Pare shock caused by circulating toxins treatment with phlebotomy Blalock shock caused by hypovolemia treatment with plasma replacement Shires deficit in functional extracellular volume treatment with crystalloid fluids
Does total body water, as a percentage of body weight vary with: Age? Gender?
A decrease in the percent of body weight that is water is noted with increasing age. Men have a slightly higher percentage of body weight as water than women. Why?
Young - More percent muscle Old - Less percent muscle Males - Less percent fat Females - More percent fat What percentage of total body weight is water?
Males 60% of total body weight is water Females 50% of total body weight is water
How much volume is Total Body Water in a typical 70-kg man?
70 kg x 1 L/kg x 60% = 42 L
What are the compartments? What fractions of total body water?
2/3 1/3 3/4 1/4 Intracellular Extracellular Interstitial Intravascular
What are 3 clinical conditions where the ratio of interstital/intravascular volume is increased?
Congestive heart failure Hypoalbuminemia Inflammation
The total osmotic activity in a solution is the sum of the individual osmotic activities of all the solute particles in the solution. What is the osmolarity of 0.9% NaCl?
0.9% NaCl = 154 meq/l Na + 154 meq/l Cl = 154 mosm/l Na + 154 mosm/l Cl = 308 mosm/l What is normal plasma osmolarity?
Normal plasma osmolarity = 280-290 mosm/l What is the difference between osmolarity and osmolality?
Osmolarity = osmotic activity per volume of solution Osmolality = osmotic activity per volume of H2O How can you estimate plasma osmolarity?
(2 x [Na]) + [Glucose]/18 + [BUN]/2.8
What are the primary electrolytes? Extracellular Intracellular
Extracellular Cation - Sodium Anion - Chloride Intracellular Cation - Potassium Anion - Bicarbonate
Where is water lost normally? How much water is lost normally? What is the ideal maintenance fluid?
70 kg man average losses Urine Insensible Stool Total 1500 ml 1000 ml negligible 2500 ml What conditions exacerbate water loss?
Diuretics Diarrhea Fever Open wound Artificial airway
In the nonstressed, fasting state, 150 g/day dextrose provides enough calories to limit proteolysis. This protein-sparing effect is not sufficient in the stressed, catabolic patient. What are the daily requirements for sodium and potassium?
70 kg man average needs Sodium 140 meq/day Potassium 50 meq/day What is the ideal maintenance fluid for the nonstressed, fasting, 70 kg man?
D5 + 1/2NS + 20meq/L KCl 100 ml/hour Provides total 2.4 L water 120 g dextrose 185 meq sodium 48 meq potassium
What is the estimated volume of fluid requirement for each degree of fever?
An extra 500 ml of fluid a day is required for every degree of fever above 37C.
What is Third Space?
Fluid compartments that are not freely mobilized by normal homeostatic mechanisms.
Body Spaces: 1.Intracellular Space 2.Extracellular Space Interstitial Intravascular 3.Third Space GI tract Peritoneal cavity Pleural cavity Pathologic interstitial
Stomach Pancreas Bile S. Bowel L. Bowel Na+ K+ Cl- HCO3-
Na+ K+ Cl- HCO3- Stomach 70 15 100 0 Pancreas Bile S. Bowel L. Bowel
Na+ K+ Cl- HCO3- Stomach 70 15 100 0 Pancreas 140 10 70 70 Bile S. Bowel L. Bowel
Na+ K+ Cl- HCO3- Stomach 70 15 100 0 Pancreas 140 10 70 70 Bile 140 10 100 40 S. Bowel L. Bowel
Na+ K+ Cl- HCO3- Stomach 70 15 100 0 Pancreas 140 10 70 70 Bile 140 10 100 40 S. Bowel 70 10 50 20 L. Bowel
Na+ K+ Cl- HCO3- Stomach 70 15 100 0 Pancreas 140 10 70 70 Bile 140 10 100 40 S. Bowel 70 10 50 20 L. Bowel 30 10 10 0
What is the homeostatic response to volume deficit?
Under normal circumstances, water intake is regulated by thirst. Receptors in the hypothalamus are stimulated by changes in plasma osmolarity or circulating volume.
Actions Maintenance of serum osmolarity Regulation of extracellular volume Sodium / Potassium ATPase Regulation ADH Aldosterone
Etiology Normoosmolar Hyperosmolar Hypoosmolar Hypovolemia Euvolemia Hypervolemia
Etiology Normoosmolar? What is pseudohyponatremia?
Extreme elevations in plasma lipids or proteins increase the plasma volume and can reduce the measured plasma sodium concentration. Extracellular sodium relative to extracellular water is not decreased.
Normoosmolar Pseudohyponatremia hyperlipidemia hyperproteinemia
Etiology Hyperosmolar?
Hyperosmolar Hyperglycemia Na decreases 1.6 meq/l per glucose increase of 100 mg/dl Mannitol
Etiology Hypoosmolar Hypovolemia? Euvolemia? Hypervolemia?
Hypoosmolar Hypovolemia Renal Diuretics, aldosterone deficiency, renal dysfuntion Nonrenal Vomiting, diarrhea, third spacing, burns, salt wasting Euvolemia SIADH, psychogenic polydipsia Hypervolemia CHF, liver failure
What is the etiology of cerebral salt wasting?
The cause is not clearly understood Excessive sympathetic stimulation Renovascular hypertension Dopamine release Circulating natriuretic factors
How do you distinguish between SIADH and psychogenic polydipsia?
SIADH Una > 20 meq/l Uosm > Posm Psychogenic polydipsia Una < 10 meq/l Uosm < 100 mosm/l H20
Why do patients with CHF and liver failure develop hyponatremia?
Activation of compensatory mechanisms Sympathetic stimulation Redistribution of blood flow Shunting from visceral organs to brain and heart Renal vasoconstriction / hypoperfusion Sodium and water retention Decreased sodium and water excretion
Manifestations?
Manifestations CNS Disorientation Irritability Seizures Lethargy Coma Constitutional Nausea Vomiting Weakness
Normoosmolar Treatment? Hyperosmolar Treatment?
Normoosmolar Treat underlying disease (hyperlipidemia) Hyperosmolar Treat underlying disease (hyperglycemia)
Hypoosmolar Hypovolemic Treatment?
Hypoosmolar Hypovolemic Treat underlying disease (bowel obstruction) Stop drug (diuretic) Replace with isotonic saline How is aldosterone deficiency treated?
Mineralicorticoid effect Fludrocortisone 50-100 mcg/d oral Excess mineralicorticoid replacement CHF, alkalosis, hypokalemia, Htn
Hypoosmolar Hypervolemic Treatment?
Hypoosmolar Hypervolemic Treat underlying cause (CHF) Give diuretic Don t give sodium supplements
Euvolemic Treatment?
Euvolemic Asymptomatic Water restriction Loop diuretic if necessary Symptomatic Normal saline or hypertonic saline Goal of > 130 meq/l Loop diuretic Na should not be increased > 12 meq/l/day
Etiology?
Etiology Water deficit? Sodium excess?
Water deficit Reduced intake GI loss (diarrhea, vomiting) Cutaneous loss (sweating, fever) Renal loss (DI, diuretics) Sodium excess sodium administration
What is the difference between central and nephrogenic diabetes insipidus?
Central Inhibition of ADH release from the posterior pituitary. Nephrogenic Defective end-organ responsiveness to ADH. Causes?
Central Traumatic brain injury Anoxic encephalopathy Meningitis Nephrogenic Hypokalemia Aminoglycosides Amphotericin Radiocontrast dyes Polyuric phase of ATN
Manifestations?
Manifestations CNS Lethargy Coma Seizures Constitutional Weakness Polyuria Polydipsia
Treatment?
Water and sodium deficit Give 1/2NS IV Water deficit Give D5W Give water enteral Sodium excess Diuresis and give water or D5W Na should not change > 20 meq/l/day
TBW deficit = Normal TBW - Current TBW = Normal TBW - (Normal TBW x 140/[Na]) = 0.5 x weight - (0.5 x weight x 140/[Na]) 70kg man with [Na] = 150 TBW deficit = 0.5 x 70 - (0.5 x 70 x 140/150) = 35 - (35 x 0.93) = 35-32.6 = 2.4 L
Changes in sodium concentrations are usually caused by water excess or deficit, not sodium. Alterations in sodium concentration primarily affect CNS function.
Actions Maintenance of membrane potential Sodium / Potassium ATPase Regulation Renal excretion Insulin Aldosterone
Etiology?
Etiology Decreased intake Renal loss Extrarenal loss Transcellular shift
Decreased intake Malnutrition, anorexia, alcoholism, TPN Renal loss Diuretics, amphotericin, hypomagnesemia Extrarenal loss Sweating, GI loss Transcellular shift Alkalosis, insulin
Manifestations?
Manifestations Cardiac Arrhythmias ST depression T wave inversion QT prolongation Constitutional Weakness Ileus
Treatment?
Treat underlying disease (bowel obstruciton) Stop drug, if possible (diuretic) Treat hypomagnesemia (cofactor for K transport) Correct alkalosis
Administer potassium Enteral replacement, if possible IV replacement Maximum concentration Peripheral 20 meq/100 ml Central 20 meq/50 ml Maximum rate Unmonitored 10 meq/h Monitored 20 meq/h Symptomatic 40 meq/h
Etiology?
What is Pseudohypokalemia?
WBC > 50 or Platelets > 1K Potassium release from cells during clot formation
Etiology Hemolysis of sample Pseudohyperkalemia Massive blood transfusion Excess supplements TPN Renal failure Acidemia Crush injury, rhabdomyolysis, burns Adrenal insufficiency, hypoaldosteronism
Manifestations Cardiac Arrhythmias Prolonged PR Wide QRS Peaked T waves Sine waves Constitutional Weakness Paresthesias
Treatment?
Treat underlying disease Stop K intake Stop TPN Treat acidemia Stabilize myocardial cell membrane effects Calcium chloride 1g IV Effect lasts 30 min May be repeated
List 3 mechanisms for potassium redistribution.
NaHCO3 50-100 meq IV D50W 50 g IV + Regular insulin 10 U IV High-dose inhaled beta-agonists Albuterol 10-20 mg
Eliminate K from body Renal excretion with loop diuretic GI elimination with K resin Sodium polystyrene sulfonate (Kayexalate) 50 g in sorbitol 30 ml oral or enema Hemodialysis
Extreme elevations in potassium concentration reflect laboratory sample hemolysis or renal failure. Alterations in potassium concentrations primarily affect cell membrane function and the cardiac effects may be life-threatening.