fluid/electrolytes Flashcards
normal range sodium
135-145; maintains h2o balance
impulse transmission, muscle contraction, fluid and electrolyte balance
normal range potassium
3.5-5; transmission of nerve and muscle impulses
resting membrane potential, action potentials of nerves and muscles, maintain intracellular volume
normal range chloride
104-106; buffer and regulates acid-base
regulating osmotic pressure, forming HCl in gastric acid. controlled indirectly by ADH and processes that affect renal reabsorption of sodium
normal range calcium
9-11; nerve impulse transmission; heart contractions
normal range BUN
10-20; urea is by product of metabolism
Normal range creatinine
0.7-1.2; produced by your muscle metabolism
normal range co2
22-26 buffer
normal range magnesium
1.5-2.5 nerve conduction and muscle tissue function
sum of cations in body=sum of anions in body
both 153
phosphates
regulate pH, controlled by aldosterone and renal system
excess Sodium
hypernatremia thirst CNS deterioration Increased interstitial fluid cellular dehydration net loss of water or sodium gain dehydration
Sodium deficit
Hyponatremia CNS deterioration often age related etiology due to decreased renal function fingerprint edema muscle cramps, weakness, fatigue nausea, vomiting, cramps, diarrhea apathy, lethargy, headache depression of deep tendon reflexes
excess potassium
hyperkalemia (decreased renal elimination, excessively rapid administration, mvmt of K+ from ICF to ECF) ventricular fibrillation ECG changes CNS changes Weakness
Potassium deficit
Hypokalemia (inadequate intake, excessive GI, skin, renal losses-diuretic therapy, or redistribution to ECF from ICF) bradycardia ECG changes CNS changes Fatigue
excess calcium
hypercalcemia
thirst
CNS deterioration
Increased interstitial fluid
calcium defict
hypocalcemia tetany Chvostek's, Trousseau's signs Muscle twitching CNS changes ECG changes
Excess Magnesium
hypermagnesemia
Loss of deep tendon reflexes (DTR’s)
Depression of CNS
Depression of neuromuscular function
Magnesium deficit
hypomagnesemia
hyperactive DTR’s
CNS changes
nonelectrolytes
urea
glucose
creatinine
bilirubin
isotonic fluid
280-300 mOsm/kg
Hypotonic fluid
less than 280 mOms/kg
used to hydrate the cells
cells draw in water and swell
Hypertonic fluid
greater than 300 mOsm/kg
draws fluid from the cells
increase ECF osmolality
cells shrink
decrease ECF osmolality
cells swell
The rules of fluid replacement
replace blood with blood plasma with colloid resuscitate with colloid ecf depletion with saline rehydrate with dextrose
how does the body regulate our fluid volume?
Thirst ADH RAAS SNS ANP
adh
increases water reabsorption
increases urine concentration
decreases serum concentration
disorders of ADH
SIADH
Diabetes Insipidis
SIADH
overproduction of ADH
fluid retention, edema
low sodium triggers increased ADH
HYPONATREMIA
diabetes insipidus
lack of ADH
damage to hypothalamus or pituitary gland
nephrogenic diabetes insipidus
failure of kidneys to respond to ADH and vasopressin
Renin
enzyme produced and released by kidney in response to decreased renal perfusion secondary to decreased circulating volume or increased SNS stimulation
Renin interacts with angiotensinogen to produce angiotensin 1
angiotensin 1
converted to angiotensin 2 in lungs by converting enzyme ACE
angiotensin 2
stimulates secretion of aldosterone
aldosterone
mineralocorticoid hormone released by the adrenal cortex which acts upon the distal portion of the renal tubule
- slowly boosts water reabsorption by the kidneys by increasing the reabsorption of NaCl
- acts as a volume regulator bc sodium retention leads to water retention
ANP
atrial natriuretic peptide
hormone released by the cardiac atria in response to increased atrial pressure
released in resonse to any condition that causes elevated cardiac filling pressures
effect of angiotensin 2
First spacing
normal distribution of fluid in ICF and ECF (the vascular space)
second spacing
abnormal accumulation of interstitial fluid (edema)
Third Spacing
Fluid accumulation in part of body where it is not easily exchanged with ECF (ascites)
hematocrit
%RBC in whole blood
increases with dehydration (hemoconcentration)
decreases with overhydration (hemodilution)
normal male 40-54%
normal female 37-47%
BMP
BUN blood urea is a byproduct of metabolism and is primarily excreted by the kidneys in urine
normal 7-20 mg/dL
urine osmolality
measures solute concentration of urine
24 hour specimen 300-900 mOsm/kg
urea, creatinine, and uric acid are the primary determinants of urine osmolality
urine specific gravity
elevates the kidney’s ability to conserve or excrete urine
normal 1.010-1.020
Fluid Volume Excess
neck vein distension pulmonary edema weight gain peripheral edema full, bounding pulses, elevated BP congestive heart failure
fluid volume deficit
sunken eyeballs dry mucus membranes weight loss increased respiratory rate decreased skin turgor flattened neck veins increased heart rate decreased BP
acidosis
an abnormal process which would lower arterial pH if there were no secondary changes in response to the primary etiological factor
too many circulating H+
Alkalosis
an abnormal procss which would raise arterial pH if there were no secondary changes in response to the primary etiological factor
not enough H+ in ECF
acidemia
arterial pH less than 7.35
alkalemia
arterial pH greater than 7.45
normal pH ACID BASE BALANCE
7.35-7.45
normal PaCO2 RESP
35-45 mm Hg
normal HCO3- KIDNEY
22-26 mEq/L
pulmonary embolism
respiratory alkalosis
hypotension
metabolic acidosis
vomiting
metabolic alkalosis
severe diarrhea
metabolic alkalosis
cirrhosis
resp alkalosis
renal failure
metabolic acidosis
sepsis
respiratory alkalosis, metabolic acidosis
pregnancy
resp alkalosis
diuretic use
metabolic alkalosis
COPD
resp acidosis
respiratory acidosis
carbonic acid excess caused by blood levels of CO2 above 45 mmHG
hypercapnia-high levels of CO2 in blood
breathing too slow
depression of respiratory center in brain -drugs, head trauma
paralysis of respiratory or chest muscles
emphysema
adult respiratory distress syndrome
acute respiratory acidosis
pulmonary edema
acute respiratory acidosis
pneumothorax
acute respiratory acidosis
treatment of respiratory acidosis
restore venitlation
IV lactate solution
treat underlying dysfunction or disease
Respiratory Alkalosis
carbonic acid defict
pCO2 less than 35 mm HG (hypocapnea)
most common acid-base imbalance
breathing is too fast
causes of respiratory alkalosis
high altitudes pulmonary disease and congestive heart failure caused by hypoxia acute anxiety fever, anemia cirrhosis gram - sepsis
treatment of respiratory alkalosis
treat underlying cause
breathe into a paper bag
IV Choloride containing colution Cl- replace lost HCO3-
metabolic acidosis
HCO3- deficit (less than 22 mEq/L)
Causes to metabolic acidosis
diarrhea or renal dysfunction (loss of HCO3-)
accumulation of acids (lactic acid or ketones)
Failur of kidneys to excrete H+
Symptoms of metabolic acidosis
headache, lethargy
nausea, vomiting, diarrhea
coma
death
treatment of metabolic acidosis
IV lactate solution
metabolic alkalosis
HCO3= excess (greater than 26 mEq/L)
causes of metabolic alkalosis
excess vomiting and diarrhea=loss of stomach acid excessive use of alkaline drugs certain diuretics endocrine disorders heavy ingestion of antacids severe dehydration
symptoms of metabolic alkalosis
respiration is slow and shallow hyperactive reflexes (tetany) often related to depletion of electrolytes atrial tachycardia dysrhythmias
treatment of metabolic alkalosis
electrolytes to replace those lost
IV Chloride containing solution
treat underlying disorder
interpreting the ABG
note whether the pH is low (acidosis) or high (alkalosis)
decide which value (pCO2=resp or HCO3- =metabolic) is outside normal range
Compensation?
look at the value that doesnt correspond to the observed pH change. If it is within normal range, then there is NO COMPENSATION occurring. If it is outside the normal range, the body is partially compensating for the problem.
hypertonic hyponatremia
osmotic shift of water from the ICF to the ECF compartment (hyperglycemia)
hypotonic hyponatremia
most common
caused by water retention
hypovolemic hyponatremia
water is lost along with sodium excessive sweating due to heat heavy exercise vomiting and diarrhea a lack of aldosterone increases renal losses of sodium and cortisol deficiency leads to increased release of ADH with water retention.
Euvolemic or Normovolemic hypotonic hyponatremia
retention of water with dilution of sodium while maintaining the ECF volume within normal range.
Result of SIADH
risk increases post op
high ADH levels increase water reabsorption by kidney
hypervolemic hypotonic hyponatremia
hyponatremia+edema associated disorders decompensated heart failure advanced liver disease renal disease effective circulating volume is often sensed as inadequate by baroreceptors resulting in increased ADH levels abuse of MDMA (ecstasy)
