Exam 2 ppt Flashcards
Insensate loss:
fluid loss that you can’t measure. (sweat and breathing) These things are always going on
Electrolytes: cations and anions
Cations (+) Sodium: outside the cells Potassium: mostly inside the cells Calcium Magnesium Hydrogen
Anions (-) Chloride Bicarbonate phosphate sulfate proteinate
How does the body regulate fluids and electrolytes ?
Kidney function Heart and blood vessels Lungs Pituitary Adrenal glands Parathyroid gland Baroreceptors Renin-angiotensin-aldosterone ADH and thirst Osmoreceptors BNP/ANP
Fluids, electrolytes and aging
Physiologic changes
↓Cardiac, renal, respiratory function
-Decreased thirst mechanism
-Alterations in ratio of body fluids to muscle mass
-Increased sensitivity to changes in fluids and electrolyte levels
-Frequent medication use that affects
-Renal function
-Cardiac function
-The elderly are particularly at risk for electrolyte imbalances
-Thirst mechanism doesn’t work as well
-Check skin turgor on forehead and sternum
Hypovolemia: Fluid volume deficit causes
Occurs when loss of ECF volume exceeds the intake of fluid
Mild – 2% of body weight loss
Moderate – 5% of body weight loss
Severe – 8% or more of body weight loss
Hypovolemia: Fluid volume deficit signs and symptoms
- Acute weight loss/flat neck veins
- Decreased skin turgor-lost elastin in the skin. Check for turgor in elderly on forehead and sternum
- Oliguria/concentrated urine
- Postural hypotension
- Weak, rapid, heart rate/circulatory collapse
- Increased temperature
- Decreased central venous pressure
Hypovolemia: Fluid volume deficit treatment
-First, find the cause (vomiting, diarrhea) then replace fluids. If someone is low because they fell, IV then push fluids orally. Vomiting excessively will also change pH, electrolytes, and fluid volume.
-Mild hypovolemia: use oral route if possible
-Acute or severe: Isotonic or hypotonic IV solutions
-Nursing: I & O, daily weights, vital signs, urine output, skin turgor, LOC
-Normal Hb: 12-14 in women 14-16 in men
drop in Hb could be bleeding, concentrated blood can skew results, dehydration
30 mls (avg) is normal urine output
Hypervolemia: Fluid volume excess contributing factors
People most at risk: pts with renal failure (can’t eliminate fluid) and Heart failure (can’t pump fluid)
An isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF
Contributing factors: CHF Renal Failure Cirrhosis of the liver Excess sodium intake Our job is to frequently assess to be able to treat these things. Measure weight daily: 1L of fluid=1kg
System Specific assessment Fluid Volume Excess : assessment findings
↑ pulse ↑ B/P ↑ weight ↑ edema ↑ ascites ↑ crackles in lungs ↑ dyspnea ↑ confusion JVD
Normal/desired expected Outcome – Fluid Balance
Pulse within client norm - B/P within client norm Weight within client norm ↓ edema ↓ ascites ↓ crackles in lungs ↓ dyspnea ↓ confusion
“Third spacing”
-Fluid is trapped in the interstitial space.
-Trapped in a space that is not beneficial to the body. (ie: ascietes from liver failure)
-Remember that fluids shift
-Anytime theres an inflammatory response, fluid is sent to that area. You can start third spacing small amounts
L-oss of albumin or protein leads to decreased oncotic pressure, causing fluid to “leak” from the intravascular into the interstitial space.
Normal albumin in the body:
3.5-5.0 (know the low end.)
When albumn is 1.7 or less you develop
anasarca: total body edema. handprint in the middle of their back if you try to turn them.
extremely malnourished patients (like those in the hospital) have reduced albumin
Most of the proteins are carrying things
ie transthyroiretin transports thyroid hormone
Examples of what can cause decreased albumin
Burns Peritonitis Cirrhosis Alcoholism Malnutrition Long/complex surgeries
causes of hyponatremia: Na+
- Caused by active losses or by dilution hyponatremia
- We need Na for nerve stimulation and muscle contraction
Hyponatremia manifestations
Clinical manifestations depend on the cause, magnitude, and speed of the deficit but are primarily neurological :
- Nausea and malaise
- Lethargy, headache
- Decreased level of consciousness: confusion
- Seizure, coma, death (cerebral edema)
- Brain herniation and death
changes can be from: n/v, diarrhea, suctioning, diuretics, fluid overload, etc
Fatal levels at 115/severe at 125
HYPONATREMIA: FIRST - Priority Nursing Interventions
S odium intake , Seizure precaution especially in high risk levels (125)
O verload—restrict water intake
D aily weight, diuretics, drugs (what are we doing that might cause it?)
I ntake & Output
U se isotonic fluids to restore ECF
M onitor: blood pressure, N/V, HR, dry mucous membranes / LOC
Look for CNS changes Increase sodium IV fluids (not 3% because its so hypertonic you risk damaging myelination in neurons)
Priority nursing intervention for hyponatremia
Protect airway:
suctioning: due to N/V and LOC
to get emesis out for aspiration risk reduction
in case of seizure
Hypernatremia: Na+>145 mEq/L overview
This is rare. But if you have a patient who can’t respond to their thirst mechanism or their thirst mechanism is impaired: dehydration=sodium level increases.
Can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium
Fluid deprivation in patients who cannot perceive, respond to, or communicate their thirst.
Diabetes insipidus
Acute: associated with rapid decrease in intercellular water and brain volume and causes an osmotic shift of free water out of the cell
Hypernatremia: Na+>145 mEq/L dangerous levels
ICU pts. increased mortality of 38-48% if their sodium reaches or exceeds 150.
Hypernatremia: Na+>145 mEq/L manifestations
Decreased urine output, Dry mouth dehydration, swollen tongue
Restless, irritable, confusion, delusions, hallucinations, seizures
Increased heart rate, temp, and flushed skin
Edema (peripheral and pulmonary)
Deep muscle reflexes increased
Hypernatremia: Na+>145 mEq/L treatment
I & O, daily weights Oral hygiene Monitor sodium intake Monitor vitals and neurological symptoms Monitor urine output
Normal potassium levels
3.5-5.0
Hypokalemia: serum K+ causes
Caused by active losses of potassium or insufficient intake
Needed for nerve stimulation and muscle contraction
Main sources of losses are:
Urinary loss
Gastrointestinal loss
Redistribution from extracellular to intracellular space
diuretics like lasix
starvation
trauma
alkalosis
laxative use and abuse (especially the elderly)
Hypokalemia: serum K+ s/s
low potassium will cause a flat or inverted T wave (nicknamed U wave)
Muscle weakness
Severe hypokalemia can cause DEATH through cardiac or respiratory arrest
Skeletal muscle weakness, cramping
U Wave EKG changes, arrythmias, inverted T waves
Constipation, ileus, hypoactive bowel sounds, N/V
Toxicity of digitalis glycosides
Irregular, weak pulse
Orthostatic hypotension
Numbness and tingling (paresthesia)
Hypokalemia: serum K+ treatment
Be very careful when administering potassium! It burns! Either slow it down or dillute it more
Potassium is NEVER administered by IV push or IM! Their heart stops and they die
IV potassium must be administered using an IV pump
Concentrations of potassium >20 mEq/100 mls should be administered through a central line
No more than 10-20 an hour. Ex if you need to give 40ml, that will take 4 hours typically.
Run alongside something else so it doesn’t burn
Potassium supplements are extremely dangerous for patients who have impaired renal function
know heart rate and rhythm
Hyperkalemia: K+ >5 mEq/L causes
Caused by decreased renal excretion, increased intake, medication effects, or a shift of potassium out of the cells as seen in acidosis or musculoskeletal injury muscle weakness paralysis nausea/vomiting colic
Hyperkalemia: K+ >5 mEq/L manifestations
Clinical manifestations are cardiac, nervous system, and GI
Hyperkalemia: K+ >5 mEq/L treatment
Mild- Restrict potassium intake and/or potassium sparing medications.
Serious- Cation exchange resins (e.g. Kayexelate. can be enema. Sticky and constipating. Tries pushing K into cells)
Emergent- Intravenous bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate
False readings of potassium levels
Random draw reveals random 7.2 potassium level. If this occurs, redraw and recalculate. False positives can occur from clotted blood. When you look at a patient’s labs, notice the trends to see where the patient is headed (upward or downward)
Hypocalcemia: causes
Inadequate intake, increased loss, malabsorption or increased binding of calcium
Most of our calcium is in our bones.
Calcium is carried by albumin
Needed for bone structure,…………….list she listed too fast
Normally 8.5 to 10.5 mg/dL circulates:
40% bound to protein
10 % chelated (attached to other electrolyetes)
50% “free” or “ionized”-this is what moves into and out of cells.
Need vitamin D. Add picture from ppt.
Hypocalcemia: s/s
Tetany- ↑ neural excitability, spasms Paresthesia- tingling Refractory hypotension Arrythmias Seizures
Hypocalcemia: treatment
Calcium replacement ! Don’t give with phosphorus because it will precitate
Seizure precautions!
Hypercalcemia: >10.5 mg/dL causes
Malignancy
Hyperparathyroidism
Hypercalcemia: >10.5 mg/dL: manifestations
↑ Calcium →↓neuromuscular excitability: Anorexia, N/V, constipation Muscle weakness/incoordination Confusion, lethargy, coma Bone pain Kidney stones/diuresis/thirst Cardiac arrest If your calcium is above 16, youre in trouble
Hypercalcemia: >10.5 mg/dL
Treatment:
Treat the underlying cause Increase fluids Restrict intake of calcium Mobilize the patient Monitor cardiac and neurological status Calcitonin: forces Ca into the bone
Magnesium normal ranges and overview
Magnesium travels with Potassium Also associated with Calcium Most ICU patients will experience depravation. Normal 1.3-2.3 1/3 bound to protein the rest is free
Hypomagnesemia causes
Helps maintain normal muscle and nerve activity
Major causes:
Chronic alcoholism
↓intake, especially TPN/PPN or tube feeding that lacks Mg (esp. after starvation)
Lower GI loss (Mg. absorbed in small intestines)
Diabetic ketoacidosis: has effect on potassium, so has an effect on Mg
Hypomagnesemia s/s
Neuromuscular Neuropsychotic Cardiac dysrhythmias deep tendon reflexes start to really see problems if levels are below 1 We really worry about heart block
Hypomagnesemia treatment
-Magnesium replacement: diet, PO supplement or IV (if severe)
-Patient education: on diet, DKA, diabetic control, and alcohol consumption
Replace gradually because it acts as a laxative. (milk of magnesia)
Hypermagnesemia >2.3 mEq/L causes
Most common cause: renal failure or laxative addicted/taking too much Mg.
If blood drawn with hemolyzed, you see a false high
Peripheral vasodilation
Don’t push magnesium
Excessive intake, Lithium therapy, untreated DKA
Hypermagnesemia >2.3 mEq/L manefestations
CNS depression
Muscle weakness/paralysis
N/V, flushed skin
Cardiac: bradycardia, heart block, arrest
Hypermagnesemia >2.3 mEq/L treatment
IV fluids: with or without calcium
Hold magnesium
Dialysis
Hypophosphatemia overview
Phosphate binds with Ca+ which pulls it out of the bone, giving these two an inverse relationship. If given to fast: tetany. We try to give it by mouth. Seen in: Refeeding syndrome: malnutrition, alcoholism, anorexia. Hyperparathyroidism Malignancies, severe burns Vit. D deficiency Overuse (binds with) of antiacids Post organ transplant
Hypophosphatemia s/s
Nonspecific, and depend on cause/duration/severity
Muscle weakness, numbness, fatigue
Bone pain/fractures
Altered mental status: anxiety, irritability, confusion, seizures, coma
Often dehydrated
decrease function of platelets=bruising
Hypophosphatemia treatment
-Education on diet
-Oral supplementation
-IV replacement- GO SLOW
Watch the site
Monitor Ca + and Phosphorus levels
Hyperphosphatemia >4.5 mg/dL causes and s/s
Common causes:
Renal failure
Hypoparathyroidism
Excessive intake &/or Vit. D toxicity
Chemotherapy
Acidosis
*Signs and symptoms are mostly related to hypocalcemia because they are inversed.
Treatment focuses on the underlying disorder, diet and patient education.
Hypochloremia overview, s/s, and treatment
Tend to travel with Na and K. Normal 97-107. Usually attached to another electrolyte. If there’s a problem, like an electrolyte imbalance,
Signs and symptoms are associated with hyponatremia, hypokalemia, and metabolic alkalosis
Chloride needed to make hydrochloric acid in the stomach
Treatment involves correcting the cause and replacing the electrolyte involved
Hyperchloremia >107 mEq/L causes
Doesn’t have its own warning signs:
Related to hypernatremia, bicarbonate loss, metabolic acidosis, and hypervolemia
Related to hypernatremia, bicarbonate loss, and metabolic acidosis
pH regulators
Lungs and kidneys control pH, but lungs are faster.
Metabolic Acidosis
Low pH (increased H+ concentration) and a low plasma bicarbonate concentration (
Metabolic acidosis manifestations
tachypnea
confusion
hypotension
decreased cardiac output
Metabolic acidosis treatment
Treatment focuses on the underlying metabolic disorder
Less than 7: decreased cardiac output
Respiratory rate speeds up
Metabolic Alkalosis overview
High pH (greater than 7.45) (decreased H+ concentration) and a high plasma bicarbonate concentration (26 ml of bicarb) Can be produced by a gain of bicarbonate or a loss of H+ (usually by vomiting or suction)
Metabolic alkalosis overview
Often accompanies hypokalemia; manifestations are similar to hypokalemia and hypocalcemia
Treatment addresses underlying disorder as well as K+ replacement and fluid volume replacement
Respiratory Acidosis
Always due to inadequate excretion of CO2 with inadequate ventilation
Respiratory alkalosis
pH is >7.45 and PaCO2 is
Hypotonic solutions
Provide salt and water to replace cellular fluid. We don’t give water because it’s so hypotonic cells take it in so fast, the cells burst
Examples:
1/2 normal NS (0.45% normal saline)
1/3 NS (0.33%)
Hypertonic solutions
3% or 5% NaCl
Given for increasing intervascular volume. The problem (like with D5NS) it starts as hypertonic, but gets metabolized so quickly that it becomes hypotonic. Not used for emergent critical situations …... talks too fast
ISOTONIC SOLUTIONS
Closest to osmolality of blood itself. Diffuses into extracellular space. Used a lot to give meds because it doesn’t interact with meds. Also with burns
0.9% NS
Lactated ringer’s solution: Used a lot in burns! Contains small amounts of calcium, potassium, ….talks too fast.
never use in a patient that’s alkalotic because it can be made worse
Never use in liver disease
5% dextrose in water-very quickly metabolizes into isotonic solutions
DEXTROSE
What happens when you add dextrose to a solution?
D5- metabolizes too fast
D10 - weaning off of something
D50-hypoglycemia
Troponin I or T (cTnI or cTnT):
peak
There are variations (I: cardiac specific/T:more sensitive)
will peak between 4-24 hours. Will peak early and stay peaked up to 24 hours. Will remain elevated after the event
Creatinine Kinase-MB (CK-MB):
this form is more Cardiac specific. Peaks at 4-24 hours, but doesn’t stay peaked
