Electrolyte Imbalances Flashcards
Major electrolyte found in ECF. Essential for acid-base, fluid balance, active and passive transport mechanism, irritability and conduction of nerve-muscle tissue
Sodium (Na+)
Explain thirst compensatory mechanism
Experience dehydration
Decrease in blood volume
Increase in Na+ osmolality (concentration)
Osmoreceptors in hypothalamus stimulates thirst centre
Pituitary releases ADH to increase water absorption in kidney to decrease osmolality and increase ECF volume
Explain ADH mechanism in response to low blood volume and increased blood osmolarity
Hypothalamus as a receptor responds to stimuli
Hypothalamus stimulates posterior pituitary to release ADH into the blood
ADH binds to effectors:
Hypothalamus - activating thirst centre to stimulate fluid intake increasing blood volume and pressure
Kidneys- increase water reabsorption, decrease water loss in kidneys to maintain blood volume and decrease blood osmolarity
Blood vessels - cause vasoconstriction to increase peripheral resistance and bp
Explain RAAS compensatory mechanism in response to low blood pressure and sympathetic division stimulation
Receptor juxtaglomerular apparatus responds to stimuli
JG apparatus release renin enzyme into the blood
Renin activates angiotensinogen to AT I
Angiotensin converting enzyme (ACE) in the lungs converts AT I to AT II
AT II binds to effectors:
Systemic blood vessels - causing vasoconstriction increasing peripheral resistance and increasing BP
Kidneys - decrease glomerular filtration rate (GFR), decreasing UO to maintain blood volume and BP
Hypothalamus - activate thirst centre to increase fluid intake, release ADH to maintain blood volume and decrease UO
Adrenal cortex - release aldosterone to maintain blood volume and decrease UO
Explain Aldosterone mechanism in response to decreased Na+ and increased K+ blood plasma levels
Receptor adrenal cortex responds to stimuli
Adrenal cortex releases aldosterone into the blood
Aldosterone binds to effectors:
Kidney - to increase Na+/ H20 reabsorption into blood, decrease Na+/H20 and increases K+ UO, increases K+ secretion into tubular fluid
Na+ is maintained and K+ decreases in the blood plasma, therefore, blood volume and BP is maintained
S&S of fluid volume deficit
Low BP and high HR Dry mouth, thirsty Rapid weight loss Low UO Confusion and lethargic
Nursing intervention for fluid volume deficit
Oral fluids
IV (normal saline - no K until UO is increased)
daily weight and strict vital signs
causes of fluid volume excess
Hypervolemia - too much IV fluid, kidney failure, corticosteroids
Water intoxication - CHF, ADH problems
Excess sodium intake - salt intake excess
S&S of fluid volume excess
rapid weight gain Oedema High BP, bounding pulses Increased UO JVD, crackles and dyspnea
Nursing intervention for fluid volume excess
Diuretics
fluid restriction (no IV fluids)
sodium intake restriction
daily weights and strict I&O
Causes of Hypernatraemia
Excess Na+ intake
Inadequate H2O intake
excess water loss
Hypernatraemia results in
fluid shift from ICF to ECF where water follows sodium
S&S of Hypernatraemia
Thirsty Fever (flushed skin) Restless, anxious, confused and irritable Increased BP and fluid retention Pitting oedema Decreased UO
Nursing intervention for Hypernatraemia
Restrict Na intake
Diuretics
Seizure precautions
Dialysis if severe
Causes of Hyponatraemia
excess water and loss of Na Increased Na excretion due to diaphoresis, diarrhoea, NGT suction and diuretics Low Na diet Kidney failure Heart failure
S&S of Hyponatraemia
Stupor/ coma anorexia lethargy tachycardia Limp muscle weakness orthostatic hypotension seizures/ headache stomach cramping
Nursing intervention for Hyponatraemia
Add Na to diet
administer IV sodium chloride infusions (hypovolemia)
administer diuretics (hypervolemia)
restrict fluid if caused by hypervolemia
Daily weights for fluid excess (as where Na goes H2O follows)
Safety precautions for orthostatic hypotension
Limit water intake
Causes of Hyperkalemia
Kidney failure Medications - potassium sparring diuretics, ACE inhibitors, NSAIDs Tissue damage Acidosis Hypoxia Hypercatabolism Hyperuricemia
S&S of Hyperkalemia
Muscle cramps & weakness
Urine abnormalities - oliguria (low UO) and anuria (inability to produce urine in the kidney)
Respiratory distress
Decreased cardiac contractility (Low HR & BP)
ECG changes (tall T waves, flat P waves, widened QRS complexes and prolonged PR intervals)
Reflexes increases DTR (deep tendon reflexes)
Causes of Hypokalemia
Loss of total body K
inadequate K intake
Vomiting and diarrhoea
NG suction
Alkalosis and Hyperinsulinism causing the movement of K from ECF to ICF
Dilution of serum K caused by water intoxication and IV therapy with K deficient solution
S&S of Hypokalemia
Dysrhythmias (thready, weak and irregular pulse)
Orthostatic hypotension
shallow RR
anxiety, lethargy, confusion and coma
paresthesias (prickling sensation to extremities)
Hyporeflexia (decreased reflex response)
Constipation
N&V
ECG changes (ST depression, inverted T wave and prominent U wave)
Nursing intervention for Hyperkalemia
Monitor ECG Discontinue potassium IV and PO Restrict K diet Administer K excreting diuretics Administer IV Ca gluconate & IV Na bicarb Dialysis
Nursing intervention for Hypokalemia
Monitor ECG
Administer PO K supplements, liquid potassium chloride and potassium retaining diuretic
K is NEVER administered via IV push, IM and subQ (IV potassium is always diluted & administered using an infusion device)
Potassium imbalance if not treated can cause
Cardiac Dysrhythmias which is life threatening
Major extracellular electrolyte, controls and regulate water balance. Where ______ goes water follows.
Sodium (Na)
Major intracellular electrolyte which helps maintain intracellular water balance. Transmit nerve impulses to muscles and contract skeletal and smooth muscles.
Potassium (K)
Plays a vital role in cell metabolism and transition of nerve impulses, the functioning of cardiac, lung, muscle tissues and acid-base balance.
Potassium (K)
found in the body’s cells, bones and teeth. Needed for proper functioning of the cardiovascular, neuromuscular, endocrine systems, blood clotting and teeth formation.
Calcium (Ca+)
Causes of Hypercalcemia
Increased calcium absorption and decreased calcium excretion
Kidney disease
Thiazide diuretics
Increased bone resorption of calcium - Hyperthyroidism
Hemoconcentration
S&S of Hypercalcemia
Bone pain
Arrhythmias (irregular heartbeat)
Cardiac arrest (bounding pulses)
Kidney stones (solid crystals formed in the kidneys which is often painful when passed)
Muscle weakness (decreased deep tendon reflexes)
Polyuria
Nursing intervention for Hypercalcemia
d/c IV or PO calcium and thiazide diuretics
administer phosphorus, calcitonin, bisphosphonates and prostaglandin synthesis inhibitors (NSAIDs)
restrict calcium rich diet
Causes of Hypocalcemia
Inhibition of calcium absorption from the GI tract
increased calcium excretion - kidney disease, diarrhoea, steatorrhea and wound drainage
conditions that decrease the ionised fraction of calcium
S&S of Hypocalcemia
Convulsions (violent seizure)
Arrhythmias
Tetany (involuntary muscle contractions and overly stimulated peripheral nerves)
Spasms (muscle cramps) and stridor (whistling sound from obstructed airway while breathing)
Nursing intervention for Hypocalcemia
Adm. IV or PO calcium Adm. aluminium hydroxide and Vit D Seizure precautions 10% calcium Consume calcium rich diet
mostly found in the bones which regulates BP, blood sugar, muscle contraction and nerve function
Magnesium (Mg)
Causes of Hypermagnesemia
Increased magnesium intake - laxatives and magnesium IVs
Decreased magnesium excretion in kidneys and increased magnesium levels in the blood
DKA
S&S of Hypermagnesemia
LOW: (since Mg is a sedative) energy HR BP RR (with shallow respirations) Bowel sounds DTR
Nursing intervention for Hypermagnesemia
Diuretics Adm. IV calcium chloride or gluconate Restrict Mg rich diet avoid laxatives and antacids containing Mg Hemodialysis
Causes of Hypomagnesemia
insufficient Mg intake - malnutrition, vomiting, diarrhoea
increased magnesium excretion - diuretics
Intracellular movement of Mg - hyperglycemia and insulin adm., sepsis
S&S of Hypocalcemia
High: since Mg is sedative (everything is not sedated) BP HR DTR shallow respirations Twitches and paresthesias Tetany and seizures Irritability and confusion
Nursing intervention for Hypomagnesemia
Amd Mg sulfate IV or PO
seizure precautions
Consume Mg rich diet
Ca and _____ have inverse actions
Phosphate - High Ca = Low PO4 vice versa
A pt with Ca imbalance is at risk of
Pathological Fracture - its important to move them carefully and slowly
Mg and ____ have the same effects
Ca+ where High Mg = High Ca+
Normal blood ph lvl?
7.35 - 7.45
If blood ph lvl is below 7.35?
Acidosis
If blood ph lvl is above 7.45?
Alkalosis
Shifts of plasma to interstitial fluid. Develops if an obstruction of lymphatic outflow causes decreased removal of interstitial fluid.
Oedema
applying pressure to swollen area causing an indention that persist for some time
Pitting oedema
Nursing intervention for Oedema
Daily weights
Position patient to reduce positional fluid accumulation
Record pitting oedema measurements
Administer diuretics if prescribed
Explain fluid shift in heart failure causing Oedema
Heart Damage (CAD and HTN)
Ventricular overload decreasing ventricular contraction
Tachycardia causing ventricular dilation and myocardial hypertrophy
Cardiac output is decreased = low BP
Renal perfusion is decreased
Increasing sodium retention and osmotic pressure
ADH is released increasing water reabsorption
Fluid accumulates causing Oedema
Occurs when ECF volume is decreased due to vomiting, diarrhoea, haemorrhage, burns, profuse sweating, water deprivation and diuretics abuse
Dehydration
how to assess hydration
skin turgor (decreased skin turgor occurs when it remains elevated after pinching up and released) urine colour (dark yellowish)
Occurs when there is insufficient intravascular fluid volume which leads to inadequate tissue perfusion
Hypovolaemic shock
A life threatening condition in which tissue perfusion is compromised leading to possible cell dysfunction, cell death or necrosis and organ failure.
Shock
Explain compensatory mechanisms from acute bleeding or any events leading to blood volume loss
CHEMORECEPTORS activated (by low blood pH) > affecting respiratory centres > increasing RR
BARORECEPTORS firing reduced (by low blood volume and pressure) > increasing HR > weak and thready pulse > skin is cold and clammy with cyanotic appearance
SYMPATHETIC NERVOUS SYSTEM is activated > intense vasoconstriction > decreased renal blood flow > renin is released > AT II is produced in the blood > Kidney retains water and salt > UO is reduced > increasing blood volume > maintaining BP
HYPOTHALAMUS activated (by low pH and blood volume) > Thirst centre affected > ADH is released in the blood targeting the kidneys to retain water > UO is reduced > increasing blood volume > maintaining BP
BRAIN - neurons are depressed by low pH > resulting in restlessness > central nervous system is depressed leading to coma (late sign)
Explain what happens to cellular level from acute bleeding
Inadequate tissue perfusion
Cells begin to metabolise anaerobically (not requiring O2) and lactic acid accumulates
Water begins to leave tissue cells shifting into the bloodstream leading to cell dehydration
Causes of Hypovolemic shock
Hemorrhagic (from bleeding) - trauma, GI bleed and postpartum
Non-Hemorrhagic (not from bleeding) - fluid shifts (oedema) and severe hydration (burns, vomiting, diarrhoea)
Common S&S of Hypovolemic shock
Weak and thready pulse
Decreased CO, BP (hypotension), CVP and O2 SAT
Increased HR (tachycardia to compensate increasing blood flow) and SVR (vasoconstriction)
Cyanotic appearance, cool and pale skin
Capillary refill is > 3 secs
Nursing treatment for hypovolemic shock
Large gauge IVs (at least 2) Fluids and blood replacement - Crystalloids (normal saline) - Colloids (albumin) - Blood plasma
