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Fluids and Electrolytes 1 - Coggle Diagram
Fluids and Electrolytes 1
Composition of Body Fluids
Total body water
Body Fluids
transporting nutrients
solvent
maintain
body temperature
Fluid comparment
2 main compartments
ICF
intracellular fluid (30-40% of body weight)
ECF
extracellular fluid (20-25% of body weight)
Hypoalbuminemia
decreased oncotic pressure
edema
Electrolyte composition
ICF
More protein,More Potassium (K) ion,
Less Sodium (Na) ion,More Phosphate ion
ECF
No protein in interstitial;Present in Plasma, Less Potassium (K) ion,More Sodium (Na) ion,More Chloride (Cl) ion
TRANSPORT PROCESS
Osmosis
low solute to high solute concentration
Diffusion
high concentration to low concentration.
Active transport
to transport solutes in and out of cells
Filtration
high hydrostatic pressure to low hydrostatic pressure
Osmolality
plasma osmolality = 285-295 mOsm/kg
Osmolality = 2 ×[Na]+[glucose]/18 +[BUN]/2.8
Effective osmolality = 2 ×[Na]+[glucose]/18
Hyperglycemia
increase in the plasma osmolality
[Na]corrected =[Na]measured + (1.6×([glucose]−100mg/dL)/100
Regulation of Osmolality
Elevated effective osmolality
ADH
urine concentration increases and water excretion decreases
SIADH (Syndrome of inappropriate antidiuretic hormone)
osmotic diuresis
EX.Glycosuria in DM and Mannitol administration
Regulation of volume
Renin–angiotensin system
RENIN>>> Cleaves Angiotensinogen >>>angiotensin I >>>Angiotensin-converting enzyme converts angiotensin I into angiotensin II
VOLUME EXPANSION
Stimulates synthesis of ANP (Atrial Natriuretic peptide)
Causes
Kidney failure,Excessive Aldosterone, Acute Glomerulonephritis (AGN)
VOLUME DEPLETION
Renal retention of Na
Causes
Decrease in intravascular volume,Na losses exceed intake,Urinary Na wasting
SODIUM (Na)
Na METABOLISM
glucose enhances sodium absorption
HyperNatremia
145 mEq/L
Causes
EXCESSIVE SODIUM
WATER DEFICIT
Increased insensible losses
WATER AND SODIUM DEFICITS
Gastrointestinal losses
Diarrhea
Cutaneous losses
Burns
Renal losses
Diabetes mellitus,Manitol
CLINICAL MANIFESTATIONS
CNS manifestations
irritable, restless, weak, and lethargic.
Brain Hemorrhage
EX.Seizures and coma
DIAGNOSIS
History
Salt poisoning
Diabetes insipidus
TREATMENT
Hypotonic fluid should be stopped.
An infusion of 3% saline
Normal saline preferred over lactated Ringer solurion
Water deficit = Body weight × 0.6
(1-145)/[current sodium])
HypoNatremia
<135 mEq/L
CAUSES
PSEUDOHYPONATREMIA
HYPEROSMOLALITY
DM
HYPOVOLEMIC HYPONATREMIA
diarrhea
EXTRARENAL LOSSES
RENAL LOSSES
Thiazide or loop diuretics
EUVOLEMIC HYPONATREMIA
Syndrome of inappropriate antidiuretic hormone secretion
Causes
Disorders of the CNS
lung disease
malignant tumors
Diagnostic Criteria
Renal, adrenal, or thyroid insufficiency,
Heart failure, nephrotic syndrome, or cirrhosis
Water intoxication
CLINICAL MANIFESTATIONS
Neurologic symptoms
anorexia, nausea, emesis, malaise, lethargy, confusion,Hypothermia and Cheyne-Stokes respirations,Rhabdomyolysis
DIAGNOSIS
HISTORY
Primary kidney disease(polyuria)
Brain injury
TREATMENT
Avoid
CPM (central pontine myelinolysis)
severe symptoms (seizures)
hypertonic saline (3% 4-6ml/kg)
Potassium (K)
Aldosterone
regulating potassium
HyperKalemia
Mechanisms
INCREASED INTAKE
TRANSCELLULAR SHIFTS
Acidosis,Rhabdomyolysis,
Tumor lysis syndrome
SPURIOUS LABORATORY VALUE
Hemolysis
K release from cells
DECREASED EXCRETION
Renal failure,Primary adrenal disease,Hyporeninemic hypoaldosteronism,Renal tubular disease
Medications
Angiotensin-converting enzyme inhibitors,Angiotensin II blockers,Potassium-sparing diuretics,Calcineurin inhibitors,Nonsteroidal antiinflammatory drugs,Trimethoprim,Heparin,Drospirenone, aldosterone
CLINICAL MANIFESTATIONS
peaking of the T waves>>>ST-segment depression,increased PR interval,flattening of the P wave,widening of the QRS complex.
ventricular fibrillation.
Asystole
DIAGNOSIS
laboratory
creatinine, BUN,acid–base status.
TREATMENT
Stop all sources
require blood transfusions
If >6.5 meq/L – obtain ECG (peak T waves 1st sign)
2 Basic GOALS
to stabilize the heart to prevent life-threatening arrhythmias
Calcium (IV)
Bicarbonate
Insulin
Nebulization with Albuterol
to remove potassium from the body
Sodium polystyrene sulfonate (Kayexalate)
Dialysis
HypoKalemia
most related to gastroenteritis
Mechanisms
SPURIOUS
High white blood cell count
TRANSCELLULAR SHIFTS
Alkalemia,Insulin
RENAL LOSSES
CLINICAL MANIFESTATIONS
ECG changes
flattened T wave,depressed ST, appearance of U wave
<2.5mEq/L
Paralysis,Ileus
DIAGNOSIS
With metabolic acidosis
diarrhea,distal and proximal RTA
With metabolic alkalosis
emesis or nasogastric losses,aldosterone excess, use of diuretics, Gitelman syndromes.
TREATMENT
oral
2-4 mEq/kg/day, maximum of 120-240 mEq/day
intravenous
0.5-1.0 mEq/kg,givenover 1 hr.
With acidosis
K acetate or K citrate
With hypophosphatemia
K phosphate
Excessive urinary losses,K-sparing diuretics
Magnesium (Mg)
normal plasma concentration =
1.5-2.3 mg/dL (1.2- 1.9 mEq/L; 0.62-0.94 mmol/L)
small intestine is the major site of absorption
HypoMagnesemia (HypoMg)
CAUSES
GASTROINTESTINAL DISORDERS
RENAL DISORDERS
MISCELLANEOUS CAUSES
Hungry bone syndrome
CLINICAL MANIFESTATIONS
secondary hypocalcemia
tetany,presence of Chvostek and Trousseau signs, and seizures
hypokalemia
magnesium therapy
DIAGNOSIS
assessment for GI disease, adequate intake, and kidney disease
TREATMENT
Severe hypomagnesemia
Mg sulfate dose of 25-50 mg/kg (0.05-0.1 mL/kg of a 50% solution; 2.5-5.0 mg/kg of elemental magnesium)
Long-term therapy
orally
HyperMagnesium (HyperMg)
CLINICAL MANIFESTATIONS
Symptoms - >4.5mg/dL
hypotonia, hyporeflexia, and weakness; paralysis
CNS depression
lethargy and sleepiness
Hypotension
vascular dilation
ECG changes
prolonged PR, QRS, and QT intervals
Severe hyperMg
15 mg/dL
complete heart block&cardiac arrest
nausea, vomiting, and hypocalcemia
TREATMENT
normal renal function
Intravenous hydration and loop diuretics
severe with renal insufficiency
Dialysis
Exchange transfusion
Acute emergencies
100 mg/kg of intravenous calcium gluconate
DIAGNOSIS
history
Phosphorus
HypoPhosphatemia
CAUSES
TRANSCELLULAR SHIFTS
Glucose infusion
Insulin
DECREASED INTAKE
Premature infants
RENAL LOSSES
Fanconi syndrome
MULTIFACTORIAL
Alcoholism
Vitamin D deficiency
CLINICAL MANIFESTATIONS
RICKETS
Severe
<1.0-1.5 mg/dL
acute hypophosphatemia
Rhabdomyolysis
DIAGNOSIS
History and basic laboratory evaluation
TREATMENT
Mild hypophosphatemia
does not require treatment
Severe
IV therapy (Na or K Phosphate)
0.08-0.16 mmol/ kg over 6 hr
Oral
2-3 mmol/kg/day
HyperPhosphatemia
Renal insufficiency
most common cause
CAUSES
TRANSCELLULAR SHIFTS
Tumor lysis syndrome
Rhabdomyolysis
Diabetic ketoacidosis and lactic acidosis
INCREASED INTAKE
Cow’s milk in infants
DECREASED EXCRETION
Renal failure
Hypoparathyroidism or pseudohypoparathyroidism
INCREASE
CLINICAL MANIFESTATIONS
plasma calcium × plasma phosphorus = >70
conjunctiva
foreign-body feeling, erythema, and injection
hypoxia
renal failure
DIAGNOSIS
creatinine and BUN
History
Measurement of potassium, uric acid, calcium, lactate dehydrogenase, bilirubin, hemoglobin, and CPK
Measurement of PTH
TREATMENT
Dietary restriction
Oral phosphorus binder
Dialysis