Fluids and Electrolytes Flashcards
Osmotic Pressure
Pulling force created by particles (i.e. plasma proteins) that do not pass through capillary pores
Capillary colloidal pressure is greater than interstitial colloidal pressure
Hydrostatic Pressure
Fluid pushing force inside the capillary
Inside capillaries hydrostatic pressure and capillary filtration pressure are equal
S/S of Dehydration
Increased thirst Dry mouth Tired or sleepy Decreased urine output Urine is low volume and more yellowish than normal Headache Dry skin Dizziness Few or no tears
Sodium, Na+2
135-145 mEq/L
- the most abundant cation in ECF
- functions: maintain water balance, nerve
impulse transmission, regulate acid-base
balance, and participate in cellular
chemical reactions.
- regulated by dietary intake & aldosterone
secretion
Hyponatremia
Na+ < 135 mEq/L sodium loss (GI, renal, & skin losses: sweating); pshychogenic polydipsia (drinking water increase); water intoxication; SIADH (Excess ADH)
Hyponatremia S/S
lethargy, edema, headache, disorientation, seizures, coma. Pure Na loss: hypovolemia Dilutional: Hypervolemia
Hypernatremia
Na+ > 145mEq/L
Causes: Excess salt intake, aldosterone secretions, Diabetes Insipidus, increased sensible & insensible water loss, water deprivation (hypertonic/hypernatremic)
Hypernatremia S/S
thirst, dry & flushed skin, dry & sticky m.m., postural hypotension, fever, CNS: agitation, decreased reflexes, convulsions, restlessness, & irritability.
Hypocalcemia
Ca2+< 8.5 mg/dL
Rapid administration of blood containing citrate, hypoalbuminemia, hypoparathyroidism, vitamin D deficiency, alkalosis, pancreatitis, Chronic Renal Failure (Vitamin D not activated), chronic alcoholism
Hypocalcemia S/S
numbness & tingling of fingers and circumoral (around mouth) region, hyperactive reflexes, +Trousseau’s (nerve excitability/tetany of fingers during BP) & +Chvostek’s sign (Stroking cheek), muscle cramps, fractures (if chronic). ECG: prolonged ST & QT…
Hypercalcemia
Ca2+> 10.5 mg/dL
Hyperparathyroidism, Cancer, Paget’s disease, osteoporosis, prolonged bed rest, thiazide diuretics.
Hypercalcemia S/S
Anorexia, abdominal pain & constipation, muscle weakness, hypoactive reflexes, lethargy, flank pain (if kidney stones), ECG: shortened QT & ST segment
Hypokalemia
K+ < 3.5 mEq/L
Causes: Use of K+ wasting diuretics (most), polyuria, GI losses (vomiting, diarrhea, NG/colostomy outputs), alkalosis, Tx of DKA with insulin.
Hypokalemia S/S
Skeletal muscle weakness U wave/ ECG changes (PR Interval increase) Constipation, ileus Toxic effects of digoxin Irregular, weak pulse Orthostatic hypotension Numbness (paresthesias)
Chvostek sign
is a clinical sign of existing nerve hyperexcitability (tetany) seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve.
Trousseu sign
a test for latent tetany in which carpal spasm is induced by inflating a sphygmomanometer cuff on the upper arm to a pressure exceeding systolic blood pressure for 3 minutes. A positive test may be seen in hypocalcemia and hypomagnesemia.
Hyperkalemia
K > 5 mEq/L
Renal failure, fluid volume deficit, massive cellular damage (burns & trauma), acidosis (esp DKA), rapid infusion of stored blood, use of K+-sparing diuretics, salt substitutes.
Hyperkalemia S/S
ECG changes (tall, tented T wave), paresthesias, muscle weakness, abdominal cramping, diarrhea.
Renin/ADH/Aldosterone/Angiotensin
- Low blood pressure/blood flow is sensed by the Juxtaglomerular apparatus in the kidney (which are cells next to the glomerulus). This is because a decrease in Na+ will reduce the amount of water in the blood, thus the blood will have a lower pressure. This follows the principle of osmosis, which states that water will diffuse to areas that have highly concentrated solutes.
- In response to this, the glomerulus releases a hormone known as renin into the blood stream.
- Renin then moves to the liver, where it converts an inactive peptide (protein) angiotensinogen to an active angiotensin I.
- Angiotensin I then travels to the lungs where an enzyme known as the Angiotensin Converting Enzyme (ACE), converts Angiotensin I to Angiotensin II. One effect Angiotensin II has on the body is in its ability to constrict blood vessel, thus increasing blood pressure. Another function of it is to stimulate the adrenal glands on top of the kidneys to produce the hormone Aldosterone.
- Aldosterone stimulates the reabsorption of sodium (Na+) in the distal convoluted tubules. Increasing sodium reabsorption means that water and chloride will follow, thus increasing blood volume.
- An increase in blood volume may also trigger the release of a hormone known as Atrial Natriuretic Hormone, which inhibits the release of Aldosterone, keeping the body’s water and sodium levels at the homeostatic levels. This last step is known as a negative feedback loop.