Med-Surg Exam 4

Front 1

Increased cranial pressure is crucial because:

Back 1

It DECREASES cerebral PP

Front 2

Causes of Increased Cranial Pressure:

Back 2

-Mass lesion
-Cerebral Edema (vasogenic, cytotoxic, interstitial)
-Head Injury
-Brain Inflammation
-Metabolic insult (retention of fluids--> fluids increase, wastes increase...etc)

Doesn't really matter how the ICP started, just matters that it did and the treatment is all the same anyway

Front 3

ICP flow chart:

Back 3

Cranial insult-->
Tissue Edema-->
INCREASED ICP-->
Pressure compresses on blood vessels-->
Cerebral blood flow is decreased-->
Decreased oxygen perfusion, death of brain cells-->
Edema accumulates around necrotic tissue-->
Increased ICP with compression of brain stem and respiratory center-->
Accumulation of CO2 from blood that is not leaving-->
Vasodilation as natural body response to acidosis-->
More increased ICP from the increase in blood volume from vasodilation-->
DEATH if no interventions

Front 4

Skull's 3 essential components:

Back 4

Brain tissue 78%
Blood 12%
CSF 10%

Front 5

The three components of the brain must remain _________

Back 5

BALANCED

Front 6

When the skull's 2 components are balanced, the pressure is somewhere around ___________ mm Hg under normal conditions

Back 6

0-15mm Hg

Front 7

Factors that influence ICP:

Back 7

-Arterial Pressure
-Venous Pressure
-Intra-abdominal and intra-thoracic pressure
-Posture (head elevated vs. laying down)
-Temperature (fever elevated pressure)
-Blood gases (because acidosis and hypoxia both cause vasodilation, increasing pressure)

Front 8

"ACCOMMODATION PRINCIPLE"

Back 8

Degree to which factors elevate ICP, depends on the ability to accommodate the changes

Front 9

Things that people do that increase pressure:

Back 9

Coughing
Sneezing
Pressure from straining during a BM
Laying down
Acidosis

Front 10

Normal ICP:

Back 10

0-15 mm Hg

Front 11

Modified Monro-Kellie doctrine says:

Back 11

"If volume in any one of the 3 components INCREASES within the cranial vault, and volume from ANOTHER COMPONENT is DISPLACED, the total intracranial volume WILL NOT CHANGE."

If they accommodate for one another, there will be a constant volume within the skull structure.

Front 12

Measuring ICP:

Back 12

Measured with a pressure transducer in the ventricles, subarachnoid space, epidural space, brain parenchymal tissue

Front 13

Pressure greater than ________ is considered abnormal

Back 13

15 mm Hg

Front 14

Normal compensatory adaptations in the skull components:

Back 14

-Alteration of the CSF absorption or production
-Displacement of CSF into spinal subarachnoid space
-Dispensability of the dura (by creating burr holes you make more space, or in the case of neonates they have displaced skull fragments that allows for more room)

Front 15

ability to compensate is limited.
If the volume increase continues...

Back 15

....ICP rises and continues to rise

Front 16

Definition of cerebral blood flow

Back 16

The amount of blood in mL that passes through 100g of brain tissue in 1 minute

**About 50mL/min 100 g of brain tissue

Front 17

Factors that affect cerebral blood flow:

Back 17

CO2
O2
Hydrogen ion concentration (acidosis)

Front 18

"Autoregulation" of cerebral blood flow

Back 18

Automatic alteration in diameter of cerebral blood vessels to maintain constant blood flow to brain (vasoconstriction or vasodilation)

Front 19

Ensuring a consistent cerebral blood flow is essential to:

Back 19

-Provide the metabolic needs of brain tissue
-Maintain cerebral perfusion pressure

Front 20

Cerebral perfusion pressure (CPP):

Back 20

-Pressure needed to ensure blood flow to the brain

Front 21

CPP=

Back 21

MAP minus ICP

Front 22

Normal cerebral perfusion pressure:

Back 22

70-100

Front 23

Less than ________ mm Hg CPP is associated with ________ and ______________

Back 23

Less than 50 mm Hg is associated with ISCHEMIA and NEURONAL DEATH

Front 24

Pressure changes:
Compliance = ______________ of the brain, which equals ________ divided by ___________

Back 24

Compliance = the EXPANDABILITY of the brain, which equals VOLUME divided by PRESSURE

Front 25

Stage 1 and 2:
At first there is high ___________, but then ___________ ___________, which means there is a risk for elevating ICP

Back 25

compliance (expandability), but then compliance (expandability) decreases, so risk for ICP raises

Front 26

Stage 3:
Once compliance (expandability) has decreased, ANY small addition in volume causes:

Back 26

a GREAT increase in ICP and loss of autoregulation

Front 27

Stage 4:
Once there is ICP and loss of autoregulation:

Back 27

ICP rises to LETAL levels

Front 28

3 types of cerebral edema:

Back 28

Vasogenic
Cytotoxic
Interstitial

Front 29

Vasogenic Cerebral Edema

Back 29

Most Common; in the white matter
Associated with BBB permeability changes
(from toxins, abscesses, tumors)

Front 30

Cytotoxic Cerebral Edema

Back 30

Most often occurs in the gray matter
Due to lesions or trauma to brain tissue, which results in hypoxia or anoxia

Front 31

Interstitial Cerebral Edema

Back 31

Due to peri-ventricular diffusion of ventricular CSF
Due to uncontrolled hydrocephalus
-Can also be caused by enlargement of the extracellular space as a result of SYSTEMIC WATER EXCESS, like renal insult

Front 32

If there is increased accumulation of fluid in the extravascular spaces of brain tissue (regardless of the cause):

Back 32

There will be increased TISSUE VOLUME, which means there is potential for increased ICP

Front 33

Clinical Manifestations of ICP: the MAIN ONE IS _____________

Back 33

CHANGE IN LEVEL OF CONSCIOUSNESS
-This is an early sign
-Can be subtle (flat affect, confusion, maybe they become really agitated all of a sudden and they have no explanation when you ask them about it, or you were right there the whole time and didn't see anything that would cause them to get agitated)
OR
-Can be dramatic, if they go into a coma
-Changes in LOC are due to poor cerebral blood flow, which leads to hypoxia, things get weird then the tissues aren't getting the oxygen they need

Front 34

Cushing's Triad

Back 34

LATE SIGN of increased ICP
-It's where the vital signs of that particular person have changed, must have their baseline vital signs first though). The 4 (even though its a triad) things to monitor are: BP (increased systolic), PP (widening pulse pressure), HR (bounding pulse), R (change in respirations)

Front 35

Temperature is a sign of ICP:

Back 35

due to ICP on the hypothalamus (temperature regulation center)

Front 36

If the person's respirations are changing due to ICP, they are at increased risk now for ________

Back 36

Airway obstruction risk, maybe from their tongue or secretions

Front 37

If their respiration pattern keeps changing:

Back 37

Identify lesion location

Front 38

Cheyne-Stokes Breathing Pattern:

Back 38

Cycles of hyperventilation and apnea (not breathing at all)

Bilateral Hemispheric brain dysfunction

Front 39

Central neurogenic hyperventilation

Back 39

Sustained, regular rapid and deep breathing

Brainstem at base

Front 40

Apneustic breathing;

Back 40

Prolonged inspiratory phase
or
pauses alternating with expiratory pauses

Mid or lower pons

Front 41

Cluster breathing

Back 41

Clusters of breaths follow each other with irregular pauses between

Medulla

Front 42

Ataxic Breathing

Back 42

Completely irregular with some breaths deep and some shallow. Random, irregular pauses, slow rate.

Retricular formation of the medulla

Front 43

Clinical Manifestations of ICP: Occular signs

Back 43

PERLA? Bilateral? Ispilateral?
Pupils dilate because of the pressure

Constricted: brisk response to light is normal
Sluggish: early pressure on CN III
Dilated/Fixed: increased ICP
BIlateral, dilated, fixed=ominous sign of brain injury

Front 44

ICP manifestation: signs of Decreased Motor function:

Back 44

Decebrate and Decorticate. Possible to even have a mixture of both, one on each side.

Front 45

Decebrate

Back 45

Extensor posturine, back away from core. This is a sign of more serious damage

Front 46

Decorticate

Back 46

Flexor Posturing, towards the core

Front 47

Opisthotonic Posturing

Back 47

Everything is arched, head and feet are the only thing touching the bed

Front 48

Headache as a manifestation of ICP:

Back 48

Often continuous
Worse in the morning (from laying down)
Its due to pressure on arteries, veins, nerves
May be due to Straining

Front 49

Vomiting as a sign of ICP:

Back 49

Nonspecific sign because everything causes vomiting
It is due to pressure in the skull
Person was not nauseas before they vomited
It is shown as projectile vomiting. Pressure triggered it, hard and fast in the brain

Front 50

Two major complications of uncontrolled increased ICP:

Back 50

1. Inadequate cerebral perfusion (decreased oxygenation)
2. Cerebral herniation

Front 51

Ways to diagnose increased ICP (9):

Back 51

MRI
CT
Cerebral angiography
EEG
Brain tissue oxygenation measurement
ICP measurement
Transcranial Doppler studies
Evoked potential studies
PET

Front 52

Gold standard for ICP monitoring is the __________

Back 52

VENTRICULOSTOMY

LICOX brain tissue oxygenation catheter--in frontal white matter monitor brain O2, especially for ischemia
Jugylar venous bulb catheter

Monitor heavily for infection

Front 53

Infection in ICP:

Back 53

a SERIOUS consideration

Front 54

ICP should be measured as a "mean pressure" at:

Back 54

the end of expiration
-Waveform should be recorded
-Shaped similar to arterial pressure tracing

Front 55

Measurement of ICP: inaccurate readings can be caused by:

Back 55

CSF leaks
Obstruction in catheter
Differenced in height of bolt/transducer
Kinks in tubing
Incorrect height of drainage system relative to patient's reference point

Front 56

With a catheter, it is possible to control ICP by:

Back 56

removing CSF. this decreases the pressure

Front 57

if you are draining the CSF:

Back 57

ESSENTIAL to monitor the volume drained

Front 58

Mannitol for ICP:

Back 58

IV osmotic diuretic that decreases ICP.
Fluid leaves the tissues and moves into the blood vessels

Must have properly functioning kidneys

Front 59

Corticosteroids for ICP:

Back 59

Dexamethasone (decadron)
Controls vasogenic edema (tumors/abscesses)
Inhibits synthesis of prostoglandins

Complications include hyperglycemia, GI bleed, hyponatremia, INFECTION

Front 60

Barbituates for ICP:

Back 60

-Decrease cerebral metabolism, so decrease ICP
-Used for inducing coma

Front 61

Dilantin for ICP:

Back 61

Will probably be administered to prevent a seizure whether or not they've had one already. avoiding a seizure decreases the risk for ICP

Front 62

Nutritional therapy during ICP:

Back 62

Early feeding improves outcome
Feeding should begin within 3 days of injury
Increased need for glucose because the person is hyper-metabolic and hyper-catabolic when in ICP. Brain also only uses glucose, not anything that needs to be broken down first

Front 63

Fluids during ICP:
Restriction of fluids

Back 63

Restriction is controversial
-Slight dehydration may reduce cerebral edema
OR
-Hypovolemia may decrease CO, BP, leading to cerebral hypoxia (decreased O2 to the brain)

Front 64

Keep patient ______volemic

Back 64

Normovolemic
IV 0.9% NaCl

Once everything is stable, give D5 and 1/2 normal saline

Front 65

Adequate oxygenation in ICP:
PaO2 must be kept at _______ mm Hg or higher

Back 65

100 mm Hg or higher.
ABG analysis guides the oxygen therapy
May require a mechanical ventilator

Front 66

Hyperventilation therapy during ICP:

Back 66

Used to be the mainstay therapy to blow off CO2 and reverse acidosis, but EBP showed that aggressive hyperventilation increases risk of cerebral ischemia and adversely affects outcome.
If do it, keep it brief

Front 67

Nursing assessments for increased ICP:

Back 67

Monitor strength and response
Vital signs
Subjective data from patient/family members (especially about LOC or about what the person might be telling you)
Glascow coma scale
Neurologic assessment: eyes, pain

Front 68

Check for pupillary changes in ICP patient

Back 68

Bilateral?
Size?
Ask about medications or drugs they might be on/taking that could also affect pupil size

Front 69

Overall goals for nursing management of ICP

Back 69

A(irway). maintain a patent airway
B(reathing). ICP within normal limits
C(irculation). Normal fluid and electrolyte balance
D. no complications secondary to immobility and decreased LOC

Front 70

Nursing interventions for respiratory function and ICP:

Back 70

Pain
Fear
Opioids
Suctioning for patent airway

Front 71

Nursing interventions: maintain fluid and electrolyte balance in ICP, may be due to:

Back 71

SIADH, Diabetes Insididus (where massive clear fluid is lost and they end up in fluid deficit, leads to pre-renal failure, BP will drop, not enough fluid to the brain

Front 72

Monitoring of intracranial pressure:
Normal=?

Back 72

0-15 mm Hg
infection?

Front 73

nursing intervention for ICP: body position

Back 73

maintain HOB at 30 degrees to decrease ICP

Front 74

Nursing intervention for safety in ICP:

Back 74

Make sure they are protected from injury and harm: the risks are seizure, confusion, agitation, decreased LOC

Front 75

Psychological considerations during ICP:

Back 75

Anxiety
must give SIMPLE directions, one mundane step at a time
Must care for the family's needs, they can be having a hard time seeing their loved one act not like themselves or in a deteriorating condition

Front 76

What does the kidney do? (4)

Back 76

-Regulates volume/composition of the ECF by secreting ADH/Aldosterone, calcium
-Excrete waste
-Acid-base balance, H ion excretion, HCO3 generated
-ANP=large, dilute urine

Front 77

Endocrine (hormone) aspects of the kidney function:

Back 77

-EPO production
-Vitamin D is activated by the kidneys (which affects calcium, heart, and bones)
-Renin production
-Prostoglandins--->vasodilation to lower BP

Front 78

Energy metabolism in the kidneys:

Back 78

Carnitine produced in the kidneys, which is derived from meat and dairy products

Front 79

Carnitine is needed for:

Back 79

transfer of fatty acids into cell mitochondria, which is how energy is produced

Front 80

Clinical manifestations of decreased energy production from renal failure:

Back 80

-Muscle weakness
-lethargy
-Hypotension during dialysis (meaning they'd be likely to pass out if they go into dialysis

Front 81

Goal in Acute Renal Failure:

Back 81

PREVENTION!

-identify and eliminate cause
-Reverse it
-know that it occurs in 15-20% of all critically ill patients
-when it happens, there is 50-80% mortality

Front 82

ARF usually occurs with something else, like:

Back 82

CVD
Diabetes
Postop

Front 83

Characteristics of ARF:

Back 83

RAPID loss of renal function
Progressive azotemia
1. accumulation of nitrogenous wastes
2. uremia; oliguria 50% of cases
3. inability of kidneys to conserve sodium

Front 84

Clinical manifestations of altered fluid imbalance:

Back 84

1. Neck vein distention and bounding pulses
2. Hypertension
3. Pulmonary edema, pleural effusion
4. Heart Failure

Front 85

Clinical manifestations of electrolyte imbalance:

Back 85

Potassium: bradycardia, irregular heart rhythm
Urea: itching (buildup of wastes)
Sodium: HTN, weight gain, edema, pulmonary edema (retention of fluids)
Calcium: weak pulse, hypotension, parasthesias, diarrhea, abdominal cramps

Front 86

Objective signs of acid-base regulation problems with the kidneys

Back 86

-Increased hydrogen concentration
-increased depth and rate of respirations (Kussmaul respirations)
-waste products: high BUN, high creatinine, high uric acid

Front 87

Clinical manifestations of altered acid-base regulation

Back 87

1. dry, itchy skin (uremic frost)
2. Yellow discoloration of the skin; bruising
3. Uremic halitosis (metallic taste in the mouth)
4. Anorexia, n/v
5. changes in mental status (lethargy)
6. Asterixis (fingers moving/tremor from waste on the nerves)

Front 88

Creatinine definition:

Back 88

end product of muscle and protein metabolism

Front 89

Serum creatinine level:

Back 89

0.1-1.2 mg/dl

Front 90

Increased creatinine level could mean:

Back 90

possible renal disease

-check 24 hour creatinine clearance UA, this is the best method. results vary with age/sex/muscle mass

Front 91

Urea nitrogen definition:

Back 91

A byproduct of liver metabolism of proteins

Front 92

Blood urea nitrogen normal level

Back 92

10-20 mg/dl

Front 93

If blood urea nitrogen is increased:

Back 93

there is decreased renal perfusion

Can also be increased from: dehydration, injured muscles, GI bleed, hemolysis

Front 94

BUN/Creatinine ratio:

Back 94

10:1 is normal

If they INCREASE at the SAME rate, this suggests renal dysfuntion

Front 95

Things that can cause an increased BUN/creatinine ratio:

Back 95

-Dehydration, hemolysis, or low BP (BUN runs out of proportion to creatinine)
-Suggests non-renal causes

Front 96

Other lab tests for ARF:

Back 96

Potassium
Calcium
Phosphate
Serum albumin
Protein
CBC
Urine (UA, 24 hr collection, creatinine clearance, electrolytes, osmolarity)

Front 97

Why check phosphate level;

Back 97

PO4 will be increased due to decreased excretion by kidneys, and release from bones

Front 98

Why check Calcium levels:

Back 98

deficient kidneys won't synthesize as much vitamin D so electrolyte level will show hypocalcemia. this is important because it can lead to fractures!

Front 99

Diagnostic tests for ARF:

Back 99

Bladder scan
KUB (kidney urine bladder) X ray
IVP
CT scan (of the kidneys, bladder, ureters)
Cystography, cytoscopy
Renal arteriography, biopsy
Ultrasonography

Front 100

Causes of prerenal ARF:

Back 100

FLUID deficit.
Not enough fluid flowing to the kidneys.
Think of all the ways you might lose fluid (hemorrhage, GI losses like diarrhea and vomiting, burns, dehydration, decreased CO/HF/MI/cardiac dysrhythmias, decreased PVR, decreased RBF)

Front 101

Causes of intra-renal ARF:

Back 101

Toxins, antibody-anigen complexes. (Things that are damaging directly to the nephrons, prolonged pre-renal ischemia, meds, radiocontrast dyes, hemolytic, renal infections like nephritis/CMV/candidiasis, SLE, thrombus, malignant HTN)

Front 102

Postrenal causes of ARF:

Back 102

Anything that is obstructing urine flow after the kidneys, such as renal calculi, strictures, tumors (bladder/prostate cancer), trauma; spinal cord injuries)

Front 103

Phases of ARF:

Back 103

initiating phase (begins with an insult until sx appear, can last hours to days)
oliguric phase
diuretic phase
recovery phase

Front 104

Clinical manifesations of oliguric phase (1-7 days AFTER insult)

Back 104

1. UO <400ml/24 hours
2. Edema
3. Increased BP
4. Pulmonary Edema
5. Excess potassium
6. Metabolic Acidosis
7. Kussmaul breathing
8. Bleeding due to a calcium deficit
9. BUN

Front 105

Nursing interventions during oliguric phase

Back 105

1. closely monitor intake (CALCULATE LOSSES PLUS 600ml FOR INSENSIBLE LOSSES)
2. Diuretics, as long as CO/intravascular volume are adequate, if ARF present, diuretics will be harmful!
3. Hyperkalemia: life threatening due to dysrhthmias.
a. Insulin and sodium bicarb will shift K into cells
b. Eventually will shift back out into vascular
c. Eventually will raise threshold for dydrhytmias
d. Kayexelate and dialysis only way to remove K from body (but be sure there are paralytic ileus or will have bowel necrosis)

Front 106

Diuretic phase goals:

Back 106

-Gradual increase in urine output (1-3L/day) (osmotic diuresis d/t excess urea concentration)
-Ability to excrete waste increases
-Monitor for hyponatremia/hypokalemia/hypovolemia, things that signify fluid deficit because this might mean an inability of the tubules to concentrate urine
-Normalization of FEAB and waste product level

Front 107

Diuretic phase: interventions for fluid volume deficit

Back 107

1. Daily weights and I&Os
2. Vital signs
3. Monitor serum Na
4. Monitor s/s of dehydration
5. Offer fluid

Front 108

Diuretic phase: interventions of hypokalemia

Back 108

1. monitor for signs of low K (cardiac stuff)
2. IV potassium if needed, never exceed 10mEq/hr
3. Control GI losses

Front 109

Diuretic phase lasts:

Back 109

1-3 weeks in duration

Front 110

Recovery phase (healing process):

Back 110

maximal renal function returns when GFR increases (shows by BUN/Cr plateau then gradually decline, may take 2 weeks-12 months)

Front 111

Functional loss during recovery phase is not clinically significant:

Back 111

Urine volume stabilizes
Body fluid and electrolytes become balanced
Uremia resolves

No additional treatment is necessary

Front 112

If too much damage has occurred...

Back 112

may progress to CRF over time


Especially with older adults

Front 113

Nursing role in AKI (ARF)

Back 113

-Identify risks and monitor closely:
-ANY episodes of hypotension
-Patients with diabetes, HTN
-Signs of UTI
-Administration of nephrotoxic drugs

Front 114

Nephrotoxic drugs:

Back 114

-NSAIDs, ASA, heroin, cocaine, lithium, capoten
-Vancomycin, Amphotericin B, sulfonamides
-Contrast medium, gold, methotrexate

Front 115

Interventions for AKI

Back 115

Eliminate precipitating CAUSE of AKI:

pharmacologic therapy (IV fluids, furosemide)
renal replacement therapy if needed

Front 116

Nutrition therapy for AKI

Back 116

Protein intake is cruicial
Na/K/PO4 restriction
Fats INCREASED
TPN if GI is non functioning
Goal is to prevent muscle breakdown

Front 117

Protein intake during AKI:

Back 117

a. 0.6 g/kg if not on dialysis
b. 1 to 1.5 g/kg if on dialysis

Front 118

Fats intake during AKI:

Back 118

30-40% of calories
30-35 kcal/kg TBW

Front 119

Na/K/PO4 during AKI:

Back 119

restricted

Front 120

Foods with a lot of sodium (restricted):

Back 120

ANYTHING that comes from a bag
-processed foods
pickles
potato chips
smoked meat/fish
processed cheese
peanut butter
baking soda toothpaste

Front 121

Foods with a lot of potassium (restricted)

Back 121

Orange Juice
Potatoes
Rice
Pasta
Bread
Coffee
Chocolate

Front 122

Fruit that is really hazardous to dialysis patients:

Back 122

Starfruit (carambola)



Can cause agitation, confusion, and even death

Front 123

Foods with a lot of calcium:

Back 123

Milk
Ice cream
Broccoli
Tofu
Navy beans
Almonds

Front 124

Foods with a lot of phosphorus (restricted):

Back 124

Milk
Beer
Chocholate
Yogurt
Bran cereals
Twizzlers
Potatoes
Dark Colas

Front 125

Medications for AKI

Back 125

Diuretics?
Antihypertensives
Phosphate binders
Potassium removing resin
Calcium replacement
Vitamin D analog

Front 126

Nursing care of AKI patients

Back 126

-Be aware of fluid restrictions
-Importance of DAILY WEIGHTS
-Recignuze that some drugs dialyze out with hemodialysis
-Care of access: graft/fistula, never take BP on this arm
acceptable lab values are different

Front 127

NEVER EVER EVER tale BP on:

Back 127

arm in dialysis

Front 128

Indications for renal dialysis:

Back 128

-If kidneys do not recover from ARF
-Hyperkalemia
-Fluid excess: HTN, pulm edema
-Metabolic acidosis
-Remove Toxins