Professional Documents
Culture Documents
Anions- negatively charged ions The concentration of electrolytes usually is expressed in terms of the
o Cl chemical combining activity, or equivalents.
o HCO3 Equivalent = atomic weight (g)/valence
o PO4 For univalent ions such as sodium, 1 mEq = 1 mmol.
Non Electrolyte solute For divalent ions such as magnesium, 1 mmol = 2 mEq.
o Proteins and glucose - important to know bec they usually o The number of milliequivalents of cations must be balanced by the
affects fluid movement in the body same number of milliequivalents of anions.
o Expression of molar equivalents alone does not allow a physiologic
comparison of solutes in a solution.
Movement of water across a cell membrane is dependent on osmosis.
Osmotic equilibrium
reached when water moves across a semipermeable membrane to
equalize the concentration
movement is determined by the concentration of the solutes on each side
of the membrane.
Osmotic pressure
measured in units of osmoles (osm) or milliosmoles (mOsm) that refer
to the actual number of osmotically active particles.
o Ex: 1 mmol of sodium chloride contributes to 2 mOsm (one from
sodium and one from chloride).
Principal determinants of osmolality- concentrations of sodium,
glucose, and urea (blood urea nitrogen, or BUN):
Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)
Osmolality of the intracellular and extracellular fluids = 290 and 310
mOsm in each compartment.
Osmotic Pressure
The physiologic activity of electrolytes in solution depends on
o # of particles per unit volume (mmol/L)
o # of electric charges per unit volume (mEq/L)
o # of osmotically active ions per unit volume (mOsm/L)
SarCy Checked by: Jaye Page 2 of 9
Fluid and Electrolytes SURGERY I
Kidneys must excrete a minimum of 500 to 800 mL of urine per day, Table 3. IV fluids concentration
regardless of the amount of oral intake To clear the products of
metabolism
The typical individual consumes 3 to 5 g of dietary salt per day, with
the balance maintained by the kidneys.
o With hyponatremia or hypovolemia, sodium excretion can be
reduced to as little as 1 mEq/d or maximized to as much as 5000
mEq/d to achieve balance except in people with salt-wasting
kidneys.
Sweat is hypotonic, and sweating usually results in only a small sodium
loss. When you infuse IV fluid to px, you have to know if its isotonic, hypo
GI losses are isotonic to slightly hypotonic and contribute little to net or hyper so you will know if it promotes water retention or water
gain or loss of free water when measured and appropriately replaced by excretion
isotonic salt solutions.
Plasma expanders- used when there is no ready blood products
Table 2. Regulation of Water Balance Ex: colloid, serum, protein, albumin
What to do?
Fluids resuscitation
Normal saline or lactated ringers (avoid potassium until urine
output in increases)- if there is hemorrhage we give blood
products (1ml loss is to 1ml), tht’s the best but if not available
we use lactated ringers or plasma expanders though it does
not give hemoglobin it increases plasma volume
Medications for sources of fluid loss (for chronic extracellular
fluid deficit like enterocutaneus fistulas, diarrhea-
antidiarrheal, infection-antibiotics, fever- antipyretic
cvomiting- antiemesis )
Daily weight and strict Intake/output (weight loss or gain is the
best indication)
B. Extracellular Fluid Excess
May be iatrogenic or secondary to renal dysfunction, congestive heart
failure, or cirrhosis.
Both plasma and interstitial volumes usually are increased.
In fit patients, edema and hyperdynamic circulation are common and well
tolerated.
However, the elderly and patients with cardiac disease may quickly
develop congestive heart failure and pulmonary edema in response to
only a moderate volume excess.
The classic signs of hypovolemic hypernatremia, (tachycardia, Next, depletional versus dilutional causes of hyponatremia are evaluated.
orthostasis, and hypotension) may be present, as well as the unique In the absence of renal disease, depletion is associated with low urine
findings of dry, sticky mucous membranes. sodium levels (<20 mEq/L), whereas renal sodium wasting shows high
urine sodium levels (>20 mEq/L).
Causes o Dilutional causes of hyponatremia usually are associated with
Water loss or excess Na hypervolemic circulation. A normal volume status in the setting of
Decrease excretion hyponatremia should prompt an evaluation for a syndrome of
Increased intake inappropriate secretion of ADH.
Increased water loss-usually due to dilution, Na elevate if you
lose a lot of water Causes
Symptoms (F-R-I-E-D) Water excess
Fever Dilution
Restless Increased excrertion of Na
Increased fluid retention and BP Decreased intake
Edema (peripheral/pitting) Symptoms
Decreased urine output, dry mouth Confusion
What to do? Headace
Treat underlying cause Seizures
Diuretics-immediate treatment Abdominal cramps
Sodium restriction There are similarities in symptoms in hyper and hypo because it
Seizure precaution-in correcting sodium, reduce the sodium affects the brain
slowly What to do?
3% saline
Hyponatremia If caused by fluid excess will need fluid restriction
A low serum sodium level occurs when there is an excess of extracellular Can’t be fixed by adding Na to the diet
water relative to sodium.
In most cases, hyponatremia is a consequence of either sodium depletion
or dilution. B. Potassium
Dilutional hyponatremia frequently results from excess extracellular Average dietary intake -50
water and therefore is associated with a high extracellular volume status. to 100 mEq/d
o Excessive oral water intake or iatrogenic intravenous (IV) excess Extracellular potassium is
free water administration can cause hyponatremia. maintained within a
Postoperative patients are particularly prone to increased secretion of narrow range, principally
antidiuretic hormone (ADH), which increases reabsorption of free water by renal excretion of
from the kidneys with subsequent volume expansion and hyponatremia. potassium, which can
o This is usually self-limiting in that both hyponatremia and volume range from 10 to 700
expansion decrease ADH secretion. mEq/d.
Additionally, a number of drugs can cause water retention and Although only 2% of the
subsequent hyponatremia, such as the antipsychotics and tricyclic total body potassium (4.5
antidepressants as well as angiotensin-converting enzyme inhibitors. mEq/L × 14 L = 63 mEq)
The elderly are particularly susceptible to drug-induced hyponatremia. is located within the
Physical signs of volume overload usually are absent, and laboratory extracellular compartment
evaluation reveals hemodilution. = critical to cardiac and
Depletional causes of hyponatremia are associated with either a neuromuscular function
decreased intake or increased loss of sodium-containing fluids. The intracellular and
A concomitant ECF volume deficit is common. extracellular distribution
o Causes include decreased sodium intake, such as consumption of a of potassium is influenced
low-sodium diet or use of enteral feeds, which are typically low in by a number of factors,
sodium; GI losses from vomiting, prolonged nasogastric suctioning, including surgical stress,
or diarrhea; and renal losses due to diuretic use or primary renal injury, acidosis, and tissue
disease. catabolism.
o Hyponatremia also can be seen with an excess of solute relative to Hyperkalemia
free water, such as with untreated hyperglycemia or mannitol
administration. serum potassium concentration above the normal range of 3.5 to 5.0
o Glucose exerts an osmotic force in the extracellular compartment mEq/L.
a shift of water from the intracellular to the extracellular space. It is caused by excessive potassium intake, increased release of potassium
Hyponatremia therefore can be seen when the effective osmotic pressure from cells, or impaired potassium excretion by the kidneys
of the extracellular compartment is normal or even high. Increased intake can be either from oral or IV supplementation, or from
o When hyponatremia in the presence of hyperglycemia is being red cell lysis after transfusion.
evaluated, the corrected sodium concentration should be calculated Hemolysis, rhabdomyolysis, and crush injuries can disrupt cell
as follows: membranes and release intracellular potassium into the ECF.
For every 100-mg/dL increment in plasma glucose above normal, the Acidosis and a rapid rise in extracellular osmolality from hyperglycemia
plasma sodium should decrease by 1.6 mEq/L or IV mannitol can raise serum potassium levels by causing a shift of
Lastly, extreme elevations in plasma lipids and proteins can cause potassium ions to the extracellular compartment.
pseudohyponatremia, because there is no true decrease in extracellular Because 98% of total body potassium is in the intracellular fluid
sodium relative to water. compartment, even small shifts of intracellular potassium out of the
Signs and symptoms of hyponatremia are dependent on the degree of intracellular fluid compartment can lead to a significant rise in
hyponatremia and the rapidity with which it occurred. extracellular potassium.
Clinical manifestations primarily have a central nervous system origin A number of medications can contribute to hyperkalemia, particularly in
and are related to cellular water intoxication and associated increases in the presence of renal insufficiency, including potassium-sparing
intracranial pressure. diuretics, angiotensin-converting enzyme inhibitors, and nonsteroidal
Oliguric renal failure also can be a rapid complication in the setting of anti-inflammatory drugs (NSAIDs).
severe hyponatremia. Spironolactone and angiotensin-converting enzyme inhibitors interfere
A systematic review of the etiology of hyponatremia should reveal its with aldosterone activity, inhibiting the normal renal mechanism of
cause in a given instance. potassium excretion.
o Hyperosmolar causes, including hyperglycemia or mannitol infusion Acute and chronic renal insufficiency also impairs potassium excretion.
and pseudohyponatremia, should be easily excluded. Symptoms of hyperkalemia are primarily GI, neuromuscular, and
cardiovascular
SarCy Checked by: Jaye Page 5 of 9
Fluid and Electrolytes SURGERY I
o GI symptoms - nausea, vomiting, intestinal colic, and diarrhea. Increase digoxin toxicity
o Neuromuscular symptoms - range from weakness to ascending Diuresis
paralysis to respiratory failure.
o Early cardiovascular signs may be apparent from electrocardiogram What to do?
(ECG) changes and eventually lead to hemodynamic symptoms of Cardiac monitor
arrhythmia and cardiac arrest. Increased intake -unlike Na, you can give supplements orally
ECG changes that may be seen with hyperkalemia include high peaked T or K rich food
waves (early), widened QRS complex, flattened P wave, prolonged PR Watch digoxin toxicity
interval (first-degree block), sine wave formation, and ventricular Potassium IV (only if good urine output- normal 500-600 ml
fibrillation. per day or 30cc/ hour for px with catheter)
Spironolactone
Causes Treat constipation
Kidney failure,
Increased intake C. Calcium
Cell destruct The vast majority of the body’s calcium is contained within the bone
Acidosis matrix, with <1% found in the ECF.
Hypoxia Serum calcium is distributed among three forms: protein found (40%),
Exercise complexed to phosphate and other anions (10%), and ionized (50%).
Catabolic state It is the ionized fraction that is responsible for neuromuscular stability
Use of potassium diuretics-spironolactone and can be measured directly.
Symptoms (M-U-R-D-E-R) -pertains to heart When total serum calcium levels are measured, the albumin
Muscle weakness concentration must be taken into consideration:
Urine oliguria, anuria Adjust total serum calcium down by 0.8 mg/dL for every 1 g/dL
Respiratory distress decrease in albumin.
Decreased cardiac contractility Unlike changes in albumin, changes in pH will affect the ionized
ECG changes calcium concentration.
Reflexes, hyperreflexia or areflexia Acidosis decreases protein binding, thereby increasing the ionized
What to do? fraction of calcium.
Cardiac monitor Daily calcium intake is 1 to 3 g/d.
Kayexalate, calcium gluconate or glucose + insulin (insulin Most of this is excreted via the bowel, with urinary excretion relatively
increases potassium uptake in cells; give glucose because low.
insulin promotes hypoglycemia Total body calcium balance is under complex hormonal control, but
Lasix if kidneys are functioning disturbances in metabolism are relatively long term and less important
Potassium retriction in the acute surgical setting.
Dialysis if severe
Hypercalcemia
Hypokalemia serum calcium level above the normal range of 8.5 to 10.5 mEq/L or an
much more common than hyperkalemia in the surgical patient. increase in the ionized calcium level above 4.2 to 4.8 mg/dL.
It may be caused by inadequate potassium intake; excessive renal Primary hyperparathyroidism in the outpatient setting and malignancy
potassium excretion; potassium loss in pathologic GI secretions, such in hospitalized patients, from either bony metastasis or secretion of
as with diarrhea, fistulas, vomiting, or high nasogastric output; or parathyroid hormone–related protein, account for most cases of
intracellular shifts from metabolic alkalosis or insulin therapy. symptomatic hypercalcemia.
The change in potassium associated with alkalosis can be calculated by Symptoms of hypercalcemia, which vary with the degree of severity,
the following formula: Potassium decreases by 0.3 mEq/L for every include neurologic impairment, musculoskeletal weakness and pain,
0.1 increase in pH above normal. renal dysfunction, and GI symptoms of nausea, vomiting, and
Additionally, drugs such as amphotericin, aminoglycosides, cisplatin, abdominal pain.
and ifosfamide that induce magnesium depletion cause renal o Cardiac symptoms can be manifest as hypertension, cardiac
potassium wastage. arrhythmias, and a worsening of digitalis toxicity.
In cases in which potassium deficiency is due to magnesium depletion, ECG changes in hypercalcemia include shortened QT interval, prolonged
potassium repletion is difficult unless hypomagnesemia is first PR and QRS intervals, increased QRS voltage, T-wave flattening and
corrected. widening, and atrioventricular block (which can progress to complete
The symptoms of hypokalemia like those of hyperkalemia, are primarily heart block and cardiac arrest).
related to failure of normal contractility of GI smooth muscle, skeletal
muscle, and cardiac muscle. Causes
Findings may include ileus, constipation, weakness, fatigue, diminished Hyperparathoid
tendon reflexes, paralysis, and cardiac arrest. In the setting of ECF Vitamin D excess
depletion, symptoms may be masked initially and then worsened by Prolonged immobilization
further dilution during volume repletion. Renal failure
ECG changes suggestive of hypokalemia include U waves, T-wave Malignancies
flattening, ST-segment changes, and arrhythmias (with digitalis Symptoms
therapy). Lethargy
Confusion
Causes Prone to fratures
Vomiting Increase clotting itme (DVT)
Nasogastric tube losses Depressed reflexes
Diarrhea Kidney stones
Medications- Lasix, diuretics What to do?
Metabolic alkalosis Lasix
Rapid cell building Hydration with normal saline
Symptoms Increased oral fluid intake
Dysrhythmia
Weakness, paralysis Hypocalcemia
Nausea a/ vomiting serum calcium level below 8.5 mEq/L or a decrease in the ionized
Paralytic ileus-important in abdominal surgeons when bowel calcium level below 4.2 mg/dL.
+
fxn does not return to normal-check K levels and correct by The causes of hypocalcemia include pancreatitis, massive soft tissue
giving potassium rich food infections such as necrotizing fasciitis, renal failure, pancreatic and
Constipation
Low BP , weak pulse
SarCy Checked by: Jaye Page 6 of 9
Fluid and Electrolytes SURGERY I
small bowel fistulas, hypoparathyroidism, toxic shock syndrome, rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe
abnormalities in magnesium levels, and tumor lysis syndrome. hypothermia, and malignant hyperthermia.
Excessive phosphate administration from IV hyperalimentation solutions
Transient hypocalcemia or phosphorus containing laxatives may also lead to elevated phosphate
o occurs after removal of a parathyroid adenoma due to atrophy of the levels.
remaining glands and avid bone remineralization, and sometimes Most cases of hyperphosphatemia are asymptomatic
requires high-dose calcium supplementation. Significant prolonged hyperphosphatemia metastatic deposition of soft
Additionally, malignancies associated with increased osteoblastic tissue calcium-phosphorus complexes
activity, such as breast and prostate cancer, can lead to hypocalcemia
from increased bone formation. Causes
Calcium precipitation with organic anions is also a cause of Renal failure
hypocalcemia and may occur during hyperphosphatemia from tumor Tumor lysis syndrome
lysis syndrome or rhabdomyolysis. Hypoparathyroidism
Pancreatitis may sequester calcium via chelation with free fatty acids. Laxatives or enemas containing phosphate
Massive blood transfusion with citrate binding is another mechanism. Symptoms
Hypocalcemia rarely results solely from decreased intake, because Calcium deposits in joinys, skins, kidneys -because of
bone reabsorption can maintain normal levels for prolonged increased in calcium resorption from the bone
periods. Hypocalcemia
Tetany
Asymptomatic hypocalcemia Neuromascular irritability
o occur when hypoproteinemia results in a normal ionized calcium What to do?
level. Treat the hypocalcemia
Conversely, symptoms can develop with a normal serum calcium level
during alkalosis, which decreases ionized calcium. Hypophosphotemia
In general, neuromuscular and cardiac symptoms do not occur until the due to a decrease in phosphorus intake, an intracellular shift of
ionized fraction falls below 2.5 mg/dL
phosphorus, or an increase in phosphorus excretion.
Clinical findings may include paresthesias of the face and extremities, Decreased GI uptake due to malabsorption or administration of phosphate
muscle cramps, carpopedal spasm, stridor, tetany, and seizures.
binders and decreased dietary intake from malnutrition are causes of
Patients will demonstrate hyperreflexia and may exhibit positive chronic hypophosphatemia.
Chvostek’s sign (spasm resulting from tapping over the facial nerve)
Most acute cases are due to an intracellular shift of phosphorus in
and Trousseau’s sign (spasm resulting from pressure applied to the
association with respiratory alkalosis, insulin therapy, refeeding
nerves and vessels of the upper extremity with a blood pressure cuff or
syndrome, and hungry bone syndrome.
tourniquet).
Clinical manifestations of hypophosphatemia usually are absent until
Hypocalcemia decreased cardiac contractility and heart failure.
levels fall significantly.
ECG changes of hypocalcemia include prolonged QT interval, T-wave
In general, symptoms are related to adverse effects on the oxygen
inversion, heart block, and ventricular fibrillation
availability of tissue and to a decrease in high-energy phosphates, and
can be manifested as cardiac dysfunction or muscle weakness.
Causes
Hypoparathyroidism -hypcalcemia is seen in patients who Causes
undergone complete thyroidectomy due to possible
Malabsorption syndormes
devascularization or excision of parathyroid
Diarrhea
Malabsorption
Deficient serum albumin Excessive use of antacids
Increased serum Ph Hyperparathyroidism
Lack of Vitamin D because Vit Anemias
Chronic Renal failure Bleeding disorder
Symptoms Symptoms
Increased neuromuscular stimulation Impaired neurologic functions
Muscle spasms, cramps Anorexia
Chvostek sign - tap facial nerve there is hyperstimulation Osteomalacia
causing twitching What to do?
Trousseau sign -place tourniquet wait for 5 min, there isrolling Oral supplements
of wrist but very uncomfortable for px Decreased calcium intake because PO4 is inversely related to
Arrhythmias Ca intake
Intestinal cramping
What to do E. Magnesium
Give oral or IV supplements with Vit D (cant give oral calcium fourth most common mineral in the body
without Vit D because it is important for absorption) found primarily in the intracellular compartments.
Approximately one half of the total body content of 2000 mEq is
D. Phosphate incorporated in bone and is slowly exchangeable.
Primary intracellular divalent anion Of the fraction found in the extracellular space, one third is bound to
Abundant in metabolically active cells. serum albumin.
involved in energy production during glycolysis o Therefore, the plasma level of magnesium may be a poor indicator
found in high-energy phosphate products such as adenosine triphosphate. of total body stores in the presence of hypoalbuminemia.
Serum phosphate levels are tightly controlled by renal excretion.
Magnesium should be replaced until levels are in the upper limit of
Hyperphosphotemia normal.
due to decreased urinary excretion, increased intake, or endogenous Normal dietary intake is approximately 20 mEq/d
mobilization of phosphorus. excreted in both the feces and urine.
Most cases of hyperphosphatemia are seen in patients with impaired renal The kidneys have a remarkable ability to conserve magnesium, with renal
function. excretion <1 mEq/d during magnesium deficiency.
Hypermagnesemia
Hypoparathyroidism or hyperthyroidism
o can decrease urinary excretion of phosphorus lead to rare but can be seen with severe renal insufficiency and parallel changes
hyperphosphatemia. in potassium excretion.
Increased release of endogenous phosphorus can be seen in association Magnesium-containing antacids and laxatives can produce toxic levels in
with any clinical condition that results in cell destruction, including patients with renal failure.
End of Transcription