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NUR4630 > Exam 2 review sheet > Flashcards

Exam 2 review sheet Flashcards

1
Q

Brain uses what for metabolism?

A

glucose and oxygen

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2
Q

Autoregulation is the brains ability to? When does it shut down

A
  • maintain constant cerebral blood flow
  • less than 60, greater than 160 systolic, or cerebral perfusion suboptimal
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3
Q

Arterial is the ? system in the brain

A
  • High Pressure System
  • Thinner & more fragile
  • Carotid & Vertebral arteries supply blood to the brain
  • Circle of Willis: where blood flows up and is able to flow over to the oppposite side
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4
Q

Venous is the ? Pressure System

A
  • Low pressure system
  • Lack valves

Compress easily with Increase Pressure

*

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5
Q

Cerebral Perfusion Pressure

A
  • CPP= MAP –ICP
  • Normally greater than 50
  • Less than 50 indicates loss of autoregulation
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6
Q

Monro Kellie Hypothesis

A
  • Changes in the brain volume result in
  • Increased ICP
  • (or) decrease in one of the other volumes
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7
Q

Compliance is the attempt to ?

A
  • Compliance is the attempt to maintain the ICP between 5-15 mm/hg
  • CSF displacement
  • CSF reabsorption
  • Venous compression and blood shuntin
  • ensure cererbral blood flow
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8
Q

Decrease in CBF leads to?

A
  • Ischemia
  • Build-up Lactate (does not cross blood brain Barrier)
  • Ultimately cerebral acidosis
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9
Q

Hyperemia

A
  • Is increased blood flow to brain. Causes arterial congestion
  • Luxury Perfusion
  • Progressive vasodilation
  • Increased CBF
  • Loss of Autoregulation: Increased ICP
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10
Q

conditions that increase cerebral blood flow

A
  • Hypertension
  • Fever
  • Pain
  • Hypercapnia
  • Ischemia
  • Cerebral vasodilation
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11
Q

conditions that decrease cerebral blood flow

A
  • Hypotension
  • Sedation
  • Paralysis
  • Hypocapnia
  • Cerebral edema
  • Decrease CO
  • Cerebral vasoconstriction
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12
Q

Confusion
Disorientation differences?

A

disorientations: agitation and anxiety plus the confusion

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13
Q

obtunded

A

responses are slower

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14
Q

stupor

A

only respond with painful stimuli

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15
Q

coma

A

don’t respond to painful stimuli

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16
Q

Vowel- TIPPS

A

Common Reasons for altered LOC

Vowel-Tipps

  • Alcohol
  • Epilepsy
  • Insulin
  • Opiates/drugs
  • Uremia
  • Trauma
  • Temperature
  • Infection
  • Psychogenic
  • Poisin
  • Shock-Stroke
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17
Q

Glascow coma scale

A
  • Looks at eye opening, verbal response, motor response.
  • Higher the score the higher the function
  • Score less than 9=concern
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18
Q

decerebate

A

arms flexed down and out, and you’re dying

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19
Q

decorticate

A

pulled in towards your core, you can fix it

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20
Q

What is a positive Dolls Eyes?

A

turn the patient and the eyes stay fixed straight. Head goes sideways and eyes go sideways too

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21
Q

Caloric Ice Test negative and positive findings?

A
  • insert 20 ml of cold water into the ear. You expect to see the eyes start moving, and then they fix over to the side you put the ice water in. This would be a normal response and a negative eyes test
  • abnormal response is the eyes staying fixed
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22
Q

Cranial Nerve Assessment

A
  • Corneal: stick something on cornea, they blink (normal)
  • Gag
  • Swallow
  • Cough
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23
Q

S/S of Increased ICP infants, children

A
  • Infants
  • Bulging fontanel
  • Separated cranial sutures
  • Cracked-pot sign: bang on head, sounds like a hollow pot (extra fluid)
  • Setting-sun sign: eyes are low set and whites are showing above it
  • Positive transillumination
  • Children: c/o headaches, projectile vomiting, and new seizure onset activity
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24
Q

neurologically small pupils

A

damage to pons

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25
Q

neurologically big pupils

A

damage to brain stem

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26
Q

fixed pupil that is dilated =

A

impending herniation

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27
Q

Early Signs of ↑ ICP

A
  1. Slight LOC changes ***MOST IMPORTANT****
  2. Pupils sluggish / Impaired eye movement
  3. Limb strength changes
  4. Headache
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28
Q

ICP Peaks?

A

48 – 72 hours after injury

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29
Q

Cushing’s Triad: Signs of ↑ ICP

A

Blood Pressure

  - Systolic   BP   Increases
  - Diastolic BP  Decreases
  - Pulse Decreases

Widening Puse Presure

Bradycardia

Might also see cheyne-stokes breathing and elevated temperature

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30
Q

Brain Herniation occurs when

A

a part of the brain pushes downward inside the skull through the opening that leads into the neck

(Foramen Magnum)

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31
Q

How To Minimize Cerebral Edema?

A

Maintain

Cerebral perfusion pressure
CPP of 50 – 70 mm Hg

Prevents Hypoxia (Hypercarbia)

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32
Q

early herniation

A
  • potentially reversible
  • level of conciousness may not be impaired initially
  • alert to stuperous, pupils sluggish, cheyne-stokes respiration, slight increase in pulse pressure
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33
Q

Herniation to the mid-brain/upper pons

A

Deep Coma, Dolls eyes, pupils fixed, posturing, hyperventilation, wide pulse pressure

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34
Q

herniation to medulla

A
  • late phase of UNCAL herniation
  • irreversible (terminal)
  • Deep Coma
  • no pupillary response
  • cluster or apneic
  • pulse pressure starts to narrow again
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35
Q

EEG

A

Used to:

  • Electrical Activity
  • Identify seizure activity
  • Determine Brain Death
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36
Q

Encephalography

A

Used to

  • Identify shifts from midline
  • May show ventricular dilation
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37
Q

CT scan vs MRI

A

CT: Show Horizontal and Vertical Cross Sections

MRI: Show tissue discrimination

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38
Q

ICP monitoring indications

A
  • Severe Head Injury
  • GCS 3-8 (less than 9)
  • Abnormal Imaging
  • SBP less than 90 mm/hg
  • Subarachnoid hemorrhage
  • Hydrocephalus
  • Brain tumors
  • Stroke
  • meningitis
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39
Q

contraindications for ICP

A
  • Central nervous system infection
  • Coagulation defects
  • Anticoagulant therapy
  • Scalp infection
  • Severe midline shift resulting in ventricular displacement
  • Cerebral edema resulting in ventricular collapse
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40
Q

normal icp for adults

A

15

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41
Q

maintaning ICP

A
  • Q 1hour Neuro Checks
  • Monitor MAP, ICP, CPP (MAP-ICP)
  • Monitor ICP wave Forms
  • Strict Asepsis
  • Assess ICP site
  • Watch for CSF leaks (ear, see halo with the fluid)
  • Watch for Blood in the ICP monitoring system (should never see blood in there)
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42
Q

Never use a ? for ICP monitoring

A
  • never use a flush device. Use only sterile 0.9% NaCl to fill the pressure tubing.
  • Never use a heparinized solution.
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43
Q

Patients are maintained in a ? head up and neutral position when necessary to minimize the ICP.

A

30-45 degree

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44
Q

Avoid ? of the neck and positioning the patient in a Trendelenberg position, all of which may increase ICP.

A

flexion and hyperextension of the neck

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45
Q

simultaneous drainage and pressure monitoring is ?

A

Simultaneous drainage and pressure monitoring is not recommended. To ensure precise pressure measurements, perform only pressure monitoring while keeping the stopcock closed to the drainage system.

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46
Q

Intraventricular monitoring advantages and disadvantages

A

*gold standard*

Advantages

  • Allows for CSF drainage
  • Provides direct measurement of CSF pressure

Disadvantages

  • Most Invasive
  • High risk for infection/ hemorrhage/ infection
  • Contraindicated with coagulopathies
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47
Q

subarachnoid advantages/disadvantages

A

Advantages

  • Less invasive
  • Easy to place
  • Low risk of infection
  • Able to sample CSF
  • Can be used if ventricles are not able to be cannulated

Disadvantages

  • Unable to drain CSF
  • Decreased accuracy with time
  • Needs frequent recalibration
  • Easy to be obstructed with bone/tissue
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48
Q

Intraparenchymal advantages/disadvantages

A

advantages

  • Easy placement
  • Low risk of infection
  • Highly accurate

disadvantages

  • Unable to drain CSF
  • Needs a separate monitoring system
  • Catheters kink easy
  • Risk of hemorrhage/ infection
  • Can not be re-zeroed
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49
Q

Epidural Probe advantages/disadvantages

A

advantages

  • Easy placement
  • Low risk of infectin

disadvantages

  • Unable to drain CSF
  • Can not be re-zeroed
  • Accuracy questionable
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50
Q

ICP monitor level

A
  • head 30 degrees
  • ear in line with transducer
  • leveler is at 90 degrees (upright)
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51
Q

osmotic diuretic for ICP

A

Mannitol

  • Pulls fluid into the cerebral vascular space
  • Reduces cerebral blood viscosity
  • Increases cerebral blood flow
  • Increased cerebral oxygen delivery
  • Dosage: 1.0 gm/kg
  • Nurse considerations: Watch serum osmolality
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52
Q

Targeted Temperature Management in ICP

A
  • Reduces ICP
  • Decrease levels of excitatory neurotransmitters
  • Cerebral edema
  • Free radicals
  • Cerebral metabolic rate
  • 33 degrees celcius
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53
Q

Nursing management of targeted temperature management

A

Monitor for S/S of:

  • Shivering
  • Arrhythmias
  • Coagulopathies
  • Hypothermia-induced diuresis
  • Electrolyte imbalance
  • Hiccoughs
  • Rewarming slowly
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54
Q

Seizure Precautions

A
  • Seizures are very common with increased ICP

Phenytoin may be initiated with

  • GCS less than 10
  • Cortical Contusions
  • Depressed skull fractures
  • Subdural, epidural and intracerebral hematomas
  • Penetrating head injuries
  • A seizure within the first 24 hours post injury

Nursing considerations: Safety

  • Oral airway
  • Side rails padded
  • Suction and oxygen set-up
  • Patient/ family teaching
  • Administration and monitoring of pharmacological interventions
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55
Q

ALL Cranial Injury things to do?

A

ATLS (asvance trauma life support)evaluation & intervention
(ABCs / Foley / NG / oxygen / Maintain traction)

Constant Monitoring

*Diagnosis:

  • CT scan (FAST!)
  • MRI
  • PET Scan (brain function assessment)

*Medical interventions depend on severity:

  • Endotracheal intubation / hyperventilation
  • Sedation
  • Diuresis
  • Rapid surgical evacuation
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56
Q

Nursing Interventions for Acute Head Injury

A
  • Continuous monitoring of Vitals, PERRL and Glasgow Coma Score
  • Report client condition changes ASAP
  • Maintain airway patency- positioning, suctioning (if necessary)
  • Minimize cerebral edema
  • Maximize cerebral perfusion
  • Implement seizure precautions / Siderails
  • Provide emotional support
  • Address all self-care deficits
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57
Q

Collaborative care for seizures

A

Anticonvulsants

  • Phenytoin (Dilantin)
    • 10-20 mg/kg loading dose
    • Mix with NS not dextrose
    • 25-50 mg/min IVP
    • Monitor MP and Heart Rate x 30 min: May use Fosphenytoin children (SIVP or IM)*

-Benzodiazepine: Given emergent with Dilantin

Keatogenic Diet: High fat, low carb, low protein

Vagus Nerve Stimullator: implanatble device that stimulates the vagus nerve. Done after trying 3 or more meds

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58
Q

nursing care for seizure pts

A
  • Make certain that the patient has the following equipment: Nasal cannula and tubing, Oxygen flow meter; , Suction gauge, Suction canister, Suction tubing to connect to canister
  • Assign patient to room in close proximity to the nurses station
  • Maintain continuous observation via video monitor or sitter
  • Pad side rails of bed
  • Keep bed in low position with all side rails up at all times
  • Keep unnecessary equipment out of patients room
  • Instruct patient not to get out of bed without assistance
  • Assure that call bell is always within patients reach. Make sure that the family knows where it is and how to use it
  • Avoid use of restraints
  • Check vital signs every fifteen minutes and maintain airway patency during the post ichtal phase (period of time immediately following the seizure, during which the patient remains comatose or stuperous).
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59
Q

Types of Head Injury

A
  • Linear (very small line) or depressed skull fracture
  • Simple, compound, or comminuted
  • Closed or open
  • Direct and Indirect
  • Coup (head goes forward quickly and the injury goes to the back of the brain) and Countercoup (head goes back quickly and injures the front of the brain)
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60
Q

Basal Skull fractures

A
  • CSF leakage through nose or ear
  • high risk for infection
  • battle signs (bruising behind ear)
  • raccoon sign (bruising around the eyes)
  • possible injury to internal carotid artery
  • permanent CSF leakage
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61
Q

Minor injury vs. Severe

A

Minor

  • May loose conciousness
  • transient period of confusion
  • somnolence
  • listlessness
  • irritability
  • pallor vomiting

Severe

  • Increased ICP
  • Bulging fontanel (infants)
  • reinal hemorrhages
  • extraocular palsises (CN111)
  • hemiparesis
  • quadraplegia
  • increase temperature
  • change in gait
  • papilledema
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62
Q

Temporary loss of consciousness, GCS 13-15

A

Mild Head Injury

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63
Q

obtunded for several hours, GCS 10-12

A

moderate head injury

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64
Q

in a coma, GCS less than or equal to 8

A

severe head injury

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65
Q

Concussion grading scale: Grade 1

A
  • Transient confusion
  • no loss of consciousness
  • symptoms resolve in less than 15 minutes
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66
Q

Grade 2 concussion grading scale

A
  • transient confusion
  • no loss of consciousness
  • symptoms last more than 15 minutes
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67
Q

concussion grading scale: Grade 3

A

Any loss of consciousness, brief or prolonged

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68
Q

contusion vs. laceration

A

contusion: bruising of brain tissue withing a focal area that maintains the integrity of the pia mater and arachnoid layers

Laceration: involve actual tearing of the brain tissue. Intracerebral hemorrhage is generally associated with cerbral laceration

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69
Q

Epidural hematoma

A

results from bleeding between the dura and the inner surgace of the skull. It is a neurologic emergency and of venous or arterial origin

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70
Q

Subdural hematoma

A

Occurs from bleeding between the dura matter and arachnoid layer of the menigeal covering of th ebrain

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71
Q

diffuse axonal injury

A

widespread axonal injury occuring after a mild, moderate, or severe tbi

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72
Q

IVH causes

A
  • Infants born before 30 weeks of pregnancy are at highest risk for such bleeding (smaller and younger, higher the risk bc blood vessels are premature and fragile)
  • IVH is more common in premature babies who have had: respiratory distress syndrome, high BP, can occur in healthy premature babies born without injury
  • Rarely present at birth
  • Develops in first several days of life, and rare after one month of age
  • Falls into 4 grades, the higher the grade the more severe the bleeding
  • Presses on or leaks into the brainm, blood clots form around that, leads to increased fluid volume creating hydrocephalus
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73
Q

grades of IVH

A
  • Grade 1 &2 involve small amounts of bleeding and do not usually cause long term problems
  • Grade 3 & 4 involve more severe bleeding
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74
Q

IVH symptoms

A
  • There may be no symptoms
  • Breathing pauses
  • Changes in BP and heart rate
  • Decreased muscle tone
  • Decreased reflexes
  • Excessive sleep
  • Lethargy
  • Weak Suck
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75
Q

3 stages of clinical presentation of IVH

A

Catastrphic

Acute IVH with bulgin fontanel, spil sutures, change in level of consciousness, pupillary and cranial nerve abnormalities, decerebrate posturing, and often with rapid decrease in blood pressure andor hematocrit.

Saltatory

Gradual deterioration in neurological status, may be subtle abnormalities in level of consciousness, movement, tone, respiration and eye/position movement

Asymptomatic

25-50%, discovered on ultrasound. Fall in hematocrit or failure of hematocrit to rise wiht tranfusion should cause concern

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76
Q

Grade 1 IVH

A

bleeding condined to periventricular area (germinal matrix)

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77
Q

Grade 2 IVH

A

Intraventricular bleeding less than 50%

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78
Q

Grade 3 IVH

A

intraventricular bleeding greater than 50%

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79
Q

Grade 4 IVH

A

Intra-Parenchymal echodensity (IPE) reperesents periventricular hemorrhagic infarction

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80
Q

diagnostic testing for meningitis

A
  • bacterial culture and gram staining of csf and blood are key diagnostic tests
  • the presence of polysaccharide antigen in csf futher supports the diagnosis of bacterial meningitis
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81
Q

signs of meningitis in child vs. adult

A

adult: vomiting, headachem drowsiness, seizures, high temp, stiff neck, joint pain, dislike of light
child: high pitched cry, dislike of being held, fearful, arching back, blank staring expression, pale blotchy skin color, refusing feeds or vomiting, fever, may have cold hands and feet, difficult to wake up, very lethargic

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82
Q

nursing managmenet of meningitis, and S/s

A
  • frequent/continual assessment including vs and LOC
  • protect patient form injury related to seizure activity or altered LOC
  • monitor daily weight, serum electrolutes, urine volume, specific gracity, and osmolality
  • prevent complications associated with immobility
  • infection control precautions
  • supportive care
  • measures to facilitate coping of patient and family

s/s meningitis

  • Look for kurnig sign: hip and knee flexed 90 degrees, and when you try to extend it it’s painful
  • brudzinski sign: pt is laying extended, bring up their neck, and their knees will flex up
  • petichiae that if you blanch it they won’t go away
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83
Q

Uniform determination of death act

A
  • irreversible cessation of circulatory and respiratory function
  • irreversible cessation of all functions of the entire brain, including the brain stem, is dead.
  • A determination of death must be made in accordance with accepted medical standards.
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84
Q

conditions must be met to determine brain death

A
  • apneaic testing
  • testing with cranial nervees
  • diagnostics with brain imaging and brain blood flow: If the first 2 are inconclusive, then this one is done or under the age of 1
  • Brain death is a clinical diagnosis. It can be made without confirmatory testing if you are able to establish the etiology, eliminate reversible causes of coma, complete fully the neurologic examination and apnea testing.
  • The diagnosis requires demonstration of the absence of both cortical and brain stem activity, and demonstration of the irreversibility of this state.
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85
Q

What are the cranial nerve responses we see in brain death?

A
  • No pupillary response to light. Pupils midline and dilated 4-6mm.
  • No oculocephalic reflex (Doll’s eyes) – contraindicated in C- spine injury.
  • No oculovestibular reflex (tonic deviation of eyes toward cold stimulus) – contraindicated in ear trauma.
  • Absence of corneal reflexes
  • Absence of gag reflex and cough to tracheal suction.
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86
Q

Apnea Testing

A
  • Once coma and absence of brain stem reflexes have been confirmed –>Apnea testing.
  • Verifies loss of most rostral brain stem function
  • Confirmed by: PaCO2 > 60mmHg, or PaCO2 > 20mmHg over baseline value.
  • Testing can cause hypotension, severe cardiac arrhythmias and elevated ICP.
  • Therefore, apnea testing is performed last in the clinical assessment of brain death.
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87
Q

Following conditions must be met before apnea test can be performed:

A
  • Core temp > 35.0 C
  • Systolic blood pressure > 90mmHg.
  • Euvolemia
  • Corrected diabetes insipitus
  • Normal PaCO2 ( PaCO2 35 - 45 mmHg).
  • Preoxygenation (PaO2 > 200mmHg).
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88
Q

Criteria for Brain Death in Children

A
  • Neonate less than 7 days —> Brain death testing is not valid.
  • 7 days – 2 months: Two clinical exams and two EEG 48 hrs apart.
  • 2 months – 1 year: Two clinical exams and two EEG 24 hrs apart, or two clinical exams, EEG and blood flow study.
  • Age > 1 year to 18 years: Two clinical exams 12 hrs apart, confirmatory study (Optional)
    *
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89
Q

Loss of brain stem function results in systemic physiologic instability including?

A
  • Loss of vasomotor control leads to a hyperdynamic state.
  • Cardiac arrhythmias
  • Loss of respiratory function
  • Loss of temperature regulation –> Hypothermia
  • Hormonal imbalance –> DI, hypothyroidism
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90
Q

Intensive care management of cardiovascular sytem rule of 100’s

A
  • Maintain SBP and PaO2> 100mmHG
  • maintain HR and Urine output < 100 BPM
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91
Q

Brain death results in a massive release of?

A

Massive release of catecholamines, aka “autonomic storm”

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92
Q

Hypotension management in brain death

A
  • Fluid Bolus – NS or LR ((Followed by MIVF (maitenance IV fluids) NS or .45 NS))
  • Consider colloids
  • Dopamine: increase contractility of the heart and promote vasoconstriction
  • Neosynephrine: increase contractility of the heart and promote vasoconstriction
  • Vasopressin: helps with urine output
  • Thyroxine (T4 protocol)
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93
Q

Vassopressin and Vassopressin protocol

A
  • Low dose shown to reduce inotrope use
  • -Plays a critical role in restoring vasomotor tone
  • Vasopressin Protocol
  • 4 unit bolus IVP
  • 1- 4 u/hour – titrate to keep SBP >100 or MAP >60
94
Q

Diabetes Insipidus Management

A
  • Treatment is aimed at correcting hypovolemia
  • Desmopressin (DDAVP) 1 mcg IV, may repeat x 1 after 1 hour.
  • Replace hourly U.O. on a volume per volume basis with MIVF to avoid volume depletion
  • Leads to electrolyte depletion/instability monitor closely to avoid hypernatremia and hypokalemia
  • Goal is UOP 1-3 ml/kg/hr
  • Rule of thumb – 500 ml UOP per hour x 2 hours is DI
  • Severe cases – Notify OPC. Assess clinical situation.
95
Q

ELECTROLYTE IMBALANCE MANAGEMENT (3 things)

A

Hypokalemia
-If K+ < 3.4 – Add KCL to MIVF
(anticipate low K+ with DI & T4 administration)

Hypernatremia
-If NA+ >155 – Change MIVF to include more free H20, —-Free H20 boluses down NG tube (this is often the result of dehydration, NA+ administration, and free H20 loss 2o to diuretics or DI)

Calcium, Magnesium, and Phosphorus
-Deficiencies here common…often related to polyuria associated with osmotic diuresis, diuretics & DI.

96
Q

Hypothermia Management

A

Monitor temperature continuously

  • NO tympanic, axillary or oral temperatures. Central only.
  • Place patient on hypothermia blanket to maintain normal body temperature
  • In severe cases (<95 degrees F) consider:
    - warming lights
    - covering patient’s head with blankets
    - hot packs in the axilla
    - warmed IV fluids
    - warm inspired gas
97
Q

Overall Management Goals in Patients with Brain Death

A
  • SBP 90-110 mmHg
  • U/O 1-3 cc/kg
  • HR 60-140
  • PAWP (pulmonary artery wedge pressure) 7-12 mmHg
  • Serum electrolytes WNL
  • CBC and coags WNL
  • SPO2 >95%
  • PaO2 90-110
  • pH 7.35-7.5
  • PCO2 25-45
  • PF ratio >300
98
Q

upper motor neurons

A
  • originate in cerebral cortex
  • -project downward
  • -result in skeletal muscle movement
  • -injury: spastic paralysis
99
Q

lower motor neurons

A
  • originates at each vertebral level
  • -project to specific parts of the body
  • -results in movement/sensation
  • -injury=flaccid paralysis
100
Q

reflex arc

A

involuntary response to a stimulus without direct input from the brain

101
Q

primary & secondary spinal cord injury

A

-primary: right when the injury happens, immediate injury to spinal cord
-secondary: physiological response to the trauma: ischemia, hypoxia, hemorrhaging, edema

102
Q

neurogenic shock

A
  • due to loss of vasomotor tone
  • -SNS loss results in arasympathetic dominance with vasomotor failure
  • -loss of SNS innervation causes peripheral pooling and decreased cardiac output
  • -hypotention and bradycardia
  • -orthostatic hypotension and poor temperature control (poikilothermic)
103
Q

Clonus

A
  • one of the first signs that spinal shock is resolving
  • -hyperflexia of foot
  • -test by flexing leg at knee and quickly dorsiflex the foot
  • -rhythmic oscillations of foot agains hand
104
Q

complete (transection) degree of SCI injury

A
  • after spinal shock:
  • -motor deficits:spastic paralysis below level of injury
  • -sensory: loss of all sensation perception
  • -autonomic deficits: vasomotor failure and spastic bladder
105
Q

incomplete degree of SCI, central cord syndrome

A
  • injury to the center of the cordd by edema and hemorrhage
  • -motor weakness and sensory loss in all extremities
  • -upper extremities affected more
106
Q

incomplete classification of SCI, brown-sequard syndrome

A

hemisection of cord

  • ipsilateral paralysis
  • ipsilateral superficial sensation, vibration and proprioception loss
  • contralateral loss of pain and temp perception
107
Q

incomplete classification of SCI, anterior cord syndrome

A
  • injury to anterior cord
  • -loss of voluntary motor, pain, and temp perception below injury
  • -retains posterior column funtion (sensations of touch, position, vibration)
108
Q

incomplete SCI, posterior cord syndrome

A
  • least frequent syndrome
  • -injury to the posterior (dorsal) columns
  • -loss of proprioception
  • -pain, temp, sensation, and motor function below the level of the lesion remain intact
109
Q

incomplete SCIs

A
  • clonus medullaris: injury to the sacral cord (conus) and lumbar nerve roots
  • -cauda equina: injury to the lumbosacral nerve roots
  • -result: are flexic (flaccid) bladder and bowel, flaccid lower limbs
110
Q

upper motor deficits result in?

A

spastic paralysis

111
Q

lower motor deficits result in?

A

flaccid paralysis and muscle atrophy

112
Q
  • usually fatal
  • -ventilator dependent
  • -no bowel/bladder control
  • -electric wheelchair with chin/mouth
A

c1-c3 injury

113
Q

loss of phrenic innervation causes?

A

dependent on ventilator

114
Q

weak grasp

  • has shoulder/biceps to transfer/push wheelchair
  • considered level of independence
115
Q
  • full use of upper extremity
  • -transfer
  • -drive car with hand controls and do ADL’s
  • -no bowel/bladder contro
116
Q

immediate care of spinal injury at scene

A
  • transport with c-collar
  • -assess abc’s
  • iv for life line
  • ng to suction
  • foley
117
Q

solumedrol

A
  • pt started within 4, treated for 24 hours of solumedrol
  • -within 8 hours, treated for 48 hours
  • -to decrease edema around spinal cord
118
Q

medications for SCI

A
  • vasopressors to maintain perfusion
  • -histamine H2 blockers to prevent stress ulcers
  • -anticoagulants
  • -stool softeners
  • -antispasmodics
119
Q

physical exam of spinal injury pt.

A

LOC and pupils, may have indirect SCI from head injury

  • respiratory status-phrenic nerve (diaphragm) and intercostals, lung sounds
  • vital signs
  • motor
  • sensory
  • bowel and bladder function
120
Q

c6, t4, t10

A

c6: thumb
t4: nipple
t10: naval

121
Q

risk for autonomic dysreflexia description

A
  • SCI above T6
  • -Results in loss of normal compensatory mechanisms when sympathetic nervous system is stimulated
  • -Life threatening-if goes unchecked BP an result in cerebral hemorrhage
  • -Vasodilation symptoms above SCI
  • -Vasoconstriction symptoms below SCI
  • -the cause of SNS stimulation
122
Q

autonomic dysreflexia nursing interventions

A
  • elevate HOB-causes orthostatic hypotention
  • -indentify cause/alleviate if full bladder/cath, if skin/ remove pressure, if full bowel/ empty, etc
  • -remove support hose/abdominal binder
  • -monitor BP- can get >300 S
  • -Give PRN medication to lower BP
  • -If above not effective-call physician
123
Q

Common manifestations/complications of herniated disk

A
  • sensory root or nerve usually affected: pain, parenthesis, or loss of sensation
  • -motor root or nerve may be affected: paresis or paralysis
  • -Manifestations: depend on what nerve root, spinal nerve is being compressed-which dermatomes
  • -radiculopathy: pathology of the nerve root
124
Q

symptoms of lumbar HNP

A
  • postural changes
  • -urinary.male sexual function changes
  • -paresis or paralysis
  • -paresthesisa
  • -numbness
  • -muscle spasms
  • -absent cord relexes
125
Q

Cervical HNP manifestations/complications

A
  • -pain-neck, shoulder, anterior upper arm to thumb
  • -absent/diminished reflexes to the arm
  • -motor changes-paresis or paralysis
  • -sensory- paresthesias or pain
  • -muscle spasms
126
Q

treatment Herniated Disk: conservative

A
  • Bed rest with firm mattress: log roll, side lying position with knees bent and pillow between legs to support legs
  • -avoid flexion of the spine: brace/corset, cervical collar to provide support
  • -medication: non-narcotic analgesiscs, anti-inflammatory, muscle relaxants, antispasmodics, tranquilizers
  • -heat and cold, massage therapy
  • -weight loss
  • -TENS units
127
Q

Laminectomy

A

remove portion of the lamina to relieve pressure to get the herniated nucleus puplosus that is protruding

128
Q

foraminotomy

A

enlargement of the bony overgrowth at the opening which is compressing the nerve

129
Q

microdiskectomy

A

use of electron microscope through a small incision to remove a portion of the HNP that is displaced

130
Q

Post op assessment for HNP

A
  • sensory/motor assessment -care not to injure op site
  • -assess for csf drainage or bleeding from op site
  • -encourage turn (log roll, cough, deep breathe)
  • -assess for postural hypotension: especially if client was on bed rest for several days/weeks prior to surgery
  • Anterior cervical: assess injury to carotid, esophagus, trachea, laryngeal nerve, respiration, neck size, swallowing and speech
  • Lumbar: asses bowel sounds, voiding, minimize stress of post op site: glat with pillow between knees, log rolling, etc.
131
Q

Nursing Problem/intervention acute Pain

A
  • post surgery the individual may have similar pain as pre-op due to lack of resiliency of the spinal nerves to ‘bounce’ back quickly
  • -donor site (iliac crest) may cause more pain than laminectomy
  • -individual may be in pain-spasm-pain cycle, therefore may need both antispasmodic as well as analgesic
132
Q

intermedullary

A

arise from neural tissues of the spinal cord

133
Q

extramedullary

A

arise from tissues outside the spinal cord may be benign or malignant

134
Q

intradural

A

from the nerve roots or meninges in subarachnoid space

135
Q

extradural

A

from the epidural tissue or vertebra

136
Q

primary

A

originating in the spinal cord or meninges

137
Q

secondary

A

metasteses from other parts of the body

138
Q

most spinal cord tumors are found?

A

in the thoracic region

139
Q

manifestations of thoracic cord tumor

A
  • paresis and spasticity of one leg then the other
  • -pain back and chest, not relieved by bedrest
  • -sensory changes
  • -babinski reflex
  • -bowel, bladder dysfunction
140
Q

common manifestations/complications (cord tumors)

A
  • symptoms depend on the anatomical level of the spinal column, the anatomical location, the type of tumor and spinal nerves affected
  • *PAIN that is NOT relieved by bed rest is the most common presenting symptom
  • -sensory and motor
141
Q

Normal Hemodynamic Values Cardiac Output

142
Q

Cardiac Output

A
  • The cardiac output pushes the blood through the vascular system.
  • Cardiac output (CO) is calculated by multiplying the heart rate (HR) by the stroke volume (SV).
  • Stroke volume is the volume of blood pumped out of the heart with each heartbeat.
  • If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
  • This is known as compensatory tachycardia.
  • heart rates greater than 150 bpm actually drop stroke volume
143
Q

Preload

A
  • he amount of stretch on the cardiac myofibril at the end of diastole.
  • When the ventricle is at its fullest
144
Q

Preload is most directly related to:

A

Fluid volume

145
Q

Starling’s curve

A
  • describes the relationship of preload to cardiac output
  • As preload (fluid volume) increases, cardiac output will also increase until the cardiac output levels off.
  • If additional fluid is added after this point, cardiac output begins to fall.
146
Q

Preload Measurement

A

Not measured directly…instead measured by physical assessment of fluid volume

147
Q

Signs of inadequate preload include:

A
  • Poor skin turgor
  • Dry mucous membranes
  • Low urine output
  • Tachycardia
  • Thirst
  • Weak pulses
  • Flat neck
148
Q

Signs of excess preload in a patient with:

A
  • distended neck veins
  • crackles in the lungs
  • Bounding pulses
149
Q

Afterload is

A

the resistance that the ventricle must overcome to eject its volume of blood.

150
Q

The first step in treating any form of hemodynamic instability is

A

to assess the patient for signs of insufficient preload (e g volume or blood loss)

151
Q

The most important determinant of afterload is

A

vascular resistance

152
Q

Other factors affecting afterload include:

A
  • blood viscosity
  • aortic compliance
  • valvular disease.
153
Q

As arterial vessels constrict, what happens to afterload?

A

the afterload increases

154
Q

As arterial vessels dilate, what happens to afterload?

A

the afterload decreases

155
Q

In general, when you have someone with signs of low preload treat with

A

volume, until you know if its a stretch issue

156
Q

High Afterload

A

ncreases myocardial work and decreases stroke volume.

157
Q

Patients with high afterload present with signs and symptoms of arterial vasoconstriction including

A
  • cool clammy skin
  • capillary refill greater than 5 seconds
  • narrow pulse pressure.
158
Q

Low afterload

A

myocardial work and results in increased stroke volume.

159
Q

Patients with low afterload present with symptoms of arterial dilation

A
  • warm flushed skin
  • Bounding pulses
  • wide pulse pressure
160
Q

What is normal pulse pressure at the brachial artery

161
Q

If the afterload is too low, what may result?

A

hypotension

162
Q

Contractility refers to

A

the inherent ability of the cardiac muscle to contract regardless of preload or afterload status.

163
Q

Contractility is enhanced by

A

exercise, catecholamines, and positive inotropic drugs

164
Q

Contractility is decreased by

A

by hypothermia, hypoxemia, acidosis, and negative inotropic drugs.

165
Q

When performing interventions designed to improve hemodynamics

A

valuation of effectivess is whether or not the intervention was successful in improving tissue perfusion.

166
Q

Reasons for Hemodynamic Monitoring

A
  • Assessment of cardiovascular function (complicated MI, Cardiogenic shock, papillary muscle rupture)
  • Peri-operative monitoring of surgical patients with major systems dysfunction
  • Shock of all type (septic, hypovolemic, any shock that is prolonged or origin is unknown)
  • Assessment of pulmonary status
  • Assessment of fluid status (dehydration, hemorrhage, GI bleed, burns)
  • Therapeutic indications (cardiac pacing )
  • Diagnostic indications (pulmonary hypertension)
167
Q

Normal Hemodynamic Values SVO2

168
Q

Normal Hemodynamic Values Stroke Volume

169
Q

Normal Hemodynamic Values Stroke Index

A

25-45mL/M2

170
Q

Normal Hemodynamic Values MAP

A

60-100mm Hg

171
Q

Normal Hemodynamic Values CVP

172
Q

Normal Hemodynamic Values PAP systolic

A

20-30mm Hg

173
Q

Normal Hemodynamic Values PAP Diastolic

A

5-15 mm Hg

174
Q

Normal Hemodynamic Values PAOP (wedge)

A

8-12 mm Hg

175
Q

Normal Hemodynamic Values SVR

A

900-1300 dynes.sec.com

176
Q

Obtaining Blood Draws from the A-Line

A
  • Using proper technique when obtaining blood from an intra-arterial catheter:
  • Maintain aseptic technique for any line access and use standard precautions
  • Withdraw blood gently and slowly from the line
  • Waste the first 5mL
  • Flush the collection port to prevent clot formation and bacterial colonization
  • Maintain sterility of the system; place a new sterile cap over the sample port
  • Fast-flush the system to the patient for no more than 3 seconds at a time
  • Do not use a syringe to manually flush arterial catheters
  • Manual flushing with a syringe generates enough pressure that the injected fluid can invade the cerebral circulation
177
Q

Right Atrial Pressure Monitoring Indications

A
  • Measure right atrial pressure (RAP)
  • Same as Central Venous Pressure (CVP)
  • 1-7 mm Hg
  • Assess blood volume; reflects preload to the right side of the heart
  • Assess right ventricular function
  • Infusion site for large fluid volume
  • Infusion site for hypertonic solutions
178
Q

he Pulmonary Artery Catheter

A

Widespread use in critically ill patients
Remains controversial

179
Q

The Pulmonary Artery Catheter measures

A
  • CVP
  • PAP
  • PAOP
  • Cardiac Index
  • SVO2
180
Q

Components of a Pulmonary Artery Catheter (PAC or Swan Ganz) The pulmonary artery catheter normally has four ports which include:

A
  • The proximal port which is used for central venous pressure monitoring
  • The distal port which measures pulmonary artery and pulmonary artery wedge pressure
  • The balloon port with 1.5ml special syringe for measurement of pulmonary artery wedge pressure
  • The thermistor connector to assist with cardiac output measurement
181
Q

Increased Systolic Pulmonary Artery Pressure Caused by any of the following:

A
  • ny Factor that increases PVR
  • Pulmonary Embolism
  • Hypoxemia
  • COPD
  • ARDS
  • Sepsis
  • Shock
  • Primary Pulmonary Hypertension
  • Restrictive Cardiomyopathy
  • Significant left-to-right shunting
182
Q

Increased Diastolic Pulmonary Artery Pressure Caused by any of the following

A
  • Any Factor that increases pulmonary artery systolic pressure
  • Intravascular volume overload
  • Left Heart Dysfunction
  • Mitral Stenosis/Regurgitation
  • Aortic Stenosis/Regurgitation
  • Decreased LV Compliance
  • Cardiac Tamponade/Effusion
183
Q

Pulmonary Artery Systolic and Diastolic Pressure Decreased

A
  • Hypovolemia
  • Severe Tricuspid or Pulmonic Stenosis
184
Q

Changes in PAWP Increased

A
  • Left Heart Dysfunction
  • Mitral Stenosis/Regurgitation
  • Aortic Stenosis/Regurgitation
  • Decreased Left Ventricular Compliance
  • Intravascular Volume Overload
  • Tamponade/Effusion
  • Obstructive Left Atrial Myxoma
  • Restrictive Cardiomyopathy
185
Q

Changes in PAWP Decreases

A

Hypovolemia
Pulmonary Embolism

186
Q

Thermodilution Method of Cardiac Output Measurement

A

Measuring Cardiac Output
Inject fluid in to r atrium, fluid migrates through, change in temp over time and tells you how well the heart is contracting

187
Q

Nursing HOURLY assessment central lines

A
  • Air in line or stopcocks
  • Precipitates
  • Leaking at site
  • Increasing resistance
  • Condition of entrance sites
188
Q

Derived Pressures

A
  • Cardiac Index (CI)
  • Stroke Volume (SV) – CO/HR
  • Stroke Volume Index (SVI) – CI/HR
  • MAP- SBP + 2(DBP)/3
  • Systemic Vascular Resistance (SVR)- (MAP-RAP) x 80/CO
  • Systemic Vascular Resistance Index (SVRI) - (MAP-RAP) X80/CI
189
Q

vasopressors/inotropes

A
  • Dopamine
  • Dobutamine
  • Epinephrine
  • Phenylephrine
  • Norepinephrine
  • Vasopressin
190
Q

Dopamine

A
  • Dose dependent receptor activation
  • Low dose (1-5mics) - increases blood flow via dopamine receptors in renal, mesenteric, cerebral circulation
  • Intermediate dose (5-10mics) - increases cardiac output via - receptors
  • High dose(>10mics) - progressive vasoconstriction via -receptors in systemic and pulmonary circulation
  • In vivo, receptor effects are often mixed
  • Tachyarrhythmias are most common complication
  • Low dose dopamine has no proven renal benefit
  • Significant immunosuppressive effects through suppression of prolactin from hypothalamus
191
Q

Dobutamine

A
  • Synthetic catecholamine generally considered the drug of choice for severe systolic heart failure
  • Increases cardiac output via Beta 1 -receptor and causes vasodilation via Beta 2 -receptor
  • Inotropic and chronotropic effects are highly variable in critically ill patients
  • Data supports use in septic shock when cardiac output remains low despite volume resuscitation and vasopressor support
192
Q

Epinephrine

A
  • The most potent adrenergic agent available
  • Potency and high risk of adverse effects limit use to cardiac arrest (and specific situations after cardiac surgery)
  • Primarily Beta receptor effects at low doses and alpha receptor effects at high doses
  • Arrhythmogenic
193
Q

Phenylephrine

A
  • Relatively pure beta adrenergic agonist
  • Minimal inotropic effects; often causes reflex bradycardia
  • Consistently decreases cardiac output
  • Increased propensity to cause ischemic complications
  • Be wary in the OR
194
Q

Norepinephrine

A
  • More potent vasoconstrictor than dopamine; some inotropic effect
  • Potent alpha 1 stimulation
  • Moderate beta 1 activity
  • Minimal beta 2 activity
195
Q

vasopressin

A
  • Acts on vascular smooth muscle via V1 receptors, independent of adrenergic receptors
  • Considered replacement therapy
  • Traditionally not titrated
  • Significant splanchnic vasoconstriction
196
Q

Principles of the IABP

A
  • A flexibile catheter is inserted into the femoral artery and passed into the descending aorta.
  • Correct positioning is critical in order to avoid blocking off the subclavian, carotid, or renal arteries.
  • When inflated, the balloon blocks 85-90% of the aorta. Complete occlusion would damage the walls of the aorta, red blood cells, and platelets.
197
Q

Nursing Responsibilities Pre-Insertion PAC

A
  • Explain procedure to patient
  • Assemble all equipment
  • Set up all monitoring lines aseptically
  • Prime all IV tubing and transducer flush lines (Pressure Bag @ 300 mmHg)
  • Connect PAC cable to monitor and attach to transducer
  • Connect CVP cable to monitor and attach to transducer
  • Check PAC packaging for to ensure sterility/expiration date
  • Zero transducers (mid axillary)
  • Place monitor in wedge/insertion mode (scale should be 30-60)
  • Turn on and set continuous cardiac monitor/Svo2 monitor for insertion (make sure previous patient data is erased)
198
Q

Nursing Responsibilities During Insertion PAC

A
  • Position patient for insertion (flat for femoral, Trendelenburg for subclavian or jugular)
  • Assist with creating a sterile field
  • With the assistance of the physician, open PAC and connect transducers to the distal and proximal lumens
  • Connect the IV line to the medication port
  • Connect the cardiac output cable and Svo2 cables
  • Remove the 1.5 ml syringe and connect it to the syringe port
  • Zero catheter while still in package
  • Inflate air into the balloon to assure balloon integrity prior to insertion
  • After physician places sterile sheath over catheter, waveform presents should be assessed on the monitor (usually a small shake of the catheter itself will confirm)
  • Once physician inserts and advances the catheter to right atrium, he will request that the RN inflate the balloon
  • If for any reason during floatation of a PAC the physician wishes to withdraw the catheter, the balloon must be deflated
  • During floatation of a PAC the right atrial (CVP), right ventricle, pulmonary artery and pulmonary artery wedge pressure (PAWP) waveforms/pressure tracings should be noted and printed
199
Q

Nursing Responsibilities Post-Insertion PAC

A
  • Make sure that PAC cap is in the lock position so catheter will not migrate
  • Secure catheter to patient with tape
  • Apply occlusive dressing
  • Set high and low alarms on monitor as appropriate for patient
  • Double check to assure that physician has disposed of all sharps
  • Double check to see that Chest X-ray was ordered
200
Q

Nursing Responsibilities For Removal of PAC

A
  • Make sure the balloon is COMPLETELY deflated. Pull back extra, then lock.
  • When removing, if piece of catheter is left in patient, IMMEDIATELY put patient in trendelenburg and place pt on left side
201
Q

Na+, K+, Cl-, Ca2+, Phosphorus, Magnesium Norms?

A

Electrolyte
Normal Range

Sodium (Na+) 135-145 mEq/L
Potassium (K+) 3.5-5 mEq/L
Chloride (Cl-) 100-110 mEq/L
Calcium (Ca2+) 8.5-10.0 (total) mg/dL
Phosphorus (Po4-) 2.5-4.5 mg/dL
Magnesium (Mg2+) 1.8-2.5 mEq/L

202
Q

Antidiuretic Hormone

A
  • Increases the permeability of collecting tubule cells to water.
  • Increases water, but not electrolyte reabsorption
203
Q

Renin

A
  • Converts angiotensin into angiotensin I which is then converted to angiotensin II
  • Angiotensin II causes vasoconstriction and the release of aldosterone (important for na+ reabsorption in the distal tubules)
204
Q

Aldosterone

A
  • Promotes sodium reabsorption in the distal tubules
  • Leads to increase water absorption
205
Q

Blood Studies for renal failure

A
  • Creatinine/ Creatinine Clearance
  • Estimated Creatinine Clearance formula
  • (140-age) X weight in kg/ (Plasma Creatinine mg/dL) X 72
  • Blood Urea Nitrogen: increases in renal failure, GI bleed, dehydration, trauma.
  • 8-20 mg/dL (normal)
  • BUN/Creatinine ratio:
  • Based on serum creatinine
  • BUN:Creatinine – 10:1 (normal)
  • -when ratio goes down: liver failure, fluid volume overload,
  • -ratio up: dehydration, catabolic states or high protein diets
  • Osmolality: Up= kidneys not filtering properly
  • Normally 280-290
  • Uric Acid: elevated=kidneys not filtering uric acid properly
  • 2-8.5 mg/dL
  • Hemoglobin & Hematocrit: decrease shows renal problems
  • Men 13.5-17.5 g/dL & 40-52%
  • Women 12-16 g/dL & 37-48%
206
Q

Contributing Factors in the Development of AKI/ARF Pre-renal

A
  • Hypotention
  • Hypovolemia
  • Decrease CO
  • Dehydration
  • Vascular Disease
  • Renal Vein Thrombosis
  • DM
207
Q

Contributing Factors in the Development of AKI/ARF Intrarenal

A
  • Nephrotoxic episodes
  • Infection
  • Systemic inflammation
  • Injured red blood cells
  • Hemolytic blood transfusion reactions
  • Glomerular diseases (systemic lupus, glomerulonephritits)
  • Rhabdomylolysis
208
Q

Contributing Factors in the Development of AKI/ARF postrenal

A
  • Medication that interferes with normal bladder emptying.
  • Benign prostatic hypertrophy (BPH)
  • Prostate cancer
  • Ovarian cancer
  • Obstruction of a urinary catheter
  • Renal calculi
  • Bladder/pelvic neoplasms
  • Urethral strictures
209
Q

Types of kidney failure

A
  • Pre-Renal: occurs before you get to the kidneys. Hypovolemia, blockages. Can lead to Intra-Renal.
  • Intra-Renal: Occurs inside the kidney. Metabolites collecting and causing damage, trauma, toxicity, etc.
  • Post-Renal: Involves ureters, prostate, and bladder.
210
Q

Pharmacological Causes and Agravators of AKI/ ARF

A

Causes:

  • Contrast media
  • Diuretics (Furosemide)
  • Heavy metals (mercury, gold lead)
  • Ibuprofen
  • Organic chemicals or solvents
  • Nephrotoxic antibiotics (Gentamycin/Piperacillin)
  • ACE Inhibitors

Aggravators:

  • Amiloride
  • Any medication containing magnesium tetracycline
  • Cisplatin
  • Aspirin
  • Lithium
  • Nonsteriodal anti-inflammatory agents
  • Spironolactone
211
Q

Clinical Manifestations of AKI/ ARF

A
  • Decreased urine output (urine may be pink or reddish in color)
  • Edema (face, arms, legs, feet eyes)
  • Flank pain/Pelvic pain
  • Poor appetite (nausea, vomiting)
  • Bitter or metallic taste in mouth
  • Dry itchy skin
  • Easy bruising
  • Fatigue
  • Seizures/LOC
  • Shortness of breath
  • Arrhythmias
  • Sudden weight gain
212
Q

The Four Phases of AKI/ARF

A

Onset Phase: from hours to a day

  • -Renal flow at 25% of normal
  • -Oxygenation to the tissue at 25% of normal
  • -Urine output at 30 ml (or less) per hour
  • -Urine sodium excretion greater than 40 mEq/L.

Oliguric Phase: lasts 8-14 days. Tubular wall damage

  • -Significant decrease in GFR
  • -Increase BUN/Creatinine
  • -Electrolyte Imbalance
  • -Metabolic Acidosis

Diuretic Phase: Occurs if problem corrected. Lasts 7-14 days.

  • -Increase in GFR
  • -Urine output as high as 2-4 L/day
  • -Renal cells that cannot concentrate urine

Recovery Phase: lasts months to a year. Cells start having some recovery and generation

  • -GFR returns to70-80% Baseline
  • -Renal Tubules begin to function
  • -Fluid/ electrolyte balance returns
213
Q

Medical Management of AKI/ARF

A
  • Address underlying cause
  • Maintain intravascular volume: monitoring how much output and dialyzing them or giving diuretics to get the volume out
  • Maintain MAP: want it above 70. For elderly person, 90-100.
  • Discontinue nephrotoxic agents
  • Correct Acidosis
  • Correct hemolytic issues
  • Correct electrolyte imbalances
  • Strict I & O’s and daily weights
  • Fluid and diet restrictions
214
Q

a loop diuretic that can be used to increase urinary flow with the intent of flushing out cellular debris that may be causing an obstruction.

A

Furosemide (Lasix)

215
Q

an osmotic diuretic that can be used to dilate renal arteries by increasing the synthesis of prostaglandins (resulting in restored renal flow).

216
Q

at low doses (1-5 mcg/kg/min), dilates renal arterioles and increases renal blood flow and glomerular filtration. Because (even at low doses) can cause tachycardia, myocardial ischemia and arrhythmias it use should be considered carefully.

217
Q

this medication can help reverse acute renal failure when the cause is thought to be from a nephrotoxic source.

A

N-acetylcysteine (Mucomyst)

218
Q

Extracorporeal Therapies in AKI/ARF

A

Hemodialysis

  • Peritoneal dialysis: Not used in ARF
  • Hemodialysis. Good for quick removal of water and toxins

CRRT

  • Less likely to cause hypotension: Hemodynamic stability
  • Correction of metabolic acidosis. Quicker kidney recovery time. Correction of malnutrition. Solute removal
219
Q

Nursing Care of the AV Fistula

A
  • Cleanse with Soap and water daily
  • Limit contact with site
  • Assess for signs of infection
  • No BP or needle sticks to arm
  • Assess site for Thrill/bruit
  • Patient teaching to avoid pressure to site

*wait 1-3 months to use

220
Q

Risk for increased clotting during dialysis. What is the reversal agent?

221
Q

Types of Continuous Renal Replacement

A
  • Slow Continuous Ultrafiltration (SCUF): 100-300 ml taken off every hour. Good for removing fluid, but not good for uremia.
  • Continuous Venovenous Hemofiltration (CVVH): 7-30 liters removed every 24 hours. Can be used for convection.
  • Continuous Venovenous Hemodialysis (CVVHD): Used a lot. Good at getting fluid off, but not the moderate sized molecules
  • Continuous Venovenous Hemodiafiltration (CVVHDF): Good for small and moderate sized molecules. Run continuously, low rate, over 24 hours. Best type for acute renal failure pt.
222
Q

t waves peaked

223
Q

prolonged PR interval

224
Q

wide qrs no p wave

225
Q

management of hyperkalemia

226
Q

Severe Metabolic Acidosis common in AKI ph?

A

Severe Metabolic Acidosis common in AKI ph?

227
Q

treatment of acidosis common in AKI

A
  • Treatment
  • Alkaline Medications
  • Sodium bicarbonate tablets)
  • Sodium bicarbonate???
  • Used in severe acidosis. Many complications. Now try to not give this bc increases sodium levels and osmolarity.
  • Hemodialysis
228
Q

Nursing Diagnosis for ARF

A
  • Alteration in urinary elimination
  • Fluid volume deficit
  • Fluid volume overload
  • Altered nutrition (less than bodily requirement)
  • Potential for impaired skin integrity
  • Decreased cardiac output
  • Activity intolerance
229
Q

management of fluids in arf

A
  • Maintenance fluids
  • Crytalloids
  • D5W
  • Normal Saline
  • .45Normal Saline
  • LR
  • Colloids
  • Albumin
  • Hetastarch
  • Dextran
  • Fluid Volume Excess
  • Loop Diuretics (Lasix & Bumex)
  • Osmotic Diuretics (Mannitol)
230
Q

How to prevent ARF?

A
  • Recognize that patients with pre‐existing renal impairment are at higher risk of developing further renal insufficiency—treat and monitor accordingly
  • Temporarily withhold nephrotoxic (especially ACE‐I, ARBs, NSAIDs) and diuretics (to prevent dehydration) when patients become unwell—either in the community or in hospital
  • Ensure that patients remain adequately hydrated, to maintain renal perfusion
  • Remember to monitor renal function after starting, or increasing the dose, of ACE‐I or ARBs (check one to two weeks later)
  • Where necessary, adjust drug doses in patients with renal impairment
  • Monitor drug levels when using aminoglycoside (gentamicin) and/or glycopeptide (vancomycin) antibiotics—and adjust dose accordingly
  • Hydrate the patient and consider using N‐acetyl cysteine before procedures entailing radiological contrast media

NUR4630 (34 decks)

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