabolic acid

alkalosis

• pH >7.45

• respiratory alkalosis = too little carbonic acid

• metabolic alkalosis = too little metabolic acid

regulating the pH - chemical buffer

• work immediately when an imbalance transpires in:

  • extracellular fluid

  • intracellular

  • urine

  • electrolytes

first line of defense of pH

• phosphate

• immediate response to condition

second line of defense of pH

• lungs

• response to action: seconds to minutes (medium reaction)

• adjust respiratory rate to expel or hold CO2

third line of defense of pH

• kidneys

• response to action: hours to days (slow)

• reabsorb: HCO3- or regeneration HCO3- from CO2 and H2O

respiratory acidosis

not expelling enough CO2 (too much acid)

respiratory acidosis symptoms

• decreased loc (level of consciousness) + immobility

• pulmonary edema + chest trauma

• airway obstruction

metabolic acidosis

• not enough HCO3- (not enough base)

• high non-carbonic acids from abnormal cellular waste (too much acid)

metabolic acidosis symptoms

• severe diarrhea

• diabetic ketoacidosis

• sepsis, shock, salicylate OD (aspirin)

• renal failure

compensation in respiratory acidosis

• kidneys attempt to reabsorb HCO3-

• kidneys excrete H+

• takes hours to days

compensation in metabolic acidosis

• called kussmaul respirations

• lungs expel CO2

• increased depth and rate of breaths

• happens in minutes

causes of respiratory alkalosis

• expel too much CO2- (not enough acid)

• anxiety

• hypoxia, fever

• pregnancy

• high altitudes

causes of metabolic alkalosis (HCO3-)

• too much HCO3- (too much base)

• overuse of antacids

• blood transfusions

causes of metabolic alkalosis (H+)

• excretion of H+ (not enough acid)

• vomiting + diarrhea

• ng tube suctioning

• potassium wasting diuretics

compensation in respiratory alkalosis

• kidneys excrete HCO3-

• kidneys reabsorb H+

• takes hours to days

compensation in metabolic alkalosis

• lungs hold CO2

• decreased depth and rate of breaths

• happens in minutes

CO2 - less and greater

• <35 mmHg → not enough acid → respiratory problem

• >45 mmHg → too much acid → respiratory problem

HCO3 - less and greater

• <22 mmHg → not enough base → metabolic problem

• >22 mmHg → too much base → metabolic problem

respiratory acidosis equation

pH <7.35 + pCO2 >45 mmHg = too much acid

respiratory alkalosis equation

pH >7.45 + pCO2 <35 mmHg = not enough acid

metabolic acidosis equation

pH <7.35 + HCO3- <22 mEq/L = not enough base or too much acid

metabolic alkalosis equation

pH >7.45 + HCO3- >26 mEq/L = too much base or not enough acid