Fluid And Electrolyte Flashcards
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
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
- Decrease in capillary colloidal osmotic pressure
Increased loss of plasma proteins - burns, kidney disease
Decreased production of plasma proteins - liver disease, malnutrition
General edema - Increase in capillary permeability
Inflammation, allergic reactions, malignancy, ascites, pleural effusion, tissue injury, burns
Localized non pitting - Produce an obstruction of lymph flow
Malignant obstruction, surgery
Localized to area of impaired drainage
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
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
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
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
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
Sodium Regulation
Sympathetic Nervous System: changes in arterial blood pressure = adjust in GFR and sodium reabsorption
RAAS - increase sodium reabsorption and vasoconstriction
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)
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
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
Diabetes Insipidus: Manifestations
Intense thirst Craving ice water Polyuria Reduced fluid volume Polydipsia Hypernatremia Dehydration
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
SIADH: manifestations
Dilutional hyponatremia
Decreased urine output
Urine osmolality high
Hematocrit, serum sodium, BUN, decreased
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
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
Isotonic Fluid Volume Deficit: Treatment
Fluid replacement and measures to correct underlying cause
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
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
Isotonic Fluid Volume Excess: Treatment
Sodium restricted diet
Diuretics
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
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
Hyponatremia: treatment
Discontinue SIADH medication
IV or oral saline solution (hypertonic)
Loop diuretics
Vasopressin receptor antagonist
Hypernatremia: Causes
Sodium above 145
Water loss through GI, urine, lungs, skin
Ingestion
IV sodium
Hypodipsia
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
Hypernatremia: treatment
Limit intake
Replace fluid oral or IV D5W
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
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
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
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
Hypokalemia: treatment
Increasing intake
Oral supplement
IV potassium and magnesium replacement
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
Hyperkalemia: manifestations
Bradycardia Cardiac arrests ECG changes Weakness Paralysis Paresthesia Cramps Diarrhea Nausea and vomiting
Hyperkalemia: treatment
Calcium Sodium bicarbonate Beta agonists Insulin Hemodialysis or peritoneal dialysis Restrict intake
Hypocalcemia: causes
Below 8.5
Decreased intake Renal failure Hypoparathyroidism Vitamin D deficiency Respiratory alkalosis Loop diuretic PPI H2 blockers Citrate
Hypocalcemia: manifestations
Tetany Bone pain Carpopedal spasm Trousseau sign Chvoskek sign Twitching facial muscle Parestheisa Confusion Lethargy Anxiety Cardiac arrhythmia Resistance to digitalis Hypotension
Hypercalcemia: Causes
Above 10.5
Neoplasms of the parathyroid gland Hyperparathyroidism Immobilization Increased absorption in intestine Excess vitamin D Lithium Thiazide drugs
Hypercalcemia: manifestations
Muscle weakness Lethargy Ataxia Personality changes Stupor Coma HTN ECG changes Anorexia Nausea and vomiting Constipation Thirst and dilute urine
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
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
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
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
Metabolic Acidosis: manifestations
Lethargy Stupor Fatigue and malaise Kussmauls respirations Hyperventilation Hypotension Arrhythmia Tachycardia Anorexia Nausea and vomiting Abdominal pain
Metabolic Acidosis: treatment
Correcting underlying cause
Restoring lost fluid and electrolytes
Insulin and fluid replacement in diabetic ketosis
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
Metabolic Alkalosis: manifestations
Hyperactive reflexes Tetany Confusion Seizures Carpopedal spasm Trosseau signs Bradypnea Shallow respirations Hypoxemia Respiratory acidosis Hypotension Arrhythmia Nausea and vomiting
Metabolic Alkalosis: treatment
Correcting underlying cause
Chloride Deficit requires correction (potassium chloride)
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
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
Respiratory acidosis: treatment
Improve ventilation
Mechanical ventilation
Respiratory alkalosis: causes
Hydrogen pulled from cells to produce carbonic acid
PaCO2 <35 and pH >7.45
Hyperventilation
Medullary stimulation
Mechanical ventilation
Disease processes
Respiratory alkalosis: manifestations
Dizzzy, Agitated Circumoral and peripheral paresthsia Tetany Twitching Muscle weakness Light headed Deep rapid respirations Dyspnea Palpitations Tachycardia
Respiratory alkalosis: treatment
Correct underlying cause
Rebreathe into a paper bag
Supplemental o2 and changing ventilator settings
