Electrolyte Functio Nursing Clients at

Hyper “high” Hypo “low”

and value n interventions risk/ Causes
Hyperkalemia Hypokalemia HYPO: HYPO:
HEART (LOW & SLOW) admin KCl heart failure
HEART (TIGHT & 1 Weak irregular pulse supplements *very hypertension
CONTRACTED) carefully low body mass
1 Severe = Vfib or Cardiac MUSCULAR - LOW & SLOW encourage dietary index
Standstill! 1 Decreased DTR intake for foods high cushing
2 Hypotension, Bradycardia 2 Muscle cramping in potassium syndrome
Potassium (K+)
3 Flaccid paralysis (paralyzed (bananas, oranges,
3.5 - 5.0 GI TRACT (TIGHT & limbs) pinto beans, ect) HYPER:
Pumps the
excreted CONTRACTED) renal failure
heart and 1 Diarrhea
through the muscles
GI - LOW & SLOW HYPER: diabetes
2 Hyperactive bowel sounds Decreased motility, hypoactive to monitor I&O overuse of ACE
kidneys
absent bowel sounds, admin insulin to inhibitors
NEUROMUSCULAR (TIGHT constipation, abdominal lower potassium
& CONTRACTED) distention (check glucose when
Paralysis in Extremities Paralytic ileus, paralyzed administering)
Increased DTR intestines! check BUN and
Profound Muscle Weakness, *PRIORITY* for SBO (small creatinine levels
(General Feeling of heaviness) bowel obstruction) (checks kidney
function)

Sodium (Na+) Swells the Hypernatremia Hyponatermia Hypo: HYPER:

body to fluid replacement dehydrated
135 – 145
maintain = BIG & BLOATED = DEFLATED using sodium diarrhea
excreted blood 1. SKIN NEURO = Seizures & Coma containing fluids constant use of
through the pressure, FLUSH ‘’Red & Rosy’’ HEART = Tachycardia, & increased oral diuretics
kidneys blood EDEMA ‘’waterbed skin’’ weak thready pulses intake disorder of
volume, pH LOW GRADE FEVER RESPIRATORY ARREST salt-replacing adrenal glands
balance medication (salt kidney disease
2. POLYDIPSIA EXCESS tabs/pills)
THIRST
Hyper:
 fluid replacement HYPO:
3. LATE SERIOUS SIGN
diuretics to older adults (due
SWOLLEN dry tongue
promote excretion to use of SSRI’s
GI = nausea & vomiting
sodium restriction and diuretics)
INCREASED muscle tone
monitor vital signs
Altered personality (confused,
(cardiac function)
lethargic)
daily weights
daily assessments
Vitals: tachycardia, low BP
of skin
daily labs
HYPER:
dehydration
kidney disease
HYPO:
cushing
rehydrate/ drink
syndrome
Hypochloremia 2L of fluid per day
HYPERchloremia metabolic
NEARLY SAME AS LOW avoid alcohol and
NEARLY SAME AS HIGH acidosis
SODIUM caffeine
Blood SODIUM
Chloride (Cl-) 1. EXCESSIVE don’t take aspirin
pressure, 1. NAUSEA & HYPO:
96 – 108 blood VOMITING
DIARRHEA, products
heart failure
excreted in the VOMITING, avoid/minimize
volume and 2. SWOLLEN DRY lung disease
urine SWEATING the use of laxatives
pH balance TONGUE Addison disease
2. FEVER TEST TIP:
3. CONFUSION (when your bodies
ONLY DIFFERENCE HYPER:
adrenal glands
restrict Na (salt)
don’t produce
chloride intake
enough of certain
hormones)
metabolic
alkalosis

Magnesium Relaxes the HYPERmagnesemia Hypomagnesemia HYPO: HYPO:

muscles 1. CARDIAC - CALM & increase greens in type 2 diabetes
(Mg+) QUIET 1. CARDIAC - BUCK WILD! diet digestions
1.5 – 2.5 Heart block SEVERE = V fib IV magnesium problems such as
excreted Prolonged PR intervals VITALS = Tachycardia admin crohns disease
through kidneys VITALS = bradycardia, 2. DEEP TENDON REFLEXES long term
Hypotension - HYPER: vomiting or
and feces 2. DEEP TENDON BUCK WILD! IV fluids (IV diarrhoea
 Hyporeflexia - increased DTR kidney problems
REFLEXES - 3. EYES - BUCK WILD! long term use of
CALM & QUIET Abnormal eye movements dietetics
calcium)
Hyporeflexia - Decreased DTR (nystagmus)
diuretics
3. LUNGS - CALM & QUIET 4. GI - BUCK WILD! HYPER:
monitor VS
Depressed Shallow respirations Diarrhea diabetic
monitor
4. GI - CALM & QUIET *remember chvosteks sign ketoacidosis
LOC/neuro
Hypoactive bowel sounds (contraction of facial muscle) and addisions disease
trousseau’s sign (carpal spasm) dehydration
kidney disease
HYPER: HYPER:
assessment for excessive
etiology supplements
HYPERcalcemia
correct (antacids)
SWOLLEN & SLOW - Hypocalcemia
monitor heart immobilizations
MOANS, 1. T - Trousseau’s
function multiple
GROANS & STONES T - Twerking arm with
Calcium (Ca+) monitor signs and myeloma
Keeps the 3 1. CONSTIPATION BP cuff on
2.10 – 2.50 B’s strong: 2. BONE PAIN 2. C - Chvostek’s
symptoms thiazide diuretics
feces, mucosal cells, Bones 3. STONES Renal Calculi C - Cheek smile when
saliva, gastric juices, HYPO:
Blood (kidney stones) touched
bile, and pancreatic HYPO: excessive
Beats (heart) 4. DEEP TENDON 3. Diarrhea
juices assessment for laxatives
REFLEXES 4. Circumoral tingling
etiology metastatic
Decreased DTR 5. Weak bones
supplementation cancers
Severe muscle weakness
monitor heart MSK disorders
function
monitor signs and
symptoms

Phosphorus Helps with HYPERphosphatemia Hypophosphatemia HYPER: HYPER:

bone and ‘’LOW CALCIUM’’ BAJA Swollen & SLOW - MOAN, Decrease intake of renal failure
(P-) teeth CA+ GROANS & STONES phosphorus food excessive
.97 – 1.45 formation. 1. TROUSSEAU’S SIGNS 1. CONSTIPATION increase water indigestion
excreted Essential for 2. CHVOSTEK’S SIGNS 2. DECREASED DTR & intake large vitamin D
through urine muscle, 3. DIARRHEA SEVERE calcium intake
RBC, and 4. WEAK B’s MUSCLE WEAKNESS supplements chemotherapeuti
nervous Strong bones? 3. DECREASED HR, RR phosphate binding c agents
system. WEAK! (fractures) 4. INCREASED BP agents enemas
Helps HYPO:
regulate alcohol
calcium: Strong blood clotting? withdrawal
Ca HIGH= WEAK! (risk for bleeding) HYPO: malabsorption
phosphate Strong heart beats? increase ketoacidosis
low WEAK! (cardiac dysthymias) phosphorus high respiratory
Ca LOW= food (dairy) alkalosis
phosphate IV admin of total parental
high sodium phosphate nutrition
 Fluid Volume Deficit/ Dehydration
equal loss of water and electrolytes
Dehydration is depletion of whole-body fluid
Hypovolemia is decreased volume of fluid in the vascular
system with or without whole body fluid depletion Lab values:
increased serum osmolality
Manifestations: increased Hct (increased amount of
Irritability * rbc in the volume, if increased then
Confusion (impaired mental status) blood is getting thicker due to fluid
* loss)
seizure, coma * increased urine specific gravity (is
dizziness the urine more concentrated?)
CAUSES: weakness increase or decrease of serum Na
Prolonged fever extreme thirst depending of cause of FVD
polyuria (hyperglycaemia) dry skin/mucous membrane decreased serum potassium
NG suction sunken eyes
Wounds low BP with high HR
Diminished kidney function low urine output
orthostatic hypotension
weight loss
SHOCK
HYPOVOLEMIA NURSING MANAGEMENT:
ABC’s, VS, Safety (mental status)
Nursing management: lower HOB to slow declining BP
monitor weight (*most reliable measurement) direct pressure if bleeding and elevate as needed
monitor VS (*postural hypotension present/ increased Maintain patent IV access
temp/insensible loss) IV fluids, vasopressors, blood transfusion
assess breath sounds CWMS
assess skin turgor I&O, catheterization
prevent skin breakdown weights
admin fluids expect labs, EKG, ABG, x-rays
monitor for shock
 Hypervolemia
usually results from Na and water retention
retention or excessive intake of fluid or Na or shift from interstitial space to intravascular space

Manifestations:
tachypnea Management:
dyspnea bedrest, o2 therapy
crackles*, frothy cough* oral and parenteral fluid intake restriction
rapid bounding pulse diuretics
distended neck and hand veins Lab values: Na intake restriction
acute weight gain lowered serum osmolality if pulmonary edema, morphine and NTG
edema lowered Hct and Hgb to reduce congestion and amount of blood
heart failure (S3 heart sound) decreased urine specific returning to heart
gravity MONITOR RESPONSE TO TX
lowered K+ and BUN VS, hemodynamic status, edema
chest x-ray reveals pulmonary respiratory assess, watch venous
congestion distention
I&O, catheterization, IV access for meds
ensure fluid restriction if ordered
monitor labs
O2 therapy, rise HOB
weights
skin care
emotional support, teaching
 Regulation of water balance

Hypothalamic regulation
a fluid deficit or an increase in plasma osmolality is sensed by the hypothalamic osmoreceptors which then stimulates thirst and ADH release
Hypothalamic ADH which is stored in the pituitary gland induces water reabsorption in the renal distal and collecting tubules
These factors result in increased free water in the body and decreased plasma osmolality. Once the plasma osmolality is normalized, secretion of
ADH is suppressed, and thus urinary excretion is restored

Role of kidneys:
Cells reabsorb bicarbonate from the urine back to the blood and they secrete hydrogen back into the urine. By adjusting the amounts of reabsorbed
and secreted they balance the blood streams pH

ADH:
causes kidneys to release less water, decreasing the amount of urine produced. A high ADH level cause the body to produce less urine and vise
versa.

Renin and angiotensin:

associated with blood pressure regulation by managing the levels of sodium and potassium in your blood.

Atrial Natriuretic peptide:

acts acutely to reduce plasma volume by at least 3 mechanisms: increased renal excretion of salt and water, vasodilation, and increased vascular
permeability

Acid-base imbalances: Respiratory Acidosis

Pathophysiology: Lab findings:

Common causes: CO2 retention by lungs from decreased plasma pH
COPD hypoventilation compensatory increased PaCO2, HCO3- normal
barbiturate or sedative response to HCO3- retention by (uncompensated)
overdose kidneys increased HCO3- (compensated)
 Clinical manifestations: (increased PCO2)
drowsiness, disorientation, dizziness,
headache, coma
lowered BP, Vfib, warm flushed skin
hypoventilation with hypoxia
Nursing interventions:
admin oxygen
encourage coughing/deep breathing
suction (pneumonia)
hold respiratory depression drugs
watch potassium levels (hyperkalemia)

Acid-base imbalances: Respiratory Alkalosis

Common cause: Pathophysiology: Lab results:

hyperventilation (cause by hypoxia, increased CO2 excretion by lungs increased plasma pH
pulmonary emboli, anxiety, fear, pain, from hyperventilation decreased PaCO2, HCO3- normal
fever) compensatory response of HCO2- (uncompensated)
stimulated respiratory centre caused excretion by kidneys HCO3- (compensated)
urine pH over 6 (compensated)
 Clinical manifestations: Nursing Interventions:
lethargy, light-headedness, confusion breathing techniques to slow breathing
tachycardia, dysrhythmias related to watch potassium levels (hypokalemia)
hypokalemia make sure p/t’s on mechanical ventilation
nausea, vomiting, epigastric pain are not being hyperventilated
tetany, numbness, tingling of
extremities, hyperreflexia, seizures
hyperventilation (lungs are unable to
compensate when there is a respiratory
problem)

Acid-base imbalances: Metabolic Acidosis

Common Cause: Pathophysiology: Lab results:

diabetic ketoacidosis gain of fixed acid, inability to decreased plasma pH, PaCO2
lactic acidosis excrete acid or loss of base normal (uncompensated)
starvation compensatory response of CO2 decreased PCO2
severe diarrhea excretion by lungs (compensated)
renal failure decreased HCO3-
gastro-intestinal fistulas urine pH less than 6
shock (compensated)
 Nursing interventions:
assess other electrolyte levels
Clinical Manifestations: (especially potassium as it will be high
drowsiness, confusion, headache, coma but when it resolves there will be an
decreased BP, dysrhythmias (related to extracellular to intracellular shift of K+
hyperkalemia from compensation) back into the cell which will cause
warm, flushed skin hypokalemia)
nausea, vomiting, diarrhea, abdominal pain watch neuro status
deep, rapid respiration (compensation action by dialysis may be needed if p/t is
the lungs) experiencing acidosis (renal failure)
diabetic ketoacidosis (admin insulin to
help glucose go back into the cell which
will help the body start regulating how it
metabolizes glucose)

Acid-base imbalances: Metabolic Alkalosis

Common Cause: Pathophysiology: Lab results:

severe vomiting loss of strong acid or gain of base increase in plasma pH, PaCO2
excess gastric suctioning compensatory response of CO2 normal (uncompensated)
diuretic therapy retention by lungs increase in PCO2
potassium deficit (compensated)
excess NaHCO3 intake increase HCO3-
urine pH more than 6
(compensated)
Clinical manifestations: Nursing management:
dizziness, irritability, nervousness, give antiemetics for vomiting, stop
confusion diuretics
tachycardia, dysrhythmias (related to monitor potassium and chloride levels
 Acid-Base normal
values:
pH: 7.35 – 7.45
PCO2: 35 – 45
Bicarbonate (HCO3-) level: 21
– 28
PO2: 80 – 100
base excess: 0 +/= 2.0