Fluid And Electrolyte Flashcards

1
Q

Intracellular and Extracellular Fluid

A

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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2
Q

Edema: mechanisms of formation

A

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

  1. Decrease in capillary colloidal osmotic pressure
    Increased loss of plasma proteins - burns, kidney disease
    Decreased production of plasma proteins - liver disease, malnutrition
    General edema
  2. Increase in capillary permeability
    Inflammation, allergic reactions, malignancy, ascites, pleural effusion, tissue injury, burns
    Localized non pitting
  3. Produce an obstruction of lymph flow
    Malignant obstruction, surgery
    Localized to area of impaired drainage
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3
Q

Edema: manifestations

A

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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4
Q

Edema: Treatment

A

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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5
Q

Third Space Accumulations

A

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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6
Q

Water gain and water loss

A

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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7
Q

Water Regulation

A

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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8
Q

Sodium Regulation

A

Sympathetic Nervous System: changes in arterial blood pressure = adjust in GFR and sodium reabsorption

RAAS - increase sodium reabsorption and vasoconstriction

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9
Q

Thirst control

A

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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10
Q

Hypodipsia and Polydipsia

A

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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11
Q

Diabetes Insipidus: Causes

A

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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12
Q

Diabetes Insipidus: Manifestations

A
Intense thirst
Craving ice water
Polyuria
Reduced fluid volume
Polydipsia
Hypernatremia
Dehydration
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13
Q

Syndrome of Inappropriate Antidiuretic Hormone: Causes

A

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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14
Q

SIADH: manifestations

A

Dilutional hyponatremia
Decreased urine output
Urine osmolality high
Hematocrit, serum sodium, BUN, decreased

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15
Q

Isotonic Fluid Volume Deficit: Causes

A

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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16
Q

Isotonic Fluid Volume Deficit: Manifestations

A
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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17
Q

Isotonic Fluid Volume Deficit: Treatment

A

Fluid replacement and measures to correct underlying cause

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18
Q

Isotonic Fluid Volume Excess: Causes

A

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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19
Q

Isotonic Fluid Volume Excess: Manifestations

A
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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20
Q

Isotonic Fluid Volume Excess: Treatment

A

Sodium restricted diet

Diuretics

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21
Q

Hyponatremia: Causes

A

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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22
Q

Hyponatremia: Manifestations

A
Muscle cramps
Weakness
Fatigue
Nausea and vomiting
Abdominal cramps
Diarrhea
Apathy
Lethargy
Headache
Disorientation
Confusion
Depression of deep tendon reflexes
Seizure and coma 
Weakness
23
Q

Hyponatremia: treatment

A

Discontinue SIADH medication
IV or oral saline solution (hypertonic)
Loop diuretics
Vasopressin receptor antagonist

24
Q

Hypernatremia: Causes

A

Sodium above 145

Water loss through GI, urine, lungs, skin
Ingestion
IV sodium
Hypodipsia

25
Q

Hypernatremia: Manifestations

A
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
26
Q

Hypernatremia: treatment

A

Limit intake

Replace fluid oral or IV D5W

27
Q

Values of Co2, Bicarbonate, and pH

A

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

28
Q

Potassium Regulation

A

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

29
Q

Hypokalemia: Causes

A

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

30
Q

Hypokalemia: manifestations

A
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
31
Q

Hypokalemia: treatment

A

Increasing intake
Oral supplement
IV potassium and magnesium replacement

32
Q

Hyperkalemia: causes

A

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

33
Q

Hyperkalemia: manifestations

A
Bradycardia
Cardiac arrests
ECG changes
Weakness
Paralysis
Paresthesia
Cramps
Diarrhea
Nausea and vomiting
34
Q

Hyperkalemia: treatment

A
Calcium
Sodium bicarbonate
Beta agonists
Insulin
Hemodialysis or peritoneal dialysis 
Restrict intake
35
Q

Hypocalcemia: causes

A

Below 8.5

Decreased intake
Renal failure
Hypoparathyroidism
Vitamin D deficiency
Respiratory alkalosis
Loop diuretic
PPI
H2 blockers
Citrate
36
Q

Hypocalcemia: manifestations

A
Tetany
Bone pain
Carpopedal spasm
Trousseau sign
Chvoskek sign
Twitching facial muscle
Parestheisa
Confusion
Lethargy
Anxiety 
Cardiac arrhythmia
Resistance to digitalis
Hypotension
37
Q

Hypercalcemia: Causes

A

Above 10.5

Neoplasms of the parathyroid gland
Hyperparathyroidism
Immobilization
Increased absorption in intestine
Excess vitamin D
Lithium
Thiazide drugs
38
Q

Hypercalcemia: manifestations

A
Muscle weakness
Lethargy
Ataxia
Personality changes
Stupor
Coma
HTN
ECG changes
Anorexia
Nausea and vomiting
Constipation
Thirst and dilute urine
39
Q

Carbon Dioxide Transport

A

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

40
Q

Mechanisms of pH regulation

A

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
Q

Primary and Secondary in Mixed acid base disorders

A

Value furthest from norm is primary

If values of predicted compensatory values fall outside range it is mixed

42
Q

Metabolic Acidosis: causes

A

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

43
Q

Metabolic Acidosis: manifestations

A
Lethargy
Stupor
Fatigue and malaise
Kussmauls respirations
Hyperventilation
Hypotension
Arrhythmia
Tachycardia
Anorexia
Nausea and vomiting 
Abdominal pain
44
Q

Metabolic Acidosis: treatment

A

Correcting underlying cause
Restoring lost fluid and electrolytes
Insulin and fluid replacement in diabetic ketosis

45
Q

Metabolic Alkalosis: causes

A

Hypoventilation
HCO3 >26 ph >7.45

Vomiting
Gastric suctioning
Ingestion of alkali - calcium carbonate, antacids
IV bicarbonate
Hyperaldosteronism 
Diuretics
Abrupt acidosis correction
46
Q

Metabolic Alkalosis: manifestations

A
Hyperactive reflexes
Tetany
Confusion
Seizures
Carpopedal spasm
Trosseau signs
Bradypnea
Shallow respirations
Hypoxemia
Respiratory acidosis
Hypotension
Arrhythmia
Nausea and vomiting
47
Q

Metabolic Alkalosis: treatment

A

Correcting underlying cause

Chloride Deficit requires correction (potassium chloride)

48
Q

Respiratory Acidosis: causes

A

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
49
Q

Respiratory acidosis: manifestations

A
Restlessness
Confusion
Depressed reflexes
Somnolence
Coma 
Blurred vision
Psychological disturbances
Dyspnea
Tachypnea
Hypoxemia
Tachycardia
Arrhythmia
HTN or Hypotension
Warm flush skin and weakness
50
Q

Respiratory acidosis: treatment

A

Improve ventilation

Mechanical ventilation

51
Q

Respiratory alkalosis: causes

A

Hydrogen pulled from cells to produce carbonic acid
PaCO2 <35 and pH >7.45

Hyperventilation
Medullary stimulation
Mechanical ventilation
Disease processes

52
Q

Respiratory alkalosis: manifestations

A
Dizzzy,
Agitated
Circumoral and peripheral paresthsia 
Tetany
Twitching
Muscle weakness
Light headed
Deep rapid respirations
Dyspnea
Palpitations
Tachycardia
53
Q

Respiratory alkalosis: treatment

A

Correct underlying cause
Rebreathe into a paper bag
Supplemental o2 and changing ventilator settings