Fluids, Electrolytes, Nutrition Flashcards
Total Body Water
50-70% total body weight
Greater in lean individuals bc fat doesn’t have much water. Avg 60%.
Newborns 70%. Decreases with age to around 50%.
1L water = 1kg
2 compartments. ICF and ECF
ICF
mostly in skeletal muscle mass, thus a little lower in females (50%) than males (60%)
Cell wall separates ICF and ECF and acts as semipermeable membrane
ECF
Plasma and interstitial fluid
Capillary membrane separates plasma and interstitial fluid and acts as a semipermeable membrane
Fluid totals
ICF = 67% Total body water
ECF = 33% Total body water
- Interstitial = 25% total body water (75% of ECF)
- Plasma = 8% Total body water (25% of ECF)
Normal plasma osmolality
285-295 mmol/L
Calculated plasma osmolality
2[Na] + [gluc]/18 + [BUN]/2.8
Na is mmol/L
The others are mg/dL
Osmolar gap
Measured osmolality - calculated plasma osmolality
Normal gap 10 = lactic acid, ketones, methanol, ethanol
How much fluid can you lose through a trach?
1500ml/day if unhumidified and hyperventilation
Renal control of fluids/lytes
Distal tubules - reabsorption of Na in exchange for K and H secretion
Affected by ACTH and aldosterone
Aldosterone directly stimulates K secretion and Na reabsorption from distal tubule
Low Extracellular volume leads to low renal perfusion. This increases renin from JGA. Angiotensin 1 increases. Then Angio 2. Then aldosterone.
Aldosterone also released when low volume receptors in R atrium activated or from ACTH which is released in response to high K.
Causes of volume deficit (dehydration)
Mimics ECF loss:
Hemorrhage
Loss of GI fluid - vomit, NG suction, diarrhea, fistula
PostOp fluid sequestration - 3rd spacing: intestinal obstruction
Intra-abdominal and retroperitoneal inflammation (pancreatitis, peritonitis)
SIRS, burns, sepsis, pancreatitis
Losses that are mostly water:
- Fever
- Osmotic diuresis
- DI
- Prolonged water deprivation
- Inadequate input during procedure
Judging degree of dehydration
Mild = 3% (adults) or 5% (kids) loss of body weight
Mod = 6% or 10%
Severe = 9% or 15%
Treatment of dehydration
Initial intervention is to give a large bolus as a volume expander: 20 ml/kg of NS or LR
During the next 8 hrs, expected maintenance fluid given plus 1/2 of remaining calculated loss.
Over next 16 hrs, the other 1/2 of remaining loss is given along with the assumed maintenance fluid
Crystalloid
Dextrose is used to deliver free water to body (dextrose quickly metabolized)
0.9% NaCl quickly adds volume to intravascular space
Goal is to expand intravascular space
Colloids
pRBCs, FFP, albumin
Stay mainly within intravascular space if the capillary membranes are intact
Possible increased incidence of pulm embolism and respiratory failure
Expensive
Indications:
- Patients with too much Na and water but hypovolemic - ascites, CHF, postcardiac bypass
- Patients unable to make enough albumin or other proteins to exert enough oncotic pressure - liver disease, transplant recipients, resections, malnutrition
- Severe hemorrhage or coagulopathy
Isotonic causes of volume excess
Iatrogenic - intravascular overload of IVFs with lytes
Increased ECF without equilibration with ICF - esp postop or trauma when hormonal responses to stress are to decrease Na and H2O excretion by kidney
Often secondary to renal insufficiency, cirrhosis, CHF
Hypotonic causes of volume excess
Inappropriate NaCl-poor solution as a replacement for GI losses (most common)
Third spacing (shift of ECF from plasma to elsewhere like interstitial or transcellular spaces)
Increased ADH with surgical stress, inappropriate ADH (SIADH)
Hypertonic causes of volume excess
1 = excessive Na load without adequate water intake
- water moves out of cells bc of increased ECF osmolarity
- Causes increase in intravascular and interstitial fluid
- Worse when renal tubular excretion of water and/or Na is poor
- Can also be caused by rapid infusion of nonelectrolyte osmotically active solutes like glucose and mannitol
What can NS cause?
hypercholemic metabolic acidosis
What can LR cause?
When patient is hypovolemic and in metabolic alkalosis (from NG tube or vomiting), may worsen the alkalosis when lactate is metabolized
Treating hypervolemia
Restrict Na and fluids for isotonic
Free water replacement for hypertonic (will correct hypertonicity which should result in diuresis)
Saline for hypotonic (same as above)
Diuresis with furosemide 10-50mg
- replete K as needed
- don’t overdiuresis
Cardiogenic drugs, O2, artificial vent as needed (heart failure or resp failure)
Causes of ongoing fluid loss
Fever - each degreeC above 37 adds 2-2.5ml/kg/day of insensible water loss
Loss of body fluids (vomit, NG suction, fistulas)
3rd space losses
Burns
How much fluid does an average adult patient need?
About 2.5L/day… about 100ml/hr
unless other factors warrant higher rate
Calculating free water deficit
FWD = normal body water - current body water
NBW = 0.6 x body weight in kg
CBW = NBW (normal serum Na/measured serum Na)
How can labs show hypovolemia?
BUN/Cr > 20
FeNa
Working up hyponatremia
True hyponatremia = excess ingestion of water that overwhelms the kidneys (either normal or diseased) or due to increased ADH. It is NOT due to increased excretion of Na.
1) Determine plasma osmolality
- Normal: pseudohyponatremia. Lab artifact due to high lipids or plasma proteins. Check a lipid profile or possible Multiple Myeloma
- High - pseudohyponatremia. Due to increase of osmotically active molecules like glucose*** or mannitol
- Low - true hyponatremia
2) Assess volume status
- hypovolemia
- euvolemia
- hypervolemia
Account for glucose in hyponatremia
For every 100 mg/dl increment in plasma glucose above normal (normal = 100), plasma Na should decrease by 1.6 mEq/L
“sweet 16”
Glucose of 500 should have decrease of 6.4. 140-6.4 = 133.6
Hyponatremia with hypotonicity (true hyponatremia) and hypovolemia
- Renal cause = diuretics
- Extrarenal = vomit, diarrhea, burns, pancreatitis
Differentiate using urine Na. Urine Na 20 indicated renal cause.
True hyponatremia with euvolemia
SIADH = #1
Increased vasopressin release from posterior pit or ectopic source causes decreased renal free water excretion
Signs:
- hypo-osmotic hyponatremia (hypotonicity)
- Inappropriately concentrated urine (urine osmolality > 100)
- Normal renal, adrenal, thyroid function
Causes:
- neuropsych disorders, malignancies (esp lung), and head trauma
- glucocorticoid deficiency (Addison’s) - cortisol deficiency causes hypersecretion of ADH
- hypothyroidism - causes decreased CO and GFR which leads to increased ADH release
- primary polydipsia - usually in psych patients who compulsively drink massive volumes of water
True hyponatremia with hypervolemia
May be from CHF, cirrhosis, nephrotic syndrome
Increased thirst and ADH
Edematous state
Signs/symptoms of true hyponatremia in general and tx
Decreased reflexes, respiratory depression, seizures, coma
N/v, HA, lethargy, muscle cramps
For hypovolemic: Give 0.9% NaCl. Na repletion with saline isotonic to patient in order to avoid rapid changes in ICF volume.
Major complication from rapid correction of chronic hyponatremia is central pontine myelinolysis
For hypervolemic: Correct underlying disorder - CHF, liver or renal failure
For euvolemic: Raise plasma Na (lower ICF volume) - restrict water intake
Hypernatremia causes and signs
ALWAYS with hyperosmolarity
Causes:
- Loss of water (dehydration!): DI, diuretics, sweating, GI loss, burns, fistulas
- Gain of Na due to excess mineralocorticoid activity: Primary hyperaldosteronism, Cushing’s, renal artery stenosis (hyperreninism), congenital adrenal hyperplasia (will also cause hypoK)
- If thirst mechanism is intact and water is available, hypernatremia will not persist. Suspect hypernatremia in young, elderly, and patients with AMS who may not have access to water
Symptoms
- thirst
- restlessness, weakness, delirium
- hypotension and tachycardia
- decreased saliva and tears
- red, swollen tongue
- Oliguria
Tx
- Calculate free water deficit
- If euvolemic - replace water deficit as D5W
- if hypovolemic- use NS. Correct 1/2 of water deficit in first 24h then remaining over next 1-2days
K balance
99% of K is in ICF so small changes in ECF K has clinical effects - impaired electrical signaling in heart, muscle, nerve.
Proper proportion of K and Ca must exist for their exchange across membrane channels that allow electrical conduction to occur
Cells act as rapid K buffer. Kidney regulates long term K control
Too much K clinical
n/v, colic, diarrhea
Weakness, paralysis, resp failure
Arrhythmia, arrest
Too much Mg clinical
N/v
Weakness, lethargy, decreased reflexes
Hypotension, arrest
Too much Ca clinical
Anorexia, n/v, abdominal pain
Weakness, confusion, coma, bone pain
Hypertension, arrhythmia, polyuria, polydipsia
Too little K clinical
Ileus, constipation
Decreased reflexes, fatigue, weakness, paralysis
Arrest
Too little Mg clinical
Hyperactive reflexes, muscle tremors, tetany, seizures
Arrhythmia
Too little Ca clinical
Hyperactive reflexes, paresthesias, carpopedal spasm, seizures
HF
Causes of hypokalemia
Usually too much renal secretion
Loss of K due to excess mineralocorticoid activity - Primary hyperaldosteronism, Cushing’s, renal artery stenosis, congenital adrenal hyperplasia (will also cause hyperNa)
Movement of K into cells due to insulin, catecholamines, alkalemia
Prolonged administration of K-free parenteral fluids
Total parenteral hyperalimentation with inadequate K replacement
Loss of excessive lower GI secretions like diarrhea, colonic fistulas, VIPoma
Diuretics
Signs/symptoms of hypokalemia
ECG - flattened T waves, ST depression, U wave
Arrhythmias, signs of low voltage
Treating hypoK
Check Mg level first as hypomagnesiemia is commonly associated with hypoK and must be corrected before/along with hypoK.
Amount of K to be replaced can be estimated as 4-current K x 100, in mEq (if current K is 3.1, give 90 mEq)
If asymptomatic patient with K > 3, oral K may be enough
No more than 40 mEq should be added to a liter of IVF since rapid infusion causes fatal arrhythmias
Rate should not exceed 40 mEq/hr
May cause burning sensation if given in PIV. Using low flow of 10 mEq/hr or adding a small amount of lidocaine to solution can lower discomfort
Causes of hyperK
Usually renal failure
Rarely found when renal function is normal and usully causes a transient hyperK due to cellular shifts: K spills from cells in severe injury; cells take up H ions in exchange for intracellular K, acting as a buffer in state of acidosis
Drugs - ACE inhibitors, K sparing diuretics
Iatrogenic - Penicillin G has 1.7 mEq of K per 1M units, KCl added to maintenance fluids, blood transfusions with old batch of pRBCs where K may have leaked out of cells, overtreatment of hypoK
Digoxin - blocks Na-K-ATPase pump
Hypoaldosteronism
PseudohyperK: Can result when RBCs lyse in test tube and release K. This is lab error. Repeat test.
Signs/symptoms of hyperK
Cardiac effects most significant. Confirm hyperK and get ECG
ECG
- early: Peaked T waves, wide QRS, ST depression
- late: disappearance of T waves, heart block, sine wave (ominous for impending fatal arrhythmia), cardiac arrest
GI
- n/v, intermittent intestinal colic, diarrhea
Tx for hyperK
10% CaGluconate 1g IV - monitor ECG. Ca temporarily suppresses cardiac arrhythmias by stabilizing the cardiac membrane and should be given first. Does not effect K load. The membrane of cardiac muscle would abnormally fire in presence of high K.
Lower extracellular K (acute treatment): Albuterol, insulin with glucose, or sodium bicarb promote cellular reuptake of K
Kayexalate - cation exchange resin. As opposed to above measures, which immediately protect against dangers of high K, this actually removes the K from the body
Dialysis (last resort)
Calcium balance
Normal: 1,000 - 1,200 mg. Most in bone in form of phosphate and carbonate
Normal daily intake = 1-3g
Most excreted via stool
Normal serum 8.5-10.5 - half of this is nonionized and bound to plasma protein
Ionized calcium is the most accurate measure of calcium, but labs report total calcium
An additional nonionized fraction (5%) if bound to other substances in ECF
Ratio of ionized to nonionized Ca is related to pH
Acidosis causes increase in ionized fraction and alkalosis causes decrease in ionized fraction
First thing you do when you notice hypoCa
Correct for low albumin
Corrected Ca = 0.8 (Normal albumin - observed albumin) + observed calcium
If corrected Ca is within normal range, do nothing
Causes of hypoCa
- Acute pancreatitis
- Massive soft-tisse infections (nec fasc)
- Acute/chronic renal failure
- Pancreatic/small bowel fistuals
- Hypoparathyroidism (common after parathyroid or thyroid surgery)
- Hypoproteinemia
- Severe depletion of Mg
- Severe alkalosis may elicit symptoms with normal serum levels bc there is a decrease in ionized fraction of total serum Ca
Signs/symptoms of hypoCa
Numbness and tingling of fingers, toes, and around mouth
Increased reflexes
Chvostek’s sign: tapping over facial nerve in front of tragus of the ear causes ipsilateral twitching
Trousseau’s sign: Carpopedal spasm following inflation of sphygmomanometer cuff to above systolic blood pressure for several minutes
Muscle and abdominal cramps
Convulsions
ECG - prolonged QT interval
Tx for hypoCa
IV Ca Gluconate or CaCl2
Monitor QT interval on ECG
Causes of hyperCa
Hyperparathyroidism
Cancer (esp breast, MM)
Drugs (thiazides)
Signs/symptoms of hyperCa
Fatigue, weakness, anorexia, weight loss, n/v
Somnambulism (sleepwalking), stupor, coma
Severe HA, pain in back and extremities, thirst, polydipsia, polyuria
Death
Tx for hyperCa
Vigorous volume repletion with salt solution - dilutes Ca and increases urinary Ca excretion
- can be augmented with furosemide
- definitive tx of acute hypercalcemic crisis in patients with hyperparathyroidism is immediate surgery
Treat underlying cause
Indications for enteral nutritional support
Gut works but oral intake not possible - AMS, ventilator, oral/pharyngeal/esophageal disorders
Oral intake not sufficient for metabolic requirements - anorexia, sepsis, severe trauma/burns
Presence of malnutrition and wasting
Indications for TPN
Enteral feeding not possible - GI obstruction, ileus
Enteral intake not enough for metabolic requirements - chronic diarrhea/emesis, malabsorption, fistulas, chemo, irradiation therapy
Biggest danger of TPN is infection (organic products in TPN can become infiltrated with bacteria and sent right into the blood)
Adjunctive support needed for managing disease - pancreatitis, hepatic failure, renal failure, chylothorax
Basal energy expenditure for males
25 kcal/kg/day
Basal energy expenditure for females
22 kcal/kg/day
Calorie requirements for nonstressed patient
BEE x 1.2
Calorie requirements for postsurgery
BEE x 1.3 - 1.5
Calorie requirements for trauma/sepsis/burns
BEE x 1.6 - 2
Calorie requirements for fever
12% increase per degree C over 37
Important to keep in mind for calorie requirements
must be met with non-protein calories. 70% carbs. 30% fat
Respiratory quotient
ratio of CO2 released to O2 consumed per unit metabolism of a substrate (VCO2/VO2)
Lipid = 0.7
Protein = 0.8
Carb = 1.0
Balanced diet = 0.83
Protein requirement
0.8 - 1 g/kg body weight
Increases in illness and is maximal in burn patients
Avg surg patient needs 1.2-1.6 g/kg
Each gram of urinary nitrogen is equivalent to 6.25g of degraded protein
Nitrogen balance = (protein intake in g/6.25) - (Urinary urea nitrogen + 4)
Goal nitrogen balance should be positive 4-6
Enteral vs parenteral
Enteral preferred. Reduces infection. May be continuous or intermittent.
Routes for GI feeding = PO, NG, gastrostomy, jejunostomy
Glutamine is the fuel for enterocytes
Short chain fatty acids serve as fuel for the colonocytes
Omega 3 fatty acids and arginine serve as immune modulating agents
Complications of enteral = diarrhea, aspiration, obstruction of tube
Causes of elevated anion gap metabolic acidosis
AG > 12
MUDPILES + CAT
Methanol/Metabolism (inborn error) Uremia DKA Paraldehyde/ Propylene glycol Iron/Isoniazid/Isopropyl alcohol Lactic acidosis Ethylene glycol Salicylates/strychnine
CO, CN-
Alcoholic ketoacidosis
Toluene
4 basic processes = ketoacidosis, lactic acidosis, renal failure, intoxication
Causes of normal anion gap metabolic acidosis
HARDUPS + G
Hyperparathyroidism/Hyperalimentation (TPN), hyperparathyroid Adrenal insufficiency/Acetazolamide, Addison's, Ammonium Chloride Renal tubular acidosis*** Diarrhea*** Ureteroenteric fistula Pancreatic fistulas Sprionolactone, Saline Glue sniffing
Causes of respiratory alkalosis
MIS[HAP]3S
Mechanical overventilation/MI/Meningitis Increased ICP Sepsis Hypoxemia/Hyperpyrexia/HF Anxiety/Asthma/Ascites Pregnancy/Pain/Pneumonia Salicylates
Figuring out acid/base disorders
1) pH in relation to 7.4
2) CO2 in relation to 40
Resp acidosis: pH 40
Metabolic acidosis: pH 7.4, CO2 7.4, CO2 > 40
So you have resp acidosis, what now?
For every change in CO2 of 10, the pH should also change by 0.08 (acute) or 0.04 (chronic)
For every change in CO2 of 10, the HCO3 should change by 1 (acute) or 3 (chronic) in direction that brings pH back to normal
If we find there’s too much HCO3 (over corrected) = coexisting metabolic alkalosis
If we find there’s too little HCO3 = coexisting metabolic acidosis
So you have metabolic acidosis, what now?
1) Is CO2 appropriate? Use Winter’s formula (1.5HCO3 + 8 +/- 2). If CO2 > expected from formula, there is also a respiratory acidosis. If CO2 2 = metabolic alkalosis
If 1-2, pure anion gap acidosis (lactic acidosis about 1.6, DKA around 1)
If
So you have respiratory alkalosis, now what?
For every change in CO2 of 10, the pH should also change by 0.08 (acute) or 0.04 (chronic)
For every change in CO2 of 10, the HCO3 should change by 2 (acute) or 4 (chronic) in direction that brings pH back to normal
Too much HCO3? Coexisting metabolic alkalosis
Too little? Coexisting metabolic acidosis
So you have metabolic alkalosis, now what?
1) Urine Cl > 10 = not volume responsive
- is there HTN? Yes = hyperaldosteronism, renal artery stenosis. No = Barter’s, Gittelman’s
2) Urine Cl
Causes of respiratory acidosis
Hypoventilation
Opiate OD
Asthma/COPD with air trapping
Muscular strength (long-term ventilators or obese/OSA)
