Week 1 - Fluid and Electrolytes Student Version NRSG 311 PDF

FLUID AND ELECTROLYTES NRSG 311 – WEEK 1 Created by LT RN 2025 Formatting revisions RS Winter 2025  HOMEOSTASIS Need proper balance of fluid and electrolytes in our body to maintain equilibrium in internal environment of the body. Composi...

FLUID AND ELECTROLYTES NRSG 311 – WEEK 1 Created by LT RN 2025 Formatting revisions RS Winter 2025  HOMEOSTASIS Need proper balance of fluid and electrolytes in our body to maintain equilibrium in internal environment of the body. Composition of body fluids needs to be kept within narrow limits Important for nurses to anticipate potential for fluid and electrolyte imbalances and intervene with appropriate action 2 LT Winter 2025  H20 Water makes up 60% of body weight. Water content varies with sex, body mass and age. Lean body mass has a higher per cent of water than adipose tissue In older adults, water content is lower because of decreased mass 3 LT Winter 2025  REGULATION OF WATER BALANCE Maintained by balance of intake and excretion A body fluid deficit or increase in plasma osmolality is sensed by hypothalamic osmoreceptors  stimulate thirst and ADH release ADH is stored in pituitary, acts on distal and collecting tubules of kidney to reabsorb water When plasma osmolality is Photo retrieved from osmosis.org 2024 4 normalized, ADH is suppressed LT Winter 2025  DO YOU DRINK ENOUGH WATER? Normally, 900ml of water is lost per day due to insensible water loss. The kidneys produce about 1.5L of urine every day 5 LT Winter 2025  WHAT TYPE OF PATIENTS ARE AT RISK FOR THE DEVELOPMENT OF HYPEROSMOLALITY? A Patient who cannot recognize a sensation of thirst… TBI or neurological disorders Alzheimer's Elderly Diabetes Certain Antipsychotics Altered kidney function Hormonal imbalances: 6 Addisons (SIADH) LT Winter 2025 MECHANISMS OF WATER BALANCE IN THE BODY Hypothalamic and Pituitary Regulation Body fluid deficit or increase in plasma osmolality triggers thirst  ADH secretion. ADH released by hypothalamus and stored in pituitary Acts on tubules of kidney to retain water Once plasma osmolality restored  ADH suppressed, urinary excretion restored 7 LT Winter 2025  MECHANISMS OF WATER BALANCE IN THE BODY Adrenal Cortical Regulation Aldosterone (mineralocorticoid): potent sodium retaining and potassium excreting effect A decrease in renal perfusion or decrease in sodium in the distal portion of the renal tubule activates RAAS  releases aldosterone Aldosterone increases sodium and water reabsorption in the renal distal tubules  plasma osmolality to decrease and fluid volume to be restored. 8 LT Winter 2025  MECHANISMS OF WATER BALANCE IN THE BODY Cardiac Regulation Atrial natriuretic factor (ANF): hormone released by cardiac atria in response to increased atrial pressure and high serum sodium levels Primary actions of ANF: vasodilation and increased urinary excretion of sodium and water  decreases blood volume. 9 LT Winter 2025  NCLEX STYLE QUESTION Following a head injury that has affected a patient's pituitary gland and thus ADH secretion, the nurse is aware to monitor for signs and symptoms of fluid overload. What are some of the clinical manifestations a patient might experience if they have too much ADH secretion? Select all that apply a) Decreased Urine output b) Nausea and vomiting c) Weight gain d) Development of crackles in their lung fields e) All of the above 10 LT Winter 2025  ANSWER E. All the above Why does this patient have nausea and vomiting? 11 LT Winter 2025  With the retention of water, what is happening to their osmolality and subsequent electrolyte balance? Are they Hypo or Hypernatremic? 12 LT Winter 2025  NCLEX STYLE QUESTION A 75-year-old lady is admitted to IPU following several days of vomiting and diarrhea at home. Family has brought her in as they are concerned. Her VS are BP 90/60mmhg, HR 110, RR 22. Skin turgor: mild tenting noted in the forearm. Dry mucous membranes and cracked lips. What orders do you anticipate receiving from the physician? Select all that apply. a) Orally rehydrate giving PRN antiemetics as needed b) Start an IV and administer 500 cc fluid bolus over 2 hours and then 100cc/hr following the bolus c) Insert Foley catheter to be able to closely monitor urine output d) Obtain a CBC and lytes the next morning e) Carefully monitor cognitive status and report changes from baseline13 LT Winter 2025  ANSWERS B, C, E Why might we avoid inserting a foley catheter on this patient? 14 LT Winter 2025  ELECTROLYTES LT Winter 2025  SODIUM Main cation of the ECF Changes in Sodium are associated with parallel changes in osmolality Sodium is important in generation and transmission of nerve impulses and the regulation of acid base balance. Typical daily intake of sodium far exceeds the body’s daily requirements Sodium leaves the body through sweat, urine and fecies. Remember water follows sodium!! 16 LT Winter 2025  HYPERNATREMIA Serum sodium may become elevated because of water loss or sodium gain Hypernatremia not typically a problem for a person who can sense thirst and is able to swallow Often result of impaired LOC or inability to obtain fluids May also be caused by deficiency in synthesis of ADH, its release from the pituitary, or a decrease in kidney responsiveness to ADH  profound diuresis, water deficit, and hypernatremia 17 LT Winter 2025  HYPERNATREMIA: SYMPTOMS Dehydrati Thirst on of Lethargy neurons Agitation leads too… Seizures Dry swollen tongue Normal or Increased ECF volume Weight Gain Peripheral and pulmonary edema Increased BP 18 LT Winter 2025  HYPERNATREMIA: MANAGEMENT AND NURSING INTERVENTIONS Hypernatremia is caused by either water loss or sodium gain Goal: treat the underlying cause Water deficit: fluid replacement orally or by IV with isotonic fluids to reduce serum levels gradually and minimize risk of cerebral edema Sodium Excess: dilute sodium with IV fluids such as 5% dextrose in water to promote excretion of sodium by administering diuretics Oral sodium restriction Pay attention to fluid intake and losses 19 LT Winter 2025  CLINICAL SCENARIO It’s been a busy night on IPU. The unit was short two nurses and the floor was over-sensus. The nurse giving you report on your patient mentions that new orders were written for Mrs. Wentworth last evening, but due to the lack of resources and other deteriorating patients, the nurse ran out of time to check them. You review the orders immediately and discover that Mrs. Wentworth’s IV of NaCl 0.9 % should have been discontinued 10 hours ago. She has poor kidney function and a reduced GFR, so you stop the infusion immediately. Her CBC that morning reveals an elevated sodium level of 152mmol/L 20 LT Winter 2025  WHAT IS YOUR PRIORITY ACTION? Perform vital signs, assess for fluid overload measure urine output Notify doctor Inform Management/charge nurse of med error Complete a PSLS 21 LT Winter 2025  CLINICAL SCENARIO Mrs. Wentworth reports increased SOB this morning and new onset swelling in her hands and feet. Fine crackles can be auscultated throughout her lower lung fields. Heart sounds are regular, no S3 S4 audible. VS are BP 140/90, RR 22, HR 99, SP02 94%, Temp 36.8 22 LT Winter 2025  WHAT ARE YOU ANTICIPATING THE DOCTOR ORDERING Administering a loop diuretic to promote sodium and water excretion. Encourage oral water intake Limit dietary sodium intake 23 LT Winter 2025  THE DOCTOR ORDERS: 20mg of IV furosemide now 24 LT Winter 2025  WHAT DO WE KNOW ABOUT FUROSEMIDE ? What route do we want to give this medication given her current status? 25 LT Winter 2025  FUROSEMIDE IS Potassium Wasting!! Risk of Autotoxicity if pushed too fast 26 LT Winter 2025  CAN YOU THINK OF ANY OTHER NURSING DIAGNOSIS FOR MRS. WENTWORTH 27 LT Winter 2025  HYPONATREMIA May result from a loss of sodium containing fluids, water excess, or combination. The body attempts to compensate by shifting fluid out of the ECF and into the cells, leading to cellular edema Common causes are use of hypotonic fluids following a major trauma or surgery, during administration of fluids in patients with renal failure 28 LT Winter 2025  HYPONATREMIA: SYMPTOMS Due to cellular swelling Nonspecific neurological symptoms, headache, irritability, difficulty concentrating More severe confusion, vomiting, seizures and coma. 29 LT Winter 2025  HYPONATREMIA: MANAGEMENT AND NURSING INTERVENTIONS Infusion of hypertonic saline Monitor serum sodium levels, patient response Rapidly increasing levels of sodium can cause osmotic demyelination syndrome with permanent damage to nerve cells influid May require the restriction brain 30 LT Winter 2025  WHAT ARE SOME EFFECTIVE WAYS TO MONITOR FOR SODIUM AND VOLUME IMBALANCES Cardiovasc Intake and Respiratory ular output Changes changes Skin Neurologica Daily Assessment l Changes Weights and Care 31 LT Winter 2025  POTASSIUM K + is major ICF cation Potassium is critical for many cellular metabolic functions: Transmission of nerve impulses Maintenance of normal cardiac rhythms Skeletal smooth muscle contraction 32 LT Winter 2025  POTASSIUM Diet is the typical source of potassium: fruit, dried fruits, vegetables Kidneys are primary route for potassium loss Plays a role in acid base balance Sodium and Potassium have inverse relationship: Factors that can cause sodium retention can cause potassium loss Large urine volumes can be associated with potassium loss Body has poor ability to conserve potassium even when stores are low 33 LT Winter 2025  FACTORS THAT CAUSE POTASSIUM TO SHIFT ECF - ICF ICF- ECF Insulin Trauma Alkalosis Acidosis B-drenergic stimulation Exercise (stress, coronary ischemia) Digoxin 34 LT Winter 2025  HYPERKALEMIA May be caused by: Massive intake of potassium Impaired renal excretion Shift from ICF to ECF Massive burn or crush injury Certain drugs – spironolactone, ACE inhibitors ** most common cause is renal failure. 35 LT Winter 2025  HYPERKALEMIA: SYMPTOMS Causes membrane depolarization, altering cell excitability, causing them to become weak and paralyzed. First signs are leg cramping ECG findings may be a tall peaked T wave, Wide QRS and prolonged PR interval (don’t worry- we will explore this in NRSG 415) Heart Block, V-Fib 36 LT Winter 2025  HYPERKALEMIA: MANAGEMENT AND NURSING INTERVENTIONS Eliminate oral and parenteral potassium intake Increase diuretics, dialysis, kayexalate Force K+ from the ECF to the ICF. (IV insulin) or by administration of IV sodium bicarb in the correction of acidosis Increasing fluid intake may enhance renal elimination Patient with mild increase may be fine to have dietary potassium decreased and increase use of fluids and diuretics. Moderate increase will require shift of potassium back into cells 37 LT Winter 2025  HYPOKALEMIA Can result from abnormal loss due to shift from the ECF to ICF or deficiency in dietary intake Most common cause is patients with diuresis, when circulating blood volume is low Causes sodium retention and loss of potassium in urine Low serum Mg contributes to potassium depletion Low plasma Mg stimulates renin release and increase in aldosterone  potassium excretion GI tract losses Administration of insulin 38 LT Winter 2025  HYPOKALEMIA: SYMPTOMS Alters membrane potential, associated with hyperpolarization (increases negative charge within cell) causes excitability problems in many types of tissue Flat T wave, presence of U wave Paralysis of respiratory muscles, cramping, rhabdomyolysis With prolonged hypokalemia kidneys unable to concentrate urine and diuresis occurs, release of insulin is impaired 39 LT Winter 2025  HYPOKALEMIA: MANAGEMENT AND NURSING INTERVENTIONS Develop habitual practices that remind us to be cognizant of patients’ potassium levels Check AM labs ALWAYS Always check before oral K+ administration, diuretics, digoxin Be aware of your patient's nutritional status, oral intake, fluid intake Know your diagnosis and pathology and how electrolyte balance will be affected Understand how your IV solution may cause fluid shifts 40 LT Winter 2025  CASE STUDY Mr. Brown has been admitted to hospital for an acute kidney injury following an accidental NSAID overdoes when he mixed up his medications. Mr. Brown was pleasant and cooperative this morning when you did you 0730 assessment. VS stable and unremarkable. Lab calls at 10am with a critical high. Mr. Browns potassium came back as 6.8mmol/l. 41 LT Winter 2025  WHAT ARE YOUR IMMEDIATE ACTIONS ? SELECT ALL THAT APPLY. a) Perform a set of VS and immediate focused Cardiac assessment b) Notify the Doctor c) Prepare for a stat ECG d) Ensure IV access e) Anticipate administration of a potassium wasting loop diuretic 42 LT Winter 2025  ANSWER B, C, D 43 LT Winter 2025  THE DOCTOR ORDERS AN IV INSULIN INFUSION 44 LT Winter 2025  THE DOCTOR ORDERS 25 GRAMS DEXTROSE IV FOLLOWED BY 20 UNITS OF INSULIN OVER 2 HOURS. WHAT SIZE OF MINI BAG ARE WE CHOOSING AND HOW MANY ML DO WE WANT TO INFUSE? 45 LT Winter 2025  AS PER THE MONOGRAPH, HOW OFTEN WILL WE BE CHECKING MR. BROWNS BLOOD GLUCOSE? 46 LT Winter 2025  I WANT YOU TO KNOW THIS !! 47 LT Winter 2025  CALCIUM Calcium is obtained from ingested foods balance controlled by PTH, calcitonin and Vit D PTH increases bone resorption Calcitonin opposes PTH by decreasing GI absorption and increasing excretion Vit D is necessary for absorption from GI tract More than 99% of body’s calcium is combined with phosphorous and concentrated in skeletal system Calcium and phosphorous have inverse relationship, as one increases other decreases Calcium plays important role in blood clotting, transmission of nerve impulses, formation of teeth and bone and muscle contraction 48 LT Winter 2025  HYPERCALCEMIA More than 90% of cases caused by hyperparathyroidism and malignancy Excess calcium blocks effect of sodium in skeletal muscle  reduced excitability of muscles and nerves Symptoms: Impaired memory Confusion, disorientation Fatigue Muscle weakness Constipation Cardiac dysrhythmias Renal calculi. 49 LT Winter 2025  TREATMENT OF HYPERCALCEMIA Promote excretion of Calcium in urine with loop diuretic (e.g. Lasix) Hydration of patient with isotonic saline Administration of synthetic calcitonin Careful monitoring if sodium and fluid overload are necessary for patients with impaired renal function 50 LT Winter 2025  HYPOCALCEMIA Can be caused by any condition that causes decrease in PTH Could be due to injury to thyroid glands in neck after surgery Due to sudden alkalosis as causes calcium to bind to protein Low calcium levels allow sodium to move into cells, increases depolarization  increased nerve excitability and sustained muscle contraction 51 LT Winter 2025  CHVOSTEK’S SIGN contraction of facial muscles due to a light tap on the facial nerve by the ear Image retrieved from: ihealthblogger.com, 52 December 2024. LT Winter 2025  TROUSSEAU’S SIGN carpal spasms induced by inflating a blood pressure cuff on the arm Image retrieved from osmosis.org, December 2024 53 LT Winter 2025  TREATMENT OF HYPOCALCEMIA Correcting underlying condition Mild imbalance: calcium rick foods, Vit D supplementation Severe Imbalances: IV preparations of calcium Any patient who undoes thyroid surgery must be monitored closely for manifestations of hypocalcemia due to proximity to parathyroid glands 54 LT Winter 2025  PHOSPHATE IMBALANCES Phosphorous is primary anion of ICF Essential to muscle function, RBCs, and bone and tooth structure Involved in acid base buffering system For maintenance of normal phosphate balance, renal function must be adequate 55 LT Winter 2025  HYPERPHOSPHATEMIA Caused by acute or chronic renal failure that results in kidneys inability to excrete phosphorous. Chemotherapy, malignancies, excessive injection of milk Manifestations: CNS dysfunction, rhabdomyolysis, cardia dysrhythmias, muscle weakness, calcium- phosphate deposits in soft tissue, joints. 56 LT Winter 2025  TREATMENT OF HYPERPHOSPHATEMIA Adequate hydration Restricting foods that contain phosphorous Correction of hypocalcemia conditions 57 LT Winter 2025  HYPOPHOSPHATEMIA Commonly seen in patients who are malnourished or have malabsorption Alcohol withdrawal Use of phosphate binding antacids Clinical manifestations: relate to deficiency of ATP, hemolytic anemia, muscle weakness 58 LT Winter 2025  TREATMENT OF HYPOPHOSPHATEMIA Supplementation of high phosphorous containing food (e.g. dairy) IV treatment of severely low levels Frequent serum level monitoring to guide IV therapy 59 LT Winter 2025  MAGNESIUM IMBALANCES Most abundant intracellular cation, important role in intracellular processes Cofactor for many enzymes Carbohydrate metabolism DNA and protein synthesis Manifestations often confused with calcium imbalance as magnesium closely related to potassium and calcium; all three cations should be assessed together 60 LT Winter 2025  HYPERMAGNESEMIA Commonly associated with patients who have chronic renal failure or ingesting products containing magnesium (milk of magnesia) Excessive magnesium inhibits acetylcholine release at myneural junction and calcium movement into cells, impairing nerve and muscle function Manifestations: hypotension, facial flushing, lethargy, urinary retention, nausea and vomiting. As serum magnesium levels increase, deep tendon reflexes are lost, followed by muscle paralysis and coma Respiratory and Cardiac arrest can occur 61 LT Winter 2025  TREATMENT OF HYPERMAGNESEMIA Avoid magnesium containing medications Limit diet intake of nuts, bananas, oranges, and peanut foods If renal function adequate, increased fluids and diuretics promote urinary excretion In patients with impaired renal function, dialysis may be necessary If hypermagnesemia is symptomatic, calcium gluconate administered by IV infusion. This opposes the effect of magnesium on cardiac muscle 62 LT Winter 2025  HYPOMAGNESEMIA Occurs in patients with limited magnesium intake or increased GI or renal losses. Starvation, chronic alcoholism, uncontrolled diabetes Manifestations mirror hypocalcemia: neuromuscular manifestations, muscle cramps, tremors, hyperactive deep tendon reflexes, Chvostek’s sign, trousseaus sign Can lead to cardiac dysrhythmias 63 LT Winter 2025  TREATMENT OF HYPOMAGNESEMIA Oral supplements, or increasing nutritional intake IV or IM MgS04 Too rapid an infusion can lead to hypotension and cardiac or respiratory arrest 64 LT Winter 2025  BREAK 65 LT Winter 2025  IV FLUIDS Commonly used to treat many different fluid and electrolyte imbalances Many patients need maintenance IV fluid therapy for losses that have already occurred 66 LT Winter 2025  HYPOTONIC SOLUTIONS Provide more water than electrolytes, thus diluting ECF and causing movement of water from ECF to ICF Maintenance fluids are often hypotonic because normal daily losses are hypotonic 67 LT Winter 2025  HYPOTONIC SOLUTIONS May cause cellular swelling What kind of patient would we NOT want to have this type of solution? 68 LT Winter 2025  EXAMPLES OF HYPOTONIC SOLUTIONS D5W isotonic but physiologically hypotonic 0.45% NaCl 69 LT Winter 2025  ISOTONIC SOLUTIONS Administration of an isotonic solution expands only the ECF, no net loss or gain from the ICF Isotonic solution is ideal fluid replacement for ECF deficit 70 LT Winter 2025 EXAMPLES OF ISOTONIC SOLUTIONS D5W – sort of 0.9% NaCl Lactated Ringers 71  WHEN MIGHT AN ISOTONIC SOLUTION BE CONTRAINDICATED? NaCl Lactated Ringers: similar in concentration to plasma except does not contain Cl-, Mg2, and HC03- 72 LT Winter 2025  HYPERTONIC SOLUTIONS Initially raises osmolality of ECF and expands it Can be useful in treatment of hyponatremia and hypovolemia May be used in cases when a patient has ICP to draw fluid out of brain tissue and reduce swelling (mannitol) 73 LT Winter 2025  EXAMPLES OF HYPERTONIC SOLUTIONS D10W 3.0% NaCl D5W in 0.45% NaCL D5W in 0.9% NaCl 74 LT Winter 2025  CONTRAINDICATIONS When might a Hypertonic solution be contraindicated? If a patient is dehydrated If a patient if hypernatremic If a patient has HF or is at risk of fluid overload If a patient has renal impairment 75 LT Winter 2025  ACID BASE IMBALANCES 76 LT Winter 2025  ACID BASE IMBALANCES PH 7.34-7.45 Patients with DM, COPD, and Kidney disease are at risk for acid base imbalances Due to the body’s metabolic processes, acids are constantly produced. The body has 3 mechanisms in which it regulates acid base balance. The buffer 77 system, the respiratory system, and the LT Winter 2025  THE BUFFER SYSTEM Reacts immediately to increase in H+ concentration Reaches maximum effectiveness within a few hours Buffers act to chemically neutralize strong acids by shifting H+ in and out of cell Carbonic acid, phosphate, protein, and hemoglobin Buffers minimize effect of acids on blood PH until they can be excreted from body When ECF levels of H+ are increased, H+ enters cell in exchange for potassium. This is why Alkalosis can cause hyperkalemia 78 LT Winter 2025  THE RESPIRATORY SYSTEM Lungs help maintain PH of body by excreting CO2 and water Amount of CO2 in blood directly relates to carbonic concentration and H+ Increased respiration rate leads to less CO2 in blood, leads to less carbonic acid and fewer H+ molecules Decreased respiration rate leads to increased carbonic acid and more H+ in blood 79 LT Winter 2025  THE RESPIRATORY SYSTEM The Respiratory system will attempt to compensate for change in PH through hyperventilation or hypoventilation If PH problem is due to respiratory condition, i.e. respiratory failure, respiratory system cannot meet usual role in pH correction 80 LT Winter 2025  LET’S LOOK AT THE EQUATION 81 LT Winter 2025  RENAL SYSTEM Normal conditions, kidneys: Reabsorb and conserve bicarb they filter Generate additional bicarb Eliminate excess H+ as a compensation for acidosis If kidneys are cause of PH disturbance, e.g. renal failure, lose ability to correct pH Kidneys have 3 mechanisms for acid elimination Secretion of H+ in renal tubule Combining H+ with ammonia to form ammonium Excretion of weak acids 82 LT Winter 2025  RESPIRATORY ACIDOSIS What does this Mean? What would we expect to see on our lab values? 83 LT Winter 2025  RESPIRATORY ACIDOSIS Blood pH 45mm hg Common Causes include: COPD, Hypoventilation Barbiturate overdose Severe pneumonia Atelectasis, respiratory muscle weakness 84 LT Winter 2025  SYMPTOMS OF RESPIRATORY ACIDOSIS Drowsiness Disorientation Dizziness Headache Coma Decreased BP, Vfib related to hyperkalemia from compensation, warm flushed 85 skin due to vasodilation LT Winter 2025  RESPIRATORY ALKALOSIS What does this mean? What will our lab findings reflect? 86 LT Winter 2025  RESPIRATORY ALKALOSIS High blood PH (>7.45), low paCO2 (