Rnur 238 Adult Ii - Unit 1 Ppt 2

Front 1

Explain the fluid breakdown %'s in the adult body.

Back 1

Adult body is 60% fluid:
Intracellular: 40%
Extracellular: 20%
* Interstitial - 15%
* Intravascular - 5%

Front 2

Anions & Cations. Which one is positively charged and which one is negatively charged?

Back 2

Cations - positive
Anions - negative

Front 3

What are the major cations and anions of extracellular fluid?

Back 3

Cation - Sodium
Anion - Chloride

Front 4

What are the major cations & anions of intracellular fluid?

Back 4

Cation - Potassium
Anion - Phosphate

Front 5

What are the functions of ions (electrolytes)?

Back 5

* Promote neuromuscular irritability
* Maintain fluid volume
* Distributes water between fluid compartments
* Regulates Acid-Base Balance

Front 6

What factors influence the amount of body fluids that we have? How or why?

Back 6

Age, Gender & Body Fat
Age - younger people have higher body fluid
Gender - men have higher body fluid
Fat - obese have lower body fluid b/c fat contains little water

Front 7

By what means do solutes move?

Back 7

DiffuSion - Solutes Descend the concentration gradient
Active tranSport - Solutes Ascend the concentration gradient

Front 8

By what means to fluids move between compartments?

Back 8

Osmosis (water)
Capillary filtration & reabsorption

Front 9

What is the major force in body fluid movement & IV fluid therapy?

Back 9

Osmosis

Front 10

Define osmolality

Back 10

The concentration of a solution which creates its osmotic pressure.

Front 11

Define osmotic pressure

Back 11

The pulling power of a solution for water.

Front 12

How is osmolality measured?

Back 12

It is a measurement of the concentration of solute particles per kg of water.

Front 13

What factors would increase serum osmolality?

Back 13

Anything that causes free water loss in the serum. ie. diabetes insipidus, sodium overload, hyperglycemia, uremia

Front 14

What situations would you find an increased urine osmolality?

Back 14

Fluid volume deficit, SIADH, HF, Acidosis

Front 15

In what situations would you find a decreased serum osmolality?

Back 15

The same ones that would cause a increased urine osmolality. SIADH, Renal Failure, Diuretic use?, Adrenal insufficiency

Front 16

In what situations would you have a decreasing urine osmolality?

Back 16

Fluid volume excess, diabetes insipidus.

Front 17

Where is albumin produced?

Back 17

In the liver.

Front 18

What are some large particles which do NOT easily pass through semi-permeable membranes?

Back 18

Urea, Glucose, Albumin

Front 19

Define Hydrostatic Pressure. Give an example.

Back 19

The pushing force of a fluid against the walls of the space it occupies. On the arterial side of capillaries hydrostatic pressure pushes fluid & solutes out of the vessel. In the middle of the capillary bed, pressure is constant. On the venous side, hydrostatic pressure pushes fluids & solutes into the vessel.

Front 20

What effect does hydrostatic pressure have on the movement of water & solutes?

Back 20

It moves solutes & water from areas of high hydrostatic pressure to areas of low hydrostatic pressure.

Front 21

Define oncotic pressure.

Back 21

It is the pulling force exerted by colloids in a solution.

Front 22

What is an important purpose of albumin?

Back 22

Maintaining normal serum oncotic pressure and adequate vascular fluid volume.

Front 23

T / F Plasma proteins cross vessel walls.

Back 23

F - therefore plasma protein concentration remains the same in arteries, veins & throughout the capillaries.

Front 24

What area does Starlings law apply? Arterial, Venous, or Capillary? Define Starlings Law.

Back 24

Capillary. Starlings law is the process of filtration into & out of the capillaries between two forces that are pushing & pulling.

Front 25

How does Starlings Law work?

Back 25

On the arterial end of the capillary, hydrostatic pressure is greater than oncotic pressure so fluid & nutrients move out of the capillary. On the venous end, hydrostatic pressure is lower than oncotic pressure so fluid and wastes are carried into the capillary.

Front 26

What impact does malnourishment have on Starlings Law?

Back 26

The only true indicators of malnourishment are Albumin & Total Protein. Since albumin is responsible for maintaining normal serum oncotic pressure, if there is a lack of Albumin, then normal serum oncotic pressure is reduced. This results in not enough protein to push fluid & waste products back into the capillaries on the venous end of starlings law & edema results.

Front 27

Explain the pathophysiology of how liver dysfunction causes edema.

Back 27

The liver produces albumin, albumin maintains normal oncotic pressure. Without it, fluids & wastes do not move back into the capillaries on the venous end of Starlings law & remains in the tissues, therefore edema results.

Front 28

What are the chemical F&E regulators?

Back 28

* Antidiuretic Hormone (ADH)
* Renin-Angiotensin-Aldosterone system
* Glucocorticoids (cortisol)
* Atrial Natriuretic Peptide (ANP)

Front 29

What are the mechanical F&E regulators?

Back 29

* Thirst mechanism
* Baroreceptors
* Active Transport

Front 30

Antidiuretic Hormone - Where is it made? Stored? What is its purpose? What triggers its release? How does it work?

Back 30

Made - Hypothalamus
Stored - Posterior Pituitary
Purpose - Regulate water in the body
Triggers - drop in BP, blood volume or rise in blood osmolality
How does it work - causes the kidneys to reabsorb water

Front 31

Explain the renin-angiotensin-aldosterone system.

Back 31

Renin does 2 things.
1 - when kidney perfusion is low, kidney releases renin into serum which travels to liver, in liver renin converts angiotensinogen to angiotensin I. Then angiotensin I is converted to angiotensin II by Agiotensin Converting Enzyme (ACE). Angiotensin II is a vasoconstrictor & increases arterial perfusion & stimulates thirst.
2 - with increased serum renin & thirst stimulation, aldosterone is released by the adrenal gland which tells the kidneys to conserve sodium & release potassium. Water follows sodium so aldosterone has a direct effect on water.

Front 32

What triggers the renin-angiotensin-aldosterone system?

Back 32

* drop in BP
* drop in blood volume
* drop in serum sodium
* rise in serum potassium

Front 33

What part does glucocorticoids (cortisol) play in F&E balance?

Back 33

Cortisol is a glucocorticoid hormone made by the adrenal gland when the body is stressed. This hormone stimulates the kidneys to retain sodium & water.

Front 34

What is ANP?

Back 34

ANP (Atrial Natriuretic Peptide) is a cardiac hormone stored in the atria that is released when the atria is stretched by high blood volume or high BP. It causes vasodilation of the blood vessels and suppresses the RAA system, decreases aldosterone, & decreases ADH causing increased urinary water excretion & increased glomerular filtration.

Front 35

How does the thirst mechanism help in F&E balance?

Back 35

Thirst receptors in the hypothalamus are stimulated when fluid losses or small increases in serum osmolality occur. Thirst also stimulates ADH & aldosterone release, which promotes reabsorption of water.

Front 36

At what age does the thirst mechanism become depressed?

Back 36

60

Front 37

How do baroreceptors help in F&E balance?

Back 37

Baroreceptors are small nerve receptors that detect changes in pressure within blood vessels. They work with the SNS & PNS as well as the endocrine system to monitor circulating volume.

Front 38

How does Active Transport influence F&E balance? Give an example.

Back 38

Active Transport moves solutes against the concentration gradient to maintain equilibrium. An example is the Sodium Potassium pump.

Front 39

What are colloids? What do they do? What do they contain or not contain?

Back 39

IV solutions that contain molecules that are too large to pass through capillary membranes and remain in the intravascular space for several days. They cause oncotic pressure and pull fluid out of the intracellular & interstitial space. Contain high molecular weight proteins & starches and do not contain clotting factors; however they can still affect the coagulation process.

Front 40

Name the 4 types of colloids. What are they used for?

Back 40

* Albumin
* Hetastarch
* Dextran
* Plasma Protein Fraction (PPF)

Used as volume expanders. Albumin, Dextran & PPF are specifically used for pts experiencing shock.

Front 41

Name some common Isotonic solutions.

Back 41

* NS
* Ringers
* Lactated Ringers
* D5W

Front 42

What is special about D5W?

Back 42

It is isotonic when it is in the bottle; however, it metabolizes quickly and converts to hypotonic in the system.

Front 43

What is the only solution that can be administered with blood products?

Back 43

Normal Saline

Front 44

What is the lactate in lactated ringers converted to? Where? What effect does this have on blood?

Back 44

Lactate is converted to bicarbonate in the liver. This is a base and will increase blood pH.

Front 45

Which IV solution is promotes renal elimination of solutes such as hypernatremia?

Back 45

D5W

Front 46

Which IV solution closely resembles the electrolyte composition of normal blood serum & plasma?

Back 46

Lactated Ringers

Front 47

Which IV solution is used to treat fluid losses from the lower GI tract or from burns?

Back 47

Lactated Ringers

Front 48

Which is the only isotonic solution that provides free water & calories?

Back 48

D5W - It is only classified isotonic b4 administration. Shortly after administration the glucose is metabolized and free water is produced. It becomes hypotonic and promotes the elimination of excess solutes.

Front 49

When are hypotonic solutions contraindicated? Why?

Back 49

Acute brain injury patients. B/c hypotonic solutions causes cells to swell and we don't want to cause additional swell of brain cells.

Front 50

When is a hypotonic solution given? What are some effects that hypotonic solution cause?

Back 50

* To reverse dehydration
* Provides extra water in the vessels to be pulled into the cells to rehydrate them.
* May cause cells to swell & possibly burst.
* Decreases vascular volume.
* Provides free water for cells & for excretion of body wastes.

Front 51

What can be the result of excessive Hypotonic solution use?

Back 51

Excessive use can lead to intravascular fluid depletion, decreased BP, cellular edema, and cell damage.

Front 52

What are the classic hypotonic solutions? What are the others and why are they "others"?

Back 52

Classic -.45 NS, .225 NS
Others - D5W, D5 1/2NS, D5 1/4NS
Why? D5W is Isotonic in the bag but hypotonic after Dextrose metabolized (about 5 mins)
D5 1/2NS & D5 1/4 NS is hypertonic in the bag but hypotonic after Dextrose metabolized

Front 53

Give examples of hypertonic solutions. What are the others & why are they "others"?

Back 53

Classic - 3% NS, D10 or greater %'s (TPN)
Others - D5LR, D5 1/2 NS, D5 1/4 NS
Why? - they are hypertonic in the bag but become hypotonic as soon as dextrose metabolized

Front 54

When are colloids contraindicated? When should you use caution?

Back 54

CI: With anemic or dehydrated patients.
Caution: Cardiac or Pulmonary problems *OR* in clinical situations where there is increased capillary leakage, such as: burns, sepsis, trauma, CHF, COPD, etc.

Front 55

Give some examples of colloids.

Back 55

Albumin
Intralipids 10%
Intralipids 20%
10% Dextran in 5% or NS
8% Amino Acids

Front 56

What is the best colloid to treat shock, burns, severe hypotension?

Back 56

10% Dextrain in 5% or NS

Front 57

Define Parenteral Nutrition

Back 57

Supplies the body with nutrients intravenously when oral intake is not possible or not adequate enough.

Front 58

What are the 4 types of parenteral nutrition? Explain them.

Back 58

TPN - Total Parenteral Nutrition - Given via a central line. > 10% dextrose concentration (usually 25-50%), usually needs lipids hung with it, typically green in color.
PPN - Peripheral Parenteral Nutrition - Not nutritionally complete, Dextrose < 10%, Therapy length 5-7 days, usually needs lipids hung with it.
TNA - Total Nutrient Admixture - 3 in 1 solution, dextrose, amino acids & lipids are all mixed together, many hospitals still call this TPN or PPN.
Intralipids/lipis - Fats. Usually given 1-3 x per week, can be up to 30% of calories.

Front 59

What are lipids if hanging alone? Isotonic, Hypotonic, Hypertonic?

Back 59

Isotonic

Front 60

Where are intralipids administered if given alone?

Back 60

via peripheral veins.

Front 61

How often is tubing on PN changed? How long is the bag of PN good for ?

Back 61

q 24 h.
24 h

Front 62

What type of tubing is needed for TPN, PPN or TNA?

Back 62

Filter tubing.

Front 63

How are lipids given if hung separately from TPN or PPN?

Back 63

They can be given separately in a peripheral vein or they can be connected to the TPN, PPN via Y tubing.

Front 64

What kind of tubing is required if the PN arrives in a glass bottle?

Back 64

Vented tubing.

Front 65

What needs to be monitored with patients receiving PN?

Back 65

I & O's, labs, weight, accuchecks.

Front 66

What type of tubing is NOT used with lipids that are separate?

Back 66

Filtered tubing.

Front 67

How often should PN bags/bottles be checked? What should be checked?

Back 67

q shift
* Verified against dr's orders, for expiration date, & for clarity (clear & no sediment (if not containing lipids))

Front 68

How do you prevent rebound hypoglycemia when d/c PN?

Back 68

Cut down rate slowly.

Front 69

What are some complications of PN?

Back 69

Pneumothorax
Air embolism
Clotted catheter line
Catheter displacement & contamination
Sepsis
Hyperglycemia
Fluid Overload
Rebound Hypoglycemia

Front 70

What are the 3 types of venous access?

Back 70

Peripheral
Midline
Central

Front 71

What is a Midline IV? How long is a midline IV good for?

Back 71

Intended to be a PICC line access but didn't reach the superior vena cava so it is left in midway.

1-2 weeks.

Front 72

How long are peripheral IV's, Peripheral IV tubing good for?

Back 72

4 days.

Front 73

What type of line is this?

Back 73

PICC line

Front 74

What are some clinical indications for PN?

Back 74

10% deficit in pre-illness weight
Pt. is not interested or unwilling to eat (anorexic/elderly)
Hypercatabolic illness (fever, infection)
Inability to take in oral foods or fluids at all due to illness or within 7 days post-op.

Front 75

What should bags of lipids be checked for b4 administration?

Back 75

Frothiness
Separation
Oily Appearance

If any of these are present, the lipids may be bad.

Front 76

How long is a PICC line good for?

Back 76

weeks to months (as long as it doesn't get infected)

Front 77

What should you remember with a heplock, saline lock, or peripheral IV?

Back 77

1 - monitor site & flush q shift.
2 - If blood will be infused, 18-20 g or larger
3 - Change site q 3-4 days.
4 - Arm veins are better than hand veins

Front 78

What are the 4 different kinds of Central Venous Access Devices?

Back 78

1 - Non-tunneled: Single, Dbl, or Triple Luman Central Cath.
2 - PICC & Power PICC
3 - Tunneled Central Cath
4 - Implanted Ports

Front 79

Non-Tunneled Central Venous Access Devices
1 - Where?
2 - What size & what use?
3 - For how long can be used?

Back 79

1 - Subclavian or Jugular
2 - 16 G distal lumen for blood/viscous fluids
2 - 18 G middle lumen for PN
2 - 18 G proximal port for blood/meds
3 - Short term (CDC recommends changing q 4 weeks)

Front 80

What is the difference between a PICC and a Power PICC?

Back 80

Power PICC can accept contrast dye, PICC cannot.

Front 81

PICC Central Venous Access Devices
1 - Where?
2 - Length of time?
3 - What can't you do on the side with the PICC?

Back 81

1 - Antecubital or Upper Arm
2 - Mid/Long term
3 - No Blood Pressures or Venipunctures

Front 82

Tunneled Central Venous Access Devices
1 - Where?
2 - Length of time?
3 - Uses?

Back 82

1 - Subclavian or internal jugular
2 - Long Term
3 - IV therapy such as chemo, abx, or TPN

Front 83

What has to be done after placement of Central Venous Access Devices?

Back 83

Placement should be checked by X-Ray b4 use

Front 84

Implanted Port Venous Access Devices
1 - explain what they are

Back 84

1 - a metal chamber is implanted and adhered to the chest wall, these require a special needle called a Huber to access it.

Front 85

How do you manage a CVAD?

Back 85

1 - Prevent infection
2 - Maintain a closed IV system
3 - Maintain a patent device
4 - Prevent damage

Front 86

Give the appropriate lab values for Sodium, Potassium & Magnesium.

Back 86

Na - 135-145
K - 3.5-4.5
Mg - 1.8-2.7

Front 87

What lab values might indicate hyponatremia?

Back 87

Decreased serum & urine sodium
Decreased urine specific gravity & osmolality

Front 88

What lab values might indicate hypernatremia?

Back 88

Increased serum, urine specific gravity & osmolality
Decreased urine sodium
Decreased central venous pressure

Front 89

What S&S might you see with both hyponatremia & hypernatremia?

Back 89

N/V
Lethargy
Muscular Twitching
Increased Pulse
Anorexia
Seizures

Front 90

What different S&S might you see between hyponatremia & hypernatremia?

Back 90

Hypo - HA, Dizziness, Confusion, Muscle cramps & weakness, Papilledema, Dry Skin, Decreased BP, Weight Gain, Edema

Hyper - Thirst, Temp, Swollen/Dry Tongue, Sticky Mucous Membranes, Hallucinations, Restlessness, Irritability, Pulmonary Edema, Hyperreflexia, Increased BP

Front 91

What S&S might you see with hypokalemia?

Hyperkalemia?

Back 91

Hypo - Fatigue, Anorexia, N/V, Muscle Weakness, Polyuria, Decreased Bowel Motility, Ventricular Asystole or Fibrillation, Paresthesias, Leg Cramps, Decreased BP, Ileus, Abdominal Distention, Hypoactive Reflexes.

Hyper - Vague Muscular Weakness, Tachycardia->Bradychardia, Dysrhythmias, Flaccid Paralysis, Paresthesias, Intestinal Colic, Cramps, Irritability, Anxiety.

Front 92

What S&S might you see with hypomagnesemia?

Hypermagnesemia?

Back 92

Hypo - Neuromuscular irritability, positive Trousseau's & Chvostek's signs, insomnia, mood changes, anorexia, vomiting, increased tendon reflexes, increased BP.

Hyper - Flushing, hypotension, drowsiness, hypoactive reflexes, depressed respirations, cardiac arrest & coma, diaphoresis, tachycardia -> bradycardia.

Front 93

What factors could contribute to hyponatremia?

Back 93

Loss of sodium, as in:
* Diuretics
* Loss of GI fluids
* Renal Disease
* Adrenal Insufficiency
* Hyperglycemia
* Heart Failure
Gain of water, as in:
* Excessive D5W & water supplements for pts receiving hypotonic tube feedings
* Diseases associated with SIADH (head trauma)
* Medications causing water retention (oxytocin, tranquilizers)
* Psychogenic Polydipsia

Front 94

What factors could contribute to hypernatremia?

Back 94

* Water deprivation in pts unable to drink @ will
* Hypertonic tube feedings w/o adequate water supplement
* Diabetes Insipidus
* Heatstroke
* Hyperventilation
* Watery Diarrhea
* Burns
* Diaphoresis
* Excess Corticosteroids
* Sodium Bicarbonate
* Sodium Chloride Administration
* Salt Water, near drowning victims

Front 95

What contributing factors could result in Hypokalemia?

Back 95

* Diarrhea
* Vomiting
* Gastric Suctioning
* Corticosteroid Administration
* Hyperaldosteronism
* Bulimia
* Osmotic Diuresis
* Alkalosis
* Starvation
* Diuretics
* Digoxin Toxicity

Front 96

What contributing factors could result in Hyperkalemia?

Back 96

* Psuedohyperkalemia
* Oliguric Renal Failure
* Potassium Conserving Diuretics
* Metabolic acidosis
* Addison's disease
* Crush Injury or Burns
* Stored Blood Bank Transfusions
* Rapid IV administration of Potassium

Front 97

What contributing factors could result in Hypomagnesemia?

Back 97

* Alcoholism
* Hyperparathyroidism
* Hyperaldosteroism
* Diuretic phase of renal failure
* Malabsorptive disorders
* Diabetic Ketoacidosis
* Refeeding after starvation
* Parenteral Nutrition
* Chronic Laxative Use
* Diarrhea
* Acute MI
* Heart Failure
* Decreased Serum K & Ca

Front 98

What contributing factors could lead to Hypermagnesemia?

Back 98

* Oliguric phase of renal failure (mostly when mag containing meds are administered)
* Adrenal Insufficiency
* Excessive IV magnesium Administration
* Diabetic Ketoacidosis
* Hypothyroidism

Front 99

Which disorder do you think SUCTION? What does it stand for?

Back 99

S & S of Hypokalemia

Skeletal muscle weakness
U wave (ECG changes)
Constipation
Toxic Digoxin
Irregular/weak pulse
Orthostatic Hypotension
Numbness (paresthesia)

Front 100

Which disorder do you think RENAL? What does it stand for?

Back 100

S & S of Hypermagnesemia.

Reflexes decreased (+weakness/paralysis)
Ecg changes
Nausea/Vomiting
Appears flushed
Lethargy (+drowsiness/coma)

Front 101

Which disorder do you think SALT? What does it stand for?

Back 101

S & S of Hypernatremia.

Skin flushed
Agitation
Low grade fever
Thirst

Front 102

Which disorder should you think STARVED? What does it stand for?

Back 102

S & S of Hypomagnesemia

Seizures
Tetany
Anorexia & Arrhythmias
Rapid Heart Rate
Vomiting
Emotional Lability
DTR's increased

Front 103

Which electrolyte disorders should you be concerned with patients taking Digoxin. Why?

Back 103

Hypokalemia
Hyperkalemia
Hypomagnesemia

Front 104

What electrolyte disorder should you think of CBIGKD? What does it stand for?

Back 104

Treatments for Hyperkalemia

Calcium gluconate
Bicarbonate
Insulin
Glucose
Kayexalate
Dialysis

Front 105

What is this? Which electrolyte disorder might you see this?

Back 105

Chvostek's Sign

Hypomagnesemia

Front 106

What is this? Which electrolyte disorder might you see this?

Back 106

Trousseau's Sign

Hypomagnesemia