Fluid Imbalance Flashcards
B. Extracellular –
outside the cell (2 areas) 1/3 of all body fluids 20% of body weight Circulates between the cells contains water, electrolytes and nutrients
1. Intravascular compartment – inside vessels; plasma 2. Interstitial compartment – between cells and vessels; fluid in and around the tissues
- Third spacing -
shift of fluid from intravascular space into a “third” or extra space.
- body cavity - out of the blood stream and into the interstitial space; such as a pleural effusion or ascites (excess fluid in the space between the tissues lining the abdomen and abdominal organs [the peritoneal cavity], caused by high pressure in the blood vessels of the liver [portal hypertension] and low albumin levels)
- interstitial spaces – edema (such as in ankles); from injury when there is a shift of fluid into the interstitial space – the body can’t use that fluid anymore because it’s not available in the cells
Objective 2 Discuss the Regulation of Fluid Balance in the Body
A. Thirst -
Thirst center in hypothalamus stimulated by:
1. dry mucous membranes in the mouth 2. drop in blood volume – stimulates the body to be thirsty 3. increase in serum osmolality – lab tests show this; an ( sodium level in extracellular fluid
B. Kidneys
Regulate excretion and retention of water and electrolytes
The glomerulus and nephron regulates this
GFR (glomerulus filtration rate) – lab tests that tells how well the kidney is functioning
1500-2600 mL of urine is produced each day
Renin-Angiotensin-Aldosterone System –
RAAS - Works to maintain intravascular fluid / blood balance and blood pressure - 👆thirst, 👆B/P (constricts vessels), and retains water
a mechanism in the body which gets triggered; renin is produced which stimulates angiotensin which clamps down on the vessels (controls the B/P) and the aldosterone gets stimulated which retains fluid.
Renin is produced by the kidneys; it works on the vessels to maintain B/P and the kidneys to maintain volume
Renin will 👆thirst
Renin will 👆B/P (by constricting the blood vessels)
Aldosterone will retain water(it’s a antidiuretic)
D. Antidiuretic Hormone
(ADH) – (antidiuretic = against losing fluid)
- produced in brain (hypothalamus) and stored in pituitary
- ADH’s release is triggered in response to low blood volume (if bleeding out the kidneys are stimulated to keep fluid in and to reabsorb fluid) or 👆serum osmolality. (Triggers for thirst)
Stimulates water reabsorption
FLUID IMBALANCES
Objective 1 Describe the Distribution of Fluids in the Body:
A. Intracellular
- inside the cell
2/3 of all body fluids
40% of body weight
Provide cell with nutrients and assist in cellular metabolism
Atrial Natriuretic Peptide (ANP)
-secreted by cells lining the atria in the heart as a response to overdistention
when atria stretch too far (pt in fluid overload) the ANP is stimulated causing an 👆in urine output (gets rid of extra fluid/ gets rid of sodium and water)
Fluid volume deficit
Dehydration =
Fluid volume deficit that is a decrease in intravascular, interstitial and/or intracellular body fluid
Fluid volume deficit
2. Hypovolemia
= decreased circulating blood volume and isotonic fluid loss from extracellular spaces
Etiology of dehydration:
- excessive fluid loss
- insufficient fluid intake
- fluid shifts – r
- failure of regulatory mechanisms that are supposed to help balance fluid levels
Clinical Manifestations of dehydration – by body system
- neurologic –
altered mental status- irritable, anxious, restless, confusion
- 👇alertness
- coma(severe FVD)
Clinical Manifestations of dehydration – by body system
- mucous membranes
dry, sticky
pale
longitudinal furrow on tongue, cracks
tongue can 👇in size
Clinical Manifestations of dehydration – by body system
3. skin
- turgor will be diminished (no longer brisk) – check under collar bone
- dry skin (but doesn’t apply to elderly who tend to have dry skin anyway)
- pale, cool extremities
- sunken eyeballs
Clinical Manifestations of dehydration – by body system
3. urinary –
Body weight: min urine output 0.5ml/kg body weight/hr (see pg 2 notes)
-👇urine output (oliguria)
-👆urine specific gravity (the concentrated amounts of particles in urine)
Normal SG:1.005-1.030 ⭐️dehydration SG>1.030
Clinical Manifestations of dehydration – by body system
5. cardiovascular
-👇 B/P
-Orthostatic hypotension
-Tachycardia (compensatory mechanism – compensating for ( B/P)
-Flat neck veins (r/t ( venous filling)
-👇pulse volume (won’t feel the normal +2)
-👇capillary refill time (ex. 👆from 3 seconds to 5 or 6 seconds)
-👆hematocrit (can use the hematocrit level to determine if pt is dehydrated or has fluid volume overload)
Hemoglobin : Hematocrit normal ratio is 1:3
-so 12:36 would be normal
-but 12:42 = dehydration
Clinical Manifestations of dehydration – by body system
6. musculoskeletal
- fatigue
- weakness
Clinical Manifestations of dehydration – by body system
7. metabolic processes
- increase or decrease in body temperature (if don’t have the fluid circulating, the body can’t cool off)
- Thirst
- ⭐️Weight loss⭐️- important ( 1kg (2.2lb)= 1L of fluid
Collaborative Management for dehydration
1. Assessment
a. assess all of the above clinical manifestations
b. laboratory assessment – look at lab results
hemoconcentration – 👆Hct: if pt is dehydrated their blood is concentrated because their volume is deficient; the hematocrit is going to look higher; hematocrit is a % of RBC as compared to the total volume of blood
increased osmolality (>300mOsm/Kg) -👆glucose,👆protein, 👆BUN,👆Na
Urine – urine will be concentrated and there will be an 👆specific gravity (> 1.030)
c. vital signs – 🔼B/P, orthostatic hypertension
d. intake and output
e. daily weight (most sensitive ) -1 Kg (2.2#) = 1 liter of fluid
Collaborative Management for dehydration
- Assessment
2. Fluid replacement
Collaborative Management for dehydration
Fluid Replacement
a. Oral rehydration: fluids that contain electrolytes and glucose (Gatorade, Pedialyte)
Medication – treat the underlying cause
- If vomiting, give antiemetic
- If diarrhea, give antidiarrheal
intravenous therapy:⭐️dr. Orders needs to include soln, rate, and additives.
-fluid challenge (fluid bonus)administer a specific amount of fluid over a short period of time to replace fluids; monitor pt closely
- D5W (hypotonic soln) if Na is high – given slowly over 48° to prevent cerebral swelling; the purpose is to put fluid back into the cells, but if done too rapidly the tissue swells causing confusion, etc.
- NS if Na is not elevated – going to use an isotonic soln (mean equal or like what’s in our body, such as normal saline); 0.9% sodium chloride is normal saline; given more rapidly because it doesn’t act like the D5W where it pulls water into the cells and causes swelling; this is given to pts with fluid volume deficit for both fluids and solutes that were lost r/t diarrhea, vomiting
INTRAVENOUS THERAPY
* Dr.’s orders need to include RATE, SOLUTION, and ADDITIVES (such as potassium)
A. Crystalloids -
Solutions with small molecules that flow easily from the bloodstream into cells and tissues
- Isotonic solutions
Ex. 0.9% Sodium Chloride (NS – normal saline) - Hypotonic solutions
Ex. 0.45% Sodium Chloride (1/2 NS) - Hypertonic solutions -
Ex. 5% Dextrose & 0.9% Sodium Chloride (D5 NS)
10% Dextrose in Water (D10W)
INTRAVENOUS THERAPY
⭐️Different types of IV soln⭐️
A. Crystalloids -
1. Isotonic solutions -
Any solution with a solute concentration equal to the osmolarity of normal body fluids
- concentration of so lutes in a solution of osmoles/L
- 0.9% Sodium Chloride (NS)- most common
- Lactated Ringers(LR) – similar to what is in plasma; contains sodium, potassium, calcium, chloride) not a soln ran for long periods of time, ICU pt.
- 5% Dextrose in Water (D5W) – isotonic in bag, but acts as hypotonic in body
- Dr.’s orders need to include RATE, SOLUTION, and ADDITIVES (such as potassium)
INTRAVENOUS THERAPY️⭐️Different types of IV soln⭐️
A. Crystalloids -
2. Hypotonic solutions -
Any solution with a solute concentration less than that of normal body fluids;
-draws water INTO cells from extracellular cells (out of vascular system), causes cells to swell (edema) and vessels to collapse.
Ex. 0.45% Sodium Chloride (1/2 NS) and 5% Dextrose in h2o(most common)
- Dr.’s orders need to include RATE, SOLUTION, and ADDITIVES (such as potassium)
INTRAVENOUS THERAPY ⭐️️Different types of IV soln⭐️
A. Crystalloids -
3. Hypertonic solutions -
- Any solution with a solute concentration greater than that of normal body fluid
- draws water OUT of intracellular space, into intravascular space causes cells to shrink and extracellular to expand
Ex. 5% Dextrose & 0.9% Sodium Chloride (D5 NS)-not given often
10% Dextrose in Water (D10W)-not given often
- Dr.’s orders need to include RATE, SOLUTION, and ADDITIVES (such as potassium)
INTRAVENOUS THERAPY ⭐️️Different types of IV soln⭐️
B. Colloids (plasma expanders) –
- pull fluid INTO bloodstream,
- large molecules that can’t leak into tissues; (stay into blood stream)
- used for aggressive fluid resuscitation (trauma victim – lost a lot of fluid);
- have to monitor pt for fluid overload which can cause cardiac arrest.
Ex. 1. Albumin
2. Dextran (synthetic) 3. Hetastarch (Hespan) (synthetic)
INTRAVENOUS THERAPY ⭐️️Different types of IV soln⭐️
C. Total Parenteral Nutrition (TPN and PPN)
- TPN- total Parenteral Nutrition:
Dextrose 10-25%(high concentration )
-IV with highly concentrated, hypertonic (because of all the solutes in it) nutrient solution administered through a large, central vein, close to the heart
-Provides calories, fluids & minerals, restore nitrogen balance
Must be given thru a central vein/PICC line (peripheral vein can’t tolerate anything higher than 10% dextrose or the vein will get a phlebitis)
TPN triggers:
- Debilitating illness greater than 2 weeks
- Loss of 10% or more of pre-illness weight
- Excessive nitrogen loss ( total protein and albumin)
- Nonfunction of GI tract lasting 5-7 days –if a pt needs to rest the gut he/she will need TPN, for example; severe pancreatitis, inflammatory bowel center, bowel surgery, or severe burns (need the extra calories to heal)
- Complications of TPN
a. fluid imbalances- fluid shifts between body compartments - r/t hypertonic soln
- hyperglycemia leading to diuresis (👆excretion of urine) & dehydration (pt may need insulin to control the temporary high BS caused by the high amounts of glucose he/she is receiving thru TPN)
- fluid overload and pulmonary edema – r/t hypertonic soln (fluid back up into avoli in the lungs)
b. electrolyte imbalances – daily lab draws check the levels. Monitoring sugar and electrolyte imbalance.
INTRAVENOUS THERAPY ⭐️️Different types of IV soln⭐️
C. Total Parenteral Nutrition (TPN and PPN)
- PPN- Peripheral Parenteral Nutrition
Like TPN, EXCEPT maximum of 10% dextrose in peripheral vein.
Identify Various Delivery Methods for IV Solutions
Peripheral Lines –
- used for short-term or intermittent therapy; usually use veins in arm or hand
- a short, plastic, flexible catheter is inserted into the vein
Identify Various Delivery Methods for IV Solutions
B. Central lines
IV infused into the large vein close to the heart
- Central venous catheter
- Peripherally inserted central catheter (PICC)
- Vascular access port
- Tunneled external catheters
- Hickman, Broviac or Groshong
Identify Various Delivery Methods for IV Solutions
B. Central lines
- Central venous catheter –
placed in a central vein such as subclavian, sits right above the right atria
- Short term use
- Big risk for infection
Identify Various Delivery Methods for IV Solutions
B. Central lines
- Peripherally inserted central catheter (PICC) –
Upper arm, long catheter (less chance of infection this way r/t the bacteria has a long way to travel before getting to the heart)
- left in for months at a time
- commonly used in hospital and homecare settings when venous access is difficult or treatment is prolonged
- nse can be certified in inserting PICC’s or is done in interventional radiology/ fluoroscopy.
Identify Various Delivery Methods for IV Solutions
B. Central lines
3.Vascular access port –
- Central vein under the skin close to the heart
- long-term therapy such as chemotherapy;
- access port with a 90° bent needle (Huber)
- physician placement
Identify Various Delivery Methods for IV Solutions
B. Central lines
4. Tunneled external catheters/Hickman, Broviac or Groshong –
long-term therapy (ex. Chemo, for nutrition or antibiotic therapy); tunnel deep into the skin external catheter; still a central line, but tunnels into abdomen area for easy access for pt
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
- Infiltration
- Phlebitis or thrombophlebitis
- Infection
- Hematoma
- Extravasation
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
1. Infiltration
-Catheter is dislodged from vein
-fluid leaks from the catheter into the surrounding tissue
symptoms of infiltration include:
tight, hard, swollen skin; skin is COLD to touch; painful
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
2.Phlebitis or thrombophlebitis
inflammation of the vein
Vein wall inflamed, small lumen
symptoms of phlebitis (inflammation) or thrombophlebitis (inflammation caused by a blood clot) include: pain, redness, red streak; sluggish flow; vein that is cordlike; skin may feel a little warm
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
3.Infection
-bacterial contamination at the site
symptoms of infection include:
tender, warm, redness, drainage, bacterial contamination
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
3. Hematoma –
large amount of bruising
- leaking of blood into surrounding tissue
– usually occurs during insertion or with a pt who has clotting disease
symptoms of hematoma include: pain, bruising (ecamosis)
Possible Complications of IV Therapy
Assess the pt. for Local Complications Of IV site
4. Extravasation
infiltration of a vesicant drug (causes vessels to constrict) – such as chemo, emergency B/P meds, potassium; causes a lot of damage to tissue
symptoms of extravasation include: pain, burning, swelling, blistering, possible necrosis, possible disfigurement
-interventions: stop infusion, follow agency policy, disconnect tubing & aspirate any remaining drug from catheter, call dr., administer antidote per catheter or inject into subq tissue, elevate arm, apply ice. Leave catheter in place
Possible Complications of IV
Systemic Complications (Whole body reacting)
1. Bloodstream infection -
pathogens enter the bloodstream usually resulting from poor aseptic technique
Symptoms: fever, septic shock
Possible Complications of IV
Systemic Complications (Whole body reacting)
2. Fluid overload –
admin too much fluid for the body to handle
Symptoms: 👆B/P (r/t 👆volume), 👆respiration (r/t fluid in lungs causing difficulty in O2 exchange), SOB (r/t fluid in lungs from leaking from vascular compartments to interstitial compartments); crackles (r/t fluid that has leaked into interstitial spaces)
Possible Complications of IV
Systemic Complications (Whole body reacting)
Speed shock -
too fast of IV push fluids or meds
Symptoms: facial flushing, dizziness, irregular pulse, 👇B/P, severe headache, loss of consciousness and cardiac arrest
Possible Complications of IV
Systemic Complications (Whole body reacting)
Allergic reaction -
local or general reaction to tape, cleansing agent, latex catheter, solution or medication
Symptoms: if systemic – itching, rash, wheezing, bronchospasm
Overhydration (fluid overload, fluid volume excess, hypervolemia)
Etiology
- Excess of isotonic fluid in the extracellular compartment
- Retention of both water and sodium – can be renal failure, CHF (an and H2O tend to move together
- Fluid shift from interstitial to intravascular space – after surgery or burn treatment; administration of hypertonic fluid ( holds onto fluids) or albumin then fluid shifts and moves into intravascular
Over Hydration (fluid overload, fluid volume excess, hypervolemia)
Clinical Manifestations (Symptoms/how pt presents)
- wt gain (critical component)- can be over a short period of time
- distended neck and hand veins
- SOB, crackles, cough, or dyspnea because of fluid in lungs
- bounding pulse (+3 or +4)
- pitting edema, periorbital edema
Over Hydration (fluid overload, fluid volume excess, hypervolemia)
Collaborative Management ( what are we going to do about it?!)
- Fluid restriction -limit how much fluid is taken in
- Sodium restriction – where sodium goes, water follows; teach pt low salt diet (processed foods are high in sodium)
- Diuretics - 👆urination from diuretics is directly related to the amount of sodium reabsorption that is blocked, so the more sodium the drug blocks the more water is going to be released
Physiologic action of Diuretics
- basic mechanism of action is blocking of sodium and H2O reabsorption from the glomerulus in the nephron; as blood flows thru the kidney and glomerulus and nephron there are certain spots in the Loop of Henle where it reabsorbs and takes back some fluid (if everything flushed thru us we would die); diuretics block this reabsorption – says “let that fluid go”
- drugs whose action is ⭐️earliest (most proximal to glomerulus) in the nephron produce the greatest diuresis ⭐️
- drugs whose action occurs in the ⭐️distal parts of the nephron produce less diuresis ⭐️
- ⬆️in urine output, from diuretics, is directly related to the amount of sodium reabsorption that is blocked. The more sodium that is blocked from being reabsorbed, the more water that will go out.
Adverse effects of diuretics
hypovolemia (lost too much fluid) which causes ⭐️low B/P
electrolyte imbalances, especially potassium
acid/base imbalances⭐️ (acidic or alkalotic depending on which electrolyte the pt is losing)
c. Classification of diuretics
get more diuresis if med works in proximal portion of convoluted tube; get less diuresis if med works in distal portion of convoluted tube
1.) High-ceiling “LOOP” diuretics Ex: Furosemide (Lasix ) 2. Thiazide and related diuretics (HCTZ) Ex: hydrochlorothiazide 3.) Potassium-sparing Diuretics Ex:spironolactone (Aldactone ) 4.) Osmotic Diuretics Ex: Mannitol-
c. Classification of diuretics
1. ) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Action:
acts in loop of Henle to block reabsorption of sodium and chloride, prevents passive (water follows sodium) reabsorption of water (water follows sodium, so by blocking the reabsorption of sodium it prevents reabsorption of water); acts early in the nephron so has ⭐️high diuresis⭐️
c. Classification of diuretics
1. ) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Pharmacokinetics:
- Oral: diuresis begins in 60 minutes and lasts for 8 hours- don’t give at bedtime
- IV: diuresis begins in 5 minutes and lasts for 2 hours – used for immediate/critical action( heart failure pt)
c. Classification of diuretics
1.) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Therapeutic Uses
- pulmonary edema – such as a pt with CHF (heart doesn’t pump effectively so fluid backs up in lungs); need to diureses the pt
- edema - ex injured ankle
- hypertension – if not controlled with other diuretics
- severe renal impairment – usually dose 20-40 mg IV, but will use even over 100mg for severe renal impairment
c. Classification of diuretics
1.) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Adverse Effects
- dehydration –
- hypotension – r/t ⬇️in blood volume; if B/P is low don’t give Lasix
- hypokalemia – loop diuretic block potassium from reabsorption; ⬇️potassium is the most common side effect; may need to give potassium replacement; monitor the K levels and ( K in diet
- ototoxicity – ringing in ears, difficulty hearing, hearing impairment
- hyperglycemia - uncommon unless pt is already DM
- hyperuricemia – elevated uric acid levels; leads to gout and kidney stones
c. Classification of diuretics
1.) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Drug Interactions
- Digoxin – if pt has third factor of low potassium level that ⬆️ the risk of becoming dig toxic (heart med will reach toxic level; too high); Lasix + Digoxin + low potassium = dig toxic
- Potassium-sparing diuretics – if use loop diuretic with a potassium sparing one there is less risk of hypokalemia
- Antihypertensive agents – blood pressure is all about BLOOD VOLUME and VESSEL SIZE; if diuretic lowers volume which makes B/P lower and give a antihypertensive drug, the B/P could drop even more; a low B/P med + a loop diuretic can = an even lower B/P
c. Classification of diuretics
1.) High-ceiling “LOOP” diuretics
Lasix (Furosemide)
Nursing Implications
Timing of doses – give oral in the AM if daily (lasts 6-8 hours); if BID, give in AM and early afternoon to avoid nighttime voiding
IV push administration – need to know how much to dilute it with and over what period of time; slow IV 20mg/min; 80mg minimum is 4 minutes
Patient teaching – weigh self and report weight gain/loss
c. Classification of diuretics
2. Thiazide and related diuretics
a. ) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
- Action
- promotes urine production by blocking reabsorption of sodium and h2o in the ⭐️early segment of the distal convoluted tubule (produces less diuresis than Loop diuretics)⭐️action depends on adequate kidney function; if pt doesn’t have good kidney function then we shouldn’t give this drug
c. Classification of diuretics
2. Thiazide and related diuretics
a.) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
Pharmacokinetics
onset: 2 hours (oral)
peak: 4-6 (oral)
duration: 12 hours (oral)
c. Classification of diuretics
2. Thiazide and related diuretics
a. ) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
Therapeutic Uses
- essential hypertension – first drug of choice for HTN if cause unknown
- edema – for mild to moderate edema
c. Classification of diuretics
2. Thiazide and related diuretics
a.) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
Adverse Effects
- dehydration
- hypokalemia – add potassium to diet or supplement(teaching)
- hyperglycemia – especially in diabetics (can raise BS)
- hyperuricemia - ⬆️ uric acid
c. Classification of diuretics
2. Thiazide and related diuretics
a.) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
Drug Interactions :
Dosage:
Nursing Implications:
Drug Interactions :same as loop diuretics
Dosage: 25-50 mg po q day, qod or bid
Nursing Implications – same as loop
c. Classification of diuretics
2. Thiazide and related diuretics
a. ) hydrochlorothiazide (Esidrix, Oretic, Hydrodiuril)
Other thiazide related diuretics:
- Diuril, Diurigen (chlorothiazide)
- Zaroxolyn, Mykrox (metolazone) -Zaroxolyn potentiates (enhances) the effect of Lasix; often will give Zaroxolyn 30 mins before Lasix
c. Classification of diuretics
3. ) Potassium-sparing Diuretics
spironolactone (Aldactone )
2 useful responses: moderate ⬆️ in urine production and substantial ⬇️ in K loss Rarely used alone (because it’s only a moderate diuretic)
Holds onto k+
c. Classification of diuretics
Examples of other loop diuretics:
Edecrin (ethacrynic acid)
Bumex (bumetanide)
Demadex (torsemide)
c. Classification of diuretics
3.) Potassium-sparing Diuretics
Aldactone (spironolactone)
Action
blocks action of aldosterone in the distal nephron and allows diuresis.
Causes retention of potassium and excretion of sodium – water will go with sodium. Very specific diuretic – wants to let sodium out which will take water with it, but wants to keep potassium in
retention of K
excretion of Na+
scant diuresis – not a powerful drug
slow acting – can take up to 48°
c. Classification of diuretics
3.) Potassium-sparing Diuretics
Aldactone (spironolactone)
Therapeutic Uses
- long term treatment of hypertension
- edema from heart failure (if in real trouble, will give Lasix)
- commonly used with loop or thiazide diuretic( to counter act K+ wasting)
c. Classification of diuretics
3.) Potassium-sparing Diuretics
Aldactone (spironolactone)
Adverse Effects
-hyperkalemia – too much potassium – don’t expect this to happen, but it can
c. Classification of diuretics
3.) Potassium-sparing Diuretics
Aldactone (spironolactone)
Nursing Implications
- cut back on K in diet
c. Classification of other Potassium-sparing Diuretics
Dyrenium (triamterene)
Action –
inhibits reuptake of sodium and excretion of potassium (pushes sodium out and saves potassium)
- Midamor (amiloride) – another potassium-sparing diuretic
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Action
most common osmotic diuretic; this is the generic and brand name
– creates an osmotic force within the nephron that prohibits reabsorption of water. The greater concentration of Mannitol, the greater the diuresis; Mannitol doesn’t effect electrolytes; works on water (osmotic force) alone
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Pharmacokinetics
Route: must be given IV only
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Therapeutic Uses
- Prophylaxis of renal failure
- Reduction of intracranial pressure – pulls fluid out of edematous brain tissue. Most often ICU
- Reduction of intraocular pressure
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Adverse Effects
Edema – because we are pulling fluid out of tissues and shifting it, so we may see some edema; edema can leave capillary beds anywhere except in brain (so we can’t effect it there)
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Administration
- IV infusion concentrations of 5% to 25%
- crystallizes at low temps; can be warmed to dissolve crystals then cooled to body temperature
- administer with inline filter in tubing (comes with one from the pharmacy), so nse doesn’t administer any crystals by accident
c. Classification of diuretics
4.) Osmotic Diuretics
a.) Mannitol-
Additional collaborative management of overhydration
- monitor VS (helps determine if B/P is getting too low)
- I & O
- FIRST SIGN comes from daily weights
Etiology of dehydration:
1.excessive fluid loss –
from diarrhea, vomiting, sweating, blood loss, fever, insensible loss with expiration (moisture from lungs), over use of laxatives, use of diuretics, NG tube
Etiology of dehydration:
- insufficient fluid intake -
nausea, NPO, starvation, difficulty swallowing, not enough r/t lack of education, cognitive level, bed ridden, infants
Etiology of dehydration:
- fluid shifts –
r/t burns over large area of body, edema from injury, pleural effusion, ascites
Etiology of dehydration:
4. failure of regulatory mechanisms that are supposed to help balance fluid levels
- Diabetes Insipidus-results from ADH deficiency leading to excretion of large amounts (up to 30 LITERS/day) of dilute urine
- Brain injury – damages part of the brain that controls the ADH
- Surgery
Fluid Deficit
⬇️B/P Postural hypotension ⬆️heart rate ⬇️pulse amplitude Normal respirations Flat jugular veins No edema Tenting/poor skin turgor Low urine output Concentrated urine output High urine specific gravity >1.030 Weight loss – good indicator of FVD
Electrolyte imbalance
Hypokalemia
1. Pathophysiology
- normal = 3.5-5.0 mEq/L
- serum potassium level
Electrolyte imbalance
Hypokalemia
Etiology
- Diuretics – except K+ sparing diuretics (loop are the worst)
- Diarrhea – large amount of K+ in intestinal fluids, so lose K+ with diarrhea; enemas; laxative use
- Vomiting or NG suction
- Inadequate potassium intake – eating disorder; alcoholism
- IV therapy with potassium poor solutions – NPO = ⬇️potassium
- Low magnesium levels – make it hard for kidneys to conserve K+; if pt has low magnesium level or is at risk for hypokalemia
Electrolyte imbalance
Hypokalemia
Clinical Manifestations -
- EKG changes – inverted T Wave or flat T wave; might see a U Wave
- Rapid, weak and thready pulse
- Orthostatic hypotension – lying to sitting; sitting to standing
- Shallow respirations – with diminished breath sounds
- Lethargy and confusion – happens a lot with electrolyte imbalances
- Polyuria – frequent urination (Foley fills up fast)
- Nausea and vomiting – HYPOactive bowel sounds
- Generalized weakness – especially in legs
- Constipation
- Paresthesia - numbness in fingers and toes
- Leg cramps
Electrolyte imbalance
Hypokalemia
Collaborative Management
- Assess for signs and symptoms
- Monitor lab work results ordered by MD
- Close monitoring of dig levels (if on Dig and add Lasix the potassium level can drop causing dig toxic r/t the Lasix makes the Dig work better and better)
Electrolyte imbalance
Hypokalemia
Collaborative Management
Potassium replacement (oral or IV)
-Oral K+ rich diet (chocolate, dried fruit, nuts & seeds, oranges, bananas, tomatoes, mushrooms, potatoes, apricots, cantaloupe, carrots) oral K+ supplements IRRITANT TO STOMACH so give with food DO NOT CRUSH if extended release
IV – we don’t add K+ to bags anymore
1) Administration
Mix well – pharmacy does this now; gently rotate bag
Dilute - NEVER add it to bag without diluting; very vesicant drug
NEVER give it IV push; causes cardiac arrest /cardioplegia soln (this is how animals are put to sleep; think Dr. Kevorkian)
Don’t exceed 40-60 mEq/liter of solution
(IVPB)Give at 10 mEq/hour – no faster except in an extreme emergency); have to figure out how much in bag, how fast giving it, therefore how much pt given
Use an infusion device – never use gravity because it can get away from you and run in way too quickly; use a pump
-Patient monitoring
Cardiac rhythm – pt put on telemetry
Watch IV site – for burning; phlebitis - infuse slowly
Watch for infiltration
Electrolyte imbalance
Hyperkalemia
- Pathophysiology – > 5.0 mEq/L
- Most serious/ dangerous affect on cardiac function slows conduction system in heart; potassium has a depressant effect on the heart
- Less common to have a high potassium than a low potassium, but is more serious (6X more serious)
Treated as an emergency
-Most dangerous of all electrolyte disorders
Electrolyte imbalance
Hyperkalemia
2.Etiology
- Impaired renal function – can’t excrete the potassium properly
- Injury causing hemolysis – when a lot of tissue is damaged r/t a traumatic accident (especially a crushing injury) potassium is released from the cells and is picked up by the bloodstream
Too much intake – eating too much/supplements
Potassium sparing diuretics – can cause too much retention of potassium. ex:spironolactone
Blood transfusions – infuse within 4 hours is the limit for transfusing blood into a pt r/t potassium is being release from the RBC cells; 1 unit in 2 hrs is ideal
Electrolyte imbalance
Hyperkalemia
Clinical Manifestations
- Paresthesia – an early symptom; numbness that can’t explain
- Abdominal cramping
- Diarrhea
- EKG changes – peaked T Wave (tall and tented)
- Hypotension
- Irregular pulse rate
- Irritability - not feeling like self
- Muscle weakness – especially in legs
Electrolyte imbalance
Hyperkalemia
Collaborative Management
-Loop diuretic - in mild cases; but if pt has renal insufficiencies the loop diuretic won’t work as well.
- Kayexalate – must get into GI tract; can be given orally, thru NG tube, or rectally as an enema pt to hold for 30-60 min
- Cation exchange medication – gets into bowel and pulls out K+ to be excreted
- Onset of action: several hours
- Duration: 4-6 hours; gives pt diarrhea
Insulin – drives/forces/moves K+ from intravascular system back into cells
-Given with D10W (the dextrose balances the insulin; insulin drops the BS) - typical amount of insulin is 10 units of short or rapid acting insulin
Hemodialysis – filters blood to level out electrolytes
Electrolyte imbalance
Hyponatremia
1. Pathophysiology
a. sodium’s function –
- Responsible for regulating fluid balance in the body
- it is the MAJOR electrolyte in EXTRACELLULAR fluid
- It’s involved in impulse transmission in nerves and muscles – sodium works to get message from nervous system to muscular system to tell you to remove your hand from the hot burner on the stove
Electrolyte imbalance
Hyponatremia
b. low sodium –
is a level
Electrolyte imbalance
Hyponatremia
Etiology
- Excessive diaphoresis (loss)– ex. sweating in summer
- Diuretics
- Wound drainage –
- Renal disease – kidneys not functioning
- Low salt diet
- Vomiting – loss from GI tract
- Diarrhea – loss from GI tract
- Hyperglycemia – high BS r/t high amounts of diuresis; when sugar is high, the bloodstream becomes hyperosmotic (thicker), so the body’s response is to diureses – the more diureses the more Na+ loss
- Excessive water intake – don’t go overboard on water intake = water intoxication
- Schizophrenic disorder– may be compulsive with drinking water (dilutes sodium)
Electrolyte imbalance
Hyponatremia
Clinical Manifestations
- Altered mental status( most significant)
- Headache, stupor, coma – r/t cerebral edema
- Peripheral edema – Na+ intravascular is low, so it’s higher in the cells which pulls water with it causing interstitial spaces/cells to swell
- Nausea & vomiting, abdominal cramps
- Weakness, muscle twitching, tremors – neurovascular function
- Decreased body temperature
- Tachycardia
- Shortened attention span – r/t cerebral edema
- Confusion, altered mental status, lethargy – r/t cerebral edema
Electrolyte imbalance
Hyponatremia
Collaborative Management
Fluid restriction – especially if dilutional hyponatremia; sodium will shift back if restrict the fluids.
Might give loop diuretic to move fluid out – get the water off and the sodium will come back to a normal level
Oral Na+ supplement
If replacing with IV – use normal saline (0.9% NS) which will gradually replace sodium in bloodstream
Electrolyte imbalance
Hypernatremia
- Pathophysiology
– sodium level > 145 mEq/L
– higher level of sodium in bloodstream because it’s been pulled from cells (cells shrink)
Electrolyte imbalance
Hypernatremia
2. Etiology
- Too much Na+ intake (chips, popcorn)
- Osmotic diuretics (Mannitol)
- Excessive GI drainage, excessive diuresis – diarrhea; losing so much water that the sodium level ends up concentrated
- Excessive diaphoresis – lost volume; lost so much water that sodium levels are concentrated
Electrolyte imbalance
Hypernatremia
Clinical Manifestations
S (skin flushed)
A (agitation)
L (low-grade fever, lethargy, low urine output)
T (thirst, twitching, tachycardia)
-Hypertension
-Orthostatic hypotension – can drop pressure with position changes
Electrolyte imbalance
Hypernatremia
Collaborative Management
- Treat underlying cause
- Give hypotonic (D5W or 0.45% NS) fluid replacement gradually over 48°
- Restrict sodium in diet (teach pt to read labels)
- Oral fluid replacement
Electrolyte imbalance
Hypocalcemia -Calcium Imbalances
1. Pathophysiology
– normal range 9-10 mg/dL
-Calcium level
Electrolyte imbalance
Hypocalcemia -Calcium Imbalances
2. Etiology
- Lack of dietary intake
- Lack of Vitamin D – need Vit D to absorb Ca+; found in fortified milk
- Malabsorption in GI tract
- Pancreatitis
Hypoparathyroidism – parathyroids not functioning well or removed; parathyroid hormone is involved in regulating Ca+ levels. Low thyroid level causes low Ca+ level – PTH is not stimulating osteoclasts to “chew” bone = less bone in bloodstream
Electrolyte imbalance
Hypocalcemia -Calcium Imbalances
3. Clinical Manifestations
- Increased neuromuscular excitability – twitching, tremors
- Trousseau’s sign – pt does a palmer flexion; occurs with hypoxia (B/P cuff is inflated systolically 20mmHg greater than pt’s normal and left in place for 1-4 minutes – pt’s hand will naturally do a palmer flexion which may be a sign of hypoglycemia)
- Chvostek’s sign – tapping on the face (the facial nerve) will cause a twitch of the mouth, nose and/or cheek
- brittle nails, dry skin and hair
paresthesias – (numbness and tingling)because of neuromuscular involvement; hands, feet and mouth
- cardiac arrhythmias – abnormal rhythm
- muscle cramps or spasms
- tetany – neuromuscular rigidity with severe cases of hypocalcemia; can lead to cardia arrest(all muscle in body are contracting)
- fractures – if a young, healthy pt has a fracture or breaks a lot of bones the MD should check Ca+ levels
Electrolyte imbalance
Hypocalcemia -Calcium Imbalances
Collaborative Management
- treat underlying cause – check Ca+ levels, Vit D levels, etc
- IV calcium replacement if severely low – calcium is considered vesicant, so monitor IV site closely, infuse slowly, have pt notify nse if experiencing any pain
- Calcium gluconate
- Calcium chloride
-Oral calcium supplements - avoid giving with other medications, especially thyroid meds because they could block absorption
Electrolyte imbalance
Hypercalcemia
- Etiology
– serum level > 10mg/dL
-Increase calcium resorption from bone (being pulled out of bone and put into the bloodstream)– most common cause; happens with:
- malignancies
- hyperparathyroidism (parathyroid regulates Ca+)
- Excessive calcium or vit D intake (ex. antacid overuse)
- Kidney disease – doesn’t filter correctly
Immobility with lack of weight bearing; Ca+ is reabsorbed from the bone and put into the bloodstream
Electrolyte imbalance
Hypercalcemia
2. Clinical Manifestations
- Lethargy, depression, confusion
- Muscle weakness
- Bradycardia
- Anorexia, N/V – GI symptoms
- Constipation, decreased bowel sounds
- Bone pain – get too much Ca+
- Thirst
- Polyuria
Electrolyte imbalance
Hypercalcemia
Collaborative Management
-Decrease dietary intake
-Medications - increase excretion (from kidneys) and decrease bone reabsorption
Ex:Loop diuretics, Glucocorticoids (steroids)
-Isotonic IV solutions (meaning matching body)
Ex:Normal saline,D5W, Lactated Ringers
-Sodium phosphate or potassium phosphate (if severe) IV – help reduce Ca+; phosphorus has an inverse relationship with Ca+. If give phosphorus it will reduce Ca+ (when Ca+ is high phosphate is low)
- Prevention is key
- physical activity with weight-bearing to help prevent Ca+ loss from bone (when lost from bones, many times it shows up in the bloodstream = hypercalcemia)
- early ambulation after injury with bedrest
Electrolyte imbalance
Hypomagnesemia - Magnesium Imbalances
- Etiology
normal = 1.5 or 2.5mg/dL
Electrolyte imbalance
Hypomagnesemia - Magnesium Imbalances
2. Clinical Manifestations
- Anorexia
- Dysphagia – difficulty swallowing
- N/V
- Tremors, twitching, tetany
- Seizures – (a lot of electrolyte imbalances have to do with neuromuscular function)
- Mood changes
- Cardiac arrhythmias
Electrolyte imbalance
Hypomagnesemia - Magnesium Imbalances
3. Collaborative Care
Oral or IV replacement
Increase dietary intake
Electrolyte imbalance
Hypermagnesemia - Magnesium Imbalances
1. Etiology
serum level >2.5mg/dL
- Renal dysfunction – most common cause
- High doses of magnesium containing medications
- Such as laxatives and antacids – especially in elderly since their kidneys aren’t functioning top-notch to begin with to filter out the excess
Electrolyte imbalance
Hypermagnesemia - Magnesium Imbalances
- Clinical Manifestations
- Depressed reflexes
- Weak pulses
- Bradycardia
- Warm and flushed
- Weakness
- Drowsiness
- Hypotension
- Diaphoresis( profuse sweating)
- Depressed respirations
Electrolyte imbalance
Hypermagnesemia - Magnesium Imbalances
3. Collaborative Care
- Oral and IV fluid and diuretics to try to flush out excess Mg+
- Treat underlying cause
