Flashcards in Fluid And Electrolyte Deck (53)
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1
Intracellular and Extracellular Fluid
2/3 is intracellular 1/3 is extracellular
Intracellular = potassium, magnesium (small amounts of sodium, chloride, bicarbonate, phosphate)
Extracellular = sodium and chloride (small amounts of bicarbonate, phosphate, calcium, magnesium, and potassium)
ICF and ECF always have equal amounts of cations and anions
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Edema: mechanisms of formation
I. Increase in capillary filtration pressure
Increased vascular volume - HF, kidney disease, IV overload
Venous obstruction - thrombophlebitis
Liver disease - portal vein obstruction
Acute pulmonary edema
Dependent edema
2. Decrease in capillary colloidal osmotic pressure
Increased loss of plasma proteins - burns, kidney disease
Decreased production of plasma proteins - liver disease, malnutrition
General edema
3. Increase in capillary permeability
Inflammation, allergic reactions, malignancy, ascites, pleural effusion, tissue injury, burns
Localized non pitting
4. Produce an obstruction of lymph flow
Malignant obstruction, surgery
Localized to area of impaired drainage
3
Edema: manifestations
Edema to brain, larynx, lungs, pericardial, pleural, peritoneum = life threatening
Joint spaces, coccyx, ankles, feet = discomfort, impaired rom
Tourniquet - blood vessel compression
Pressure ulcers - further for nutrients to diffuse
Psychological self concept
Non pitting edema = proteins accumulated in tissues and coagulated
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Edema: Treatment
elevation - counter gravity
Diuretic therapy - decrease fluid volume
Massage - promote lymphatic and vascular return
ROM - lymphatic and venous return
Serum albumin - given to IV to raise colloid plasma oncotic
Elastic support stockings - oppose fluid movement
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Third Space Accumulations
Loss or movement and trapping of ECF in trans compartment all spaces (serous, pericardial, peritoneal, pleural)
Cavities are often closely linked with lymphatic drainage
Milking action of moving structures (lungs) moves fluid and proteins back into lymphatic channels
Gain in body weight doesn't contribute to fluid reserve or function
Hydrothorax - edema in the pleural cavity
Ascites - fluid in peritoneal cavity due to liver failure
Effusion - transmutation of fluid into serous cavities
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Water gain and water loss
Positive water balance = decreased osmolality and sodium
Negative water balance = increased osmolality and sodium
Gain - intake, metabolic processes
Loss - kidney, skin (insensible loss), lungs (insensible loss), GI
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Water Regulation
Aldosterone - increased sodium reabsorption and potassium excretion = increased blood volume
Renin, stress, trauma,
ADH - increases sodium reabsorption, aquaporins = increased blood volume
ECF volume and osmolality
Renin - angiotensin II = increased aldosterone, and sodium reabsorption = increased blood volume
Blood pressure low
Thirst and ADH regulate water intake and output
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Sodium Regulation
Sympathetic Nervous System: changes in arterial blood pressure = adjust in GFR and sodium reabsorption
RAAS - increase sodium reabsorption and vasoconstriction
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Thirst control
High osmolality = thirst and ADH release
Low osmolality = lack of thirst and decreased ADH release
Cellular dehydration (osmolality) and decrease in circulating volume (stretch receptors) stimulates hypothalamus to thirst and production of angiotensin II (nonosmotic thirst; back up)
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Hypodipsia and Polydipsia
Decreased ability to sense thirst
Commonly associated with lesions in the area of the hypothalamus (trauma, hemorrhage, meningiomas)
Excessive thirst
Inappropriate or false thirst - despite normal body water; CHF, chronic kidney disease
Compulsive water drinking - schizophrenia, smoking
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Diabetes Insipidus: Causes
Deficiency in ADH or a decreased renal response to ADH
Expelling large amounts of urine and excessive thirst
Danger arises when pt is unable to communicate need for water or unable to secure water
Neurogenic DI - deficit in synthesis or release of ADH
Inflammatory, autoimmune, vascular disease
Many have an incomplete form
Nephrotic DI - kidneys do not response to ADH
Congenital, pyelonephritis, lithium toxicity, electrolyte disorders
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Diabetes Insipidus: Manifestations
Intense thirst
Craving ice water
Polyuria
Reduced fluid volume
Polydipsia
Hypernatremia
Dehydration
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Syndrome of Inappropriate Antidiuretic Hormone: Causes
Failure of negative feedback system regulating ADH leading to water retention
Dilutional hyponatremia
Surgery, pain, stress, temperature changes, drugs, lung tumours, chest lesions, CNS disorders,
Tumors
Intrathoracic conditions - TB, pneumonia, positive pressure breathing
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SIADH: manifestations
Dilutional hyponatremia
Decreased urine output
Urine osmolality high
Hematocrit, serum sodium, BUN, decreased
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Isotonic Fluid Volume Deficit: Causes
Water and electrolytes lost in isotonic proportions
Severe vomiting
Diarrhea
GI suction
Excess urinary loss
Excess sweating
Endocrine disorders - adrenal insufficiency
3rd space losses
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Isotonic Fluid Volume Deficit: Manifestations
Decreased body weight
Thirst
Oliguria
Urine gravity increases
Eyes look sunken
Tissue turgor decreases
BP decrease, HR increase, weak pulses
Postural hypotension
Hypovolemic shock
Vascular collapse
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Isotonic Fluid Volume Deficit: Treatment
Fluid replacement and measures to correct underlying cause
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Isotonic Fluid Volume Excess: Causes
Isotonic expansion of ECF - increase in total body sodium and body water
Excess intake of sodium
Heart failure - compensatory increase
Liver failure - impaired aldosterone metabolism
Corticosteroid hormone excess - increased reabsorption of sodium
Circulatory overload
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Isotonic Fluid Volume Excess: Manifestations
Weight gain
Dependent edema
Distended neck veins
Slow emptying peripheral veins
Full bounding pulse
Increased central venous pressures
Fluid accumulation in lungs - SOB, dyspnea, crackles, productive cough
Ascites
Pleural effusion
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Isotonic Fluid Volume Excess: Treatment
Sodium restricted diet
Diuretics
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Hyponatremia: Causes
Serum sodium below 135
Most common disorder
Hypertonic hyponatremia - hyperglycemia
Hypovolemic hypotonic hyponatremia - excessive sweating, GI fluid loss, adrenal insufficiency
Euvolemic hypotonic hyponatremia - SIADH
Hypervolemic hypotonic hyponatremia - HF, liver disease, renal failure, MDMA abuse
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Hyponatremia: Manifestations
Muscle cramps
Weakness
Fatigue
Nausea and vomiting
Abdominal cramps
Diarrhea
Apathy
Lethargy
Headache
Disorientation
Confusion
Depression of deep tendon reflexes
Seizure and coma
Weakness
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Hyponatremia: treatment
Discontinue SIADH medication
IV or oral saline solution (hypertonic)
Loop diuretics
Vasopressin receptor antagonist
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Hypernatremia: Causes
Sodium above 145
Water loss through GI, urine, lungs, skin
Ingestion
IV sodium
Hypodipsia
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Hypernatremia: Manifestations
Thirst
Tachycardia
Decreased urine output
Fever
Flush warm skin
Dry skin and mucous membranes
Decreased salivation and lacrimation
Decreased reflexes
Agitation
Headache
Restlessness
Seizure
Coma
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Hypernatremia: treatment
Limit intake
Replace fluid oral or IV D5W
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Values of Co2, Bicarbonate, and pH
CO2 >50 = acidosis
CO2 <35 = alkalosis
PH <7.35 = acidosis
PH >7.45 = alkalosis
Bicarbonate <22 = acidosis
Bicarbonate >36 = alkalosis
Ph serum levels are not directly proportionate to CO2 levels
Arterial blood gases - indicate respiratory and metabolic function
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Potassium Regulation
Intake oral
urine output (aldosterone eliminates and hydrogen reabsorption eliminates)
transcompartmental shifts in ICF and ECF
Serum osmolality - water moves out of cell into ECF = increase in potassium concentration
Acid base balance - cation shift for buffering pH = (alkalosis = hydrogen excreted; hypokalemia and acidosis = hydrogen reabsorbed; hyperkalemia)
Insulin - temporary shift into cells; hypokalemia
Sympathetic NS - epinephrine = increase in uptake; hypokalemia
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Hypokalemia: Causes
Serum potassium below 3.5
Inadequate intake - low potassium diet or inability to obtain or ingest food
Burns and capillary injury
Excessive renal losses - diuretic, alkalosis, magnesium depletion, increased aldosterone
Insulin
Beta adrenergic agonist drugs
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Hypokalemia: manifestations
Increased urine output - polyuria
Nocturia
Thirst
Anorexia
Nausea and vomiting
Constipation
Weakness
Fatigue
Muscle cramps
ECG changes
Arrhythmias and digitalis toxicity
Alkalosis and renal chloride wasting
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Hypokalemia: treatment
Increasing intake
Oral supplement
IV potassium and magnesium replacement
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Hyperkalemia: causes
Potassium above 5
Decreased renal elimination - chronic kidney disease, nephropathy, aldosterone deficiency, potassium sparing diuretics, ace inhibitors
Shift from ICF to ECF - acidosis, tissue injury, decreased insulin, beta blockers
Increased intake
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Hyperkalemia: manifestations
Bradycardia
Cardiac arrests
ECG changes
Weakness
Paralysis
Paresthesia
Cramps
Diarrhea
Nausea and vomiting
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Hyperkalemia: treatment
Calcium
Sodium bicarbonate
Beta agonists
Insulin
Hemodialysis or peritoneal dialysis
Restrict intake
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Hypocalcemia: causes
Below 8.5
Decreased intake
Renal failure
Hypoparathyroidism
Vitamin D deficiency
Respiratory alkalosis
Loop diuretic
PPI
H2 blockers
Citrate
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Hypocalcemia: manifestations
Tetany
Bone pain
Carpopedal spasm
Trousseau sign
Chvoskek sign
Twitching facial muscle
Parestheisa
Confusion
Lethargy
Anxiety
Cardiac arrhythmia
Resistance to digitalis
Hypotension
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Hypercalcemia: Causes
Above 10.5
Neoplasms of the parathyroid gland
Hyperparathyroidism
Immobilization
Increased absorption in intestine
Excess vitamin D
Lithium
Thiazide drugs
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Hypercalcemia: manifestations
Muscle weakness
Lethargy
Ataxia
Personality changes
Stupor
Coma
HTN
ECG changes
Anorexia
Nausea and vomiting
Constipation
Thirst and dilute urine
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Carbon Dioxide Transport
Bicarbonate - plasma RBC, CA converts CO2 and H20 into H2CO3 that dissociates into H and HCO3 (bicarbonate) where HC03 is exchanged for Cl-
Hemoglobin - combination of C02 and Hgb loose reversible for exchange in lungs
Plasma - dissolved in plasma that forms carbonic acid from hydration of dissolved CO2
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Mechanisms of pH regulation
Chemical buffer - bicarbonate (weak acid H2C03 and weak base NaHC03) AND potassium hydrogen exchange AND body proteins
Bone buffering - leading to demineralization
Respiratory - ventilation to increase CO2 exchange; monitored by chemoreceptors in brain, carotid, and aortic bodies
Renal - reabsorption of HCO3 and Regulation of H+ secretion and generation of new bicarbonate; phosphate buffer system
41
Primary and Secondary in Mixed acid base disorders
Value furthest from norm is primary
If values of predicted compensatory values fall outside range it is mixed
42
Metabolic Acidosis: causes
Increasing respiratory rate
HCO3 <22 and pH <7.35
Lactic acid buildup and production of ketoacids
Inadequate o2 deliver - shock, cardiac arrest, intense exercise, cancers, liver failure
Poorly controlled diabetes
Kidney disease
Diarrhea
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Metabolic Acidosis: manifestations
Lethargy
Stupor
Fatigue and malaise
Kussmauls respirations
Hyperventilation
Hypotension
Arrhythmia
Tachycardia
Anorexia
Nausea and vomiting
Abdominal pain
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Metabolic Acidosis: treatment
Correcting underlying cause
Restoring lost fluid and electrolytes
Insulin and fluid replacement in diabetic ketosis
45
Metabolic Alkalosis: causes
Hypoventilation
HCO3 >26 ph >7.45
Vomiting
Gastric suctioning
Ingestion of alkali - calcium carbonate, antacids
IV bicarbonate
Hyperaldosteronism
Diuretics
Abrupt acidosis correction
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Metabolic Alkalosis: manifestations
Hyperactive reflexes
Tetany
Confusion
Seizures
Carpopedal spasm
Trosseau signs
Bradypnea
Shallow respirations
Hypoxemia
Respiratory acidosis
Hypotension
Arrhythmia
Nausea and vomiting
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Metabolic Alkalosis: treatment
Correcting underlying cause
Chloride Deficit requires correction (potassium chloride)
48
Respiratory Acidosis: causes
Renal adaptation
PaCO2 >45 pH <7.35
Acute respiratory failure
Narcotic overdose
Lung disease
Chest injury or obstruction
Pneumothorax
Enervation
COPD
Timor
Exercise
Fever - Hyperthermia
Sepsis
Burns
Carbohydrate rich diet
Accidental inspiration of CO2
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Respiratory acidosis: manifestations
Restlessness
Confusion
Depressed reflexes
Somnolence
Coma
Blurred vision
Psychological disturbances
Dyspnea
Tachypnea
Hypoxemia
Tachycardia
Arrhythmia
HTN or Hypotension
Warm flush skin and weakness
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Respiratory acidosis: treatment
Improve ventilation
Mechanical ventilation
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Respiratory alkalosis: causes
Hydrogen pulled from cells to produce carbonic acid
PaCO2 <35 and pH >7.45
Hyperventilation
Medullary stimulation
Mechanical ventilation
Disease processes
52
Respiratory alkalosis: manifestations
Dizzzy,
Agitated
Circumoral and peripheral paresthsia
Tetany
Twitching
Muscle weakness
Light headed
Deep rapid respirations
Dyspnea
Palpitations
Tachycardia
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