Fluids and Electrolytes Flashcards
Intravascular Compartment
Fluid inside the blood vessel
Intracellular Compartment
Fluid inside the cells
Extracellular Compartment
Fluid outside the cells. Can be referred to as the “third space”. Includes interstitial fluid, blood, lymph, bone, connective tissue, water and transcellular fluid.
Third Spacing
Accumulation of trapped extracellular fluid in an actual or potential body space as a result of disease or injury. The trapped fluid represents volume loss and is unavailable for normal physiological processes. Common places include the pericardial, pleural, peritoneal, abdomen and within soft tissues after trauma or burns. May not be reflected in weight or input/output.
Ansarca
Generalized edema in the interstitial space throughout the body and occurs as a result of cardiac, renal or liver failure
Who needs to be monitored closely for fluid imbalance?
THE YOUNG AND THE OLD due to the respective proportion of body water in each ( Young = more, Old = Less)
Isotonic Fluids
Goes into the vascular space and stays there.
Ex: 0.9% Normal Saline, Lactated Ringers, D5W and D5 1/4NS
Used in clients that has lost fluid through nausea, vomiting, burn, sweating and trauma
ALERT: Do not use isotonic fluids in clients with hypertension, cardiac disease or kidney disease as they can cause FVE, HTN or hypernatremia
Hypernatremia - Causes, Signs + Symptoms, Assessment and Treatment
Too much sodium and not enough water / Dehydration
Caused by : Decreased Sodium excretion ( kidney disease, corticosteroids, Cushing Syndrome, Hyperaldosteronism), Increased Sodium intake (too much isotonic fluid with Sodium), Decreased water intake, Increased Loss of Water (hyperventilation, Heat stroke, DI, vomiting and diarrhea)
Signs and Symptoms: Dry mouth, thirsty, Kidney damage and hypotension in the elderly, swollen tongue, Neurological changes
Assessment:
Cardiovascular: Heart rate and blood pressure respond to vascular volume status
Respiratory: Pulmonary edema if hypovolemia is present
Neuromuscular: Early - Spontaneous muscle twitches; irregular muscle contractions. Late - Skeletal muscle weakness, deep tendon reflexes diminished or absent
CNS: Altered cerebral function is the most common manifestation. THINK NEURO CHANGES. In normovolemia or hypovolemia : agitation, confusion, seizures. In Hypervolemia : Lethargy, stupor, coma
GI: Extreme thirst
Renal: Decreased Urinary output
Integumentary : Dry and flushed skin, Dry and sticky tongue and mucous membranes, presence or absence of edema, depending on fluid volume changes
Lab: Increased specific gravity
Treatment + Considerations:
Restrict Sodium, Dilute client with Fluids, Daily Weights, In + Outs, Lab work. If it the cause is inadequate renal excretion, administer diuretics. If you have a sodium problem, you have a fluid problem. In feeding tube clients, they tend to get dehydrated. Watch closely.
Renin-angiotensin system
Renin is an enzyme secreted into the blood from specialized cells that encircle the arterioles at the entrance to the glomeruli of the kidneys (the renal capillary networks that are the filtration units of the kidney). The renin-secreting cells, which compose the juxtaglomerular apparatus, are sensitive to changes in blood flow and blood pressure. The primary stimulus for increased renin secretion is decreased blood flow to the kidneys, which may be caused by loss of sodium and water (as a result of diarrhea, persistent vomiting, or excessive perspiration) or by narrowing of a renal artery. Renin catalyzes the conversion of a plasma protein called angiotensinogen into a decapeptide (consisting of 10 amino acids) called angiotensin I. An enzyme in the serum called angiotensin-converting enzyme (ACE) then converts angiotensin I into an octapeptide (consisting of eight amino acids) called angiotensin II. Angiotensin II acts via receptors in the adrenal glands to stimulate the secretion of aldosterone, which stimulates salt and water reabsorption by the kidneys, and the constriction of small arteries (arterioles), which causes an increase in blood pressure. Angiotensin II further constricts blood vessels through its inhibitory actions on the reuptake into nerve terminals of the hormone norepinephrine.
Hypotonic solutions
Goes into the vascular space and then shifts out into the cells to replace cellular fluid. They rehydrate but do not cause hypertension.
Ex: D2.5W, 1/2NS, 0.33NS
Uses: The client who has hypertension, renal or cardiac disease and needs fluid replacement because of nausea, vomiting, burns and hemorrhage. Also used for dilution when a client has hypernatremia and for cellular dehydration
ALERT: Watch for cellular edema because the fluid is moving out to the cells, which could lead to fluid volume deficit and decreased blood pressure.
Hypertonic solutions
Volume expanders that will draw fluid into the vasculature from the cells.
Ex: D10W, 3%NS, 5%NS, D5LR, D1/2NS, D5NS, TPN, ALbumin, MgSO4
Uses: The client with hyponatremia or the client who has shifted large amounts of vascular volume to a 3rd space or has severe burns, edema or ascites.
ALERT: Watch for fluid volume excess. Monitor in an ICU setting with frequent monitoring of blood pressure, pulse, CVP, especially if they are receiving 3% or 5% NS
Fluid Volume Excess / Hypervolemia - Causes, Signs + Symptoms, Assessment and Treatment
Too much fluid in the vascular space, causing it to leak into the third space. THINK HEART PROBLEMS FIRST. ACUTE WEIGHT GAIN IS FLUID.
Causes: Heart failure ( the heart is weak, cardiac output is down, kidney perfusion is decreased and urinary output decreases, Renal failure ( Not perfused kidneys/acute kidney injury, chronic kidney disease), SIADH, long term corticosteroid therapy, excessive sodium ingestion/administration ( Eating salt, IV fluid with NA and Sodium bicarb therapy)
Assessment:
Cardiovascular: Distended neck/ peripheral veins (full vessels), bounding pulse, tachycardia, Elevated blood pressure, elevated CVP. Can cause heart failure leading to pulmonary edema.
Respiratory: Increased shallow respirations, dyspnea, moist crackles in posterior bases, SOB.
Neuromuscular: Altered level of consciousness, headache, visual disturbances, skeletal muscle weakness, parenthesis
GI: Increased motility, diarrhea, increased body weight, liver enlargement, ascites
Renal: Decreased Urinary output if kidney damage is the cause, increased urine output if kidneys can compensate
Integumentary : Pitting edema, pale/cool skin
Lab: Decreased - Serum osmolality, Hct, BUN, serum sodium and urine specific gravity
Treatment:
Low sodium diet/restrict fluids
I&O/Daily Weights
Diuretics
- Watch lab work for electrolyte imbalances especially potassium. Thiazide - will cause hypokalemia. Spiranolactone - will cause hyperkalemia
Bed rest
-contraindicated in HF and kidney failure
-induces diuresis because water is coming back to the core by the release of ANP ( excrete NA and H2O) and decreased production of AHS. This can lead to fluid volume deficit/dehydration, causing the blood to become concentrated (clots), pneumonia and constipated
Fluid Volume Deficit/ Hypovolemia - Causes, Signs + Symptoms, Assessment and Treatment
Often problems with supply and demands. BIG TIME DEFiCITS = SHOCK.
Causes: Loss of fluid from ANYWHERE (Thoracentesis, paracentesis, vomiting, diarrhea and hemorrhage, ketoacidosis, ), Third Spacing (Burns, Ascites), Diseases with Polyuria (diabetes mellitus/ diabetes insipidus), hypotonic fluid replacement
Signs and Symptoms:
Decreased Weight, Decreased skin turgor, dry mucous membranes, decreased urine output ( kidneys aren’t perfusing or they are trying to hold onto the fluid/compensate), BP down (LESS VOLUME LESS PRESSURE) risk of orthostatic hypotension, pulse is increased and THREADY n WEAK, Respirations are UP as body perceives decreased volume as hypoxia, CVP is DOWN, flat veins, cool extremities because of vasoconstriction, urine specific is HIGH/ pee concentrated
Treatment:
Prevent fluid loss
Replace volume: mild deficit - PO, Severe - IV.
If the reason is third spacing, give hypertonic fluids to draw fluid into vacsculature.
Monitor electrolytes
Safety precautions:
Higher risk for Falls –> changes in v/s and lethargy
Monitor for overload
Anti Diuretic Hormone
Found in the pituitary gland, it makes you retain water in response to decreased blood volume.
ADH problems are usually secondary to something else; any condition that can increase ICP cause adverse AHD effects
Another name for ADH is vasopressin - the drug may be utilized as an ADH replacement in DI
Aldosterone: Where is it found? What does it do?
EQUATE TO SODIUM AND WATER
A steroid/mineralocorticoid that is found in the adrenal glands. When blood volume gets low ( vomiting, hemorrhage, diarrhea etc), aldosterone secretion increases, causing retention of sodium and water and blood volume goes UP. Also causes kidneys to excrete potassium.
Hyper: Cushings, Conn’s syndrome
Hypo: Addison’s disease (loss of Na and H2O leads to SHOCK)
Pulmonary edema
Fluid in the lungs that leads to impaired oxygen exchange and shortness of breath.
Causes: Heart Failure, Kidney failure
S/S : Blood or frothy pink sputum, Orthopnea, unable to speak full sentences, grunting/wheezing, abnormal heart sounds, increased pulse and RR, crackles on auscultation
Diabetes Insipidus
Too little ADH. Makes you lose water leading to fluid volume deficit and potentially, shock
Urine is diluted and blood is concentrated
USG is low, Sodium is high and Hct is High
Conn’s Syndrome
Primary aldosteronism is a type of hormonal disorder that leads to high blood pressure. Your adrenal glands produce a number of essential hormones. One of these is aldosterone, which balances sodium and potassium in your blood.
In primary aldosteronism, your adrenal glands produce too much aldosterone, causing you to lose potassium and retain sodium. The excess sodium in turn holds on to water, increasing your blood volume and blood pressure.
Diagnosis and treatment of primary aldosteronism are important because people with this form of high blood pressure have a higher risk of heart disease and stroke. Also, the high blood pressure associated with primary aldosteronism may be curable.
The main signs of primary aldosteronism are:
Moderate to severe high blood pressure
High blood pressure that takes several medications to control (resistant hypertension)
High blood pressure along with a low potassium level (hypokalemia)
This excess risk is due to the high aldosterone levels, which can cause heart and blood vessel damage independent of complications related to high blood pressure.
Hypermagnesemia - Causes, Signs + Symptoms, Assessment and Treatment
THINK MUSCLES FIRST. ACT LIKE SEDATIVES.
Causes:
Renal failure ( Magnesium is excreted by the kidneys), Antacids (contains mg), MgSO4, lithium therapy, hypothyroidism
Signs: Flushing and Warmth due to vasodilation, Decreased Deep tendon reflex. Decreased Muscle tone, Decreased LOC, Pulse and Respirations. Bradycardia, Hypotension and Prolonged PR interval and widened QRS complexes. Skeletal muscle weakness. Drowsiness and lethargy.
Treatment/interventions: Ventilator due to RR Dialysis Calcium gluconate Cardiac Monitor Safety precautions Diuretics ( increases renal excretion)
Hypercalcemia - Causes, Signs + Symptoms, Assessment and Treatment
ACT LIKE SEDATIVES. Calcium has an inverse relationship to Phosphate.
Causes:
- Hyperparathyroidism: too much PTH. When your serum calcium gets low, PTH kicks in and pulls CA from the bones and puts it into the blood - therefore serum calcium goes up.
- Hyperthyroidism. (An increase in bone turnover and mobilization of calcium from bone into the circulation are the main mechanisms responsible for the hypercalcemia associated with hyperthyroidism)
- Thiazides ( Retain Calcium)/ Kidney disease - Calcium is excreted by kidneys
- Immobilization ( you have to bear weight to keep calcium in the bones)
- Glucocorticoid/lithium use
Signs:
Cardio: increased heart rate that goes to bradycardia and then cardiac arrest, Increased BP is related to the effects of calcium on the vascular smooth muscle cells, with increased calcium ion influx through calcium channels and a direct effect on vascular smooth muscle cells and
increased vascular resistance, Bounding pulse
Resp: Ineffective respiratory movement as a result of skeletal muscle weakness
Neuromuscular: Muscle weakness, decreased DTR and muscle tone, Disorientation, lethargy and coma, Bones are brittle
Renal : UO is dependent on cause, Kidney stones
GI: Decreased motility and hypoactive BS, nausea, abd distention, constipation
ECG changes: shortened ST segment, Widened T wave
Treatment:
Movement –> calcium goes into the bones
Fluids prevent kidney stones/ flush Ca
Ingest more phosphorus
Steroids decrease Ca - They increase renal calcium excretion and decrease gastrointestinal calcium absorption, resulting in reduced serum calcium.
Safety Precautions - increased risk for pathological fracture
Meds : Biphosphates and Calcitonin ( can treat/prevent osteoporosis). D/C meds with calcium and vitamin D and THIAZIDE DIURETICS < can be replaced with a different diuretic that enhances calcium excretion
Cardiac Monitor
Dialysis if meds fail
Parathyroid hormone
When your serum calcium gets low, PTH kicks in and pulls CA from the bones and puts it into the blood - therefore serum calcium goes up while decreasing serum phosphorus.
Thiazide Diuretics. Why does it cause hypercalcemia?
Commonly used for HTN, DI, Edema associated with steroid use, estrogen therapy, heart disease or liver disease
MoA: Action is on the renal distal tubules, promoting sodium, potassium and water excretion and decreasing preload and cardiac output. Promotes Calcium reabsorption. Decreases edema. Acts on arterioles, causing vasodilation and decreasing BP. Only for ppl with adequate renal perfusion
Contraindicated in renal failure with anuria
Interactions: Will increase digoxin toxicity if hypokalemia present, Increases renal toxicity with ASA, decrease absorption with NSAIDs
Effects: Can cause hyperglycaemia, hypotension, hypokalemia, hypercalcemia, aplastic anemia, shock, N/V/D, weakness and vertigo, photosensitivity
