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CH2 > Final Exam Module 1 & 2 > Flashcards

Final Exam Module 1 & 2 Flashcards

1
Q

Status epilepticus is a medical emergency. It is continuous or rapidly occurring seizures. What does it cause?

A

brain damage, arrhythmias, hypoxemia, & acidosis

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2
Q

What is considered to be “impending status epilepticus?”

A

Seizure activity lasting longer than 5 minutes

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3
Q

What do we do for status epilepticus?

A

Initially, intravenous lorazepam/diazepam is administered to stop motor movements. This is followed by the administration of phenytoin.

May require endotracheal intubation for airway protection

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4
Q

Steps to Seizures

What do we do first?

Seizure Management Pearls

A

Protect the patient from injury.
Do not force anything into the patient’s mouth.
Turn the patient to the side to prevent aspiration and keep the airway clear.
Remove any objects that might injure the patient.
Suction oral secretions if possible without force.
Loosen any restrictive clothing the patient is wearing.
Do not restrain or try to stop the patient’s movement; guide movements if necessary.

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5
Q

Steps to Seizures

What medications?

A

IV push lorazepam or diazepam.

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6
Q

What do all anticonvulsants cause?

A

All anticonvulsants can cause drowsiness, ataxia (lack of coordination) and CNS depression (resp. depression)

Levetiracetam (Keppra): best choice for outpatient,
most popular, monitor CBC.

Phenytoin: causes gingival hyperplasia, bone marrow
suppression, rash, IV vesicant, monitor blood levels
and CBC (q3 months).

Carbamazepine: causes bone marrow suppression,
monitor blood levels and CBC.

Divalproex (Depakote): causes hepatotoxicity, bone
marrow suppression, monitor CBC, blood levels and
LFTs.

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7
Q

Steps to Seizures

What do we do once the seizure has stopped?

A

Reorient the pt.
Record the time the seizure began and ended.
Check blood glucose levels. Seizures can occur due to hypoglycemia.
Make sure airway is clear.
Ask if they have felt an aura before the seizure or have triggers.

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8
Q

How do we differentiate between bacterial
and viral meningitis? Which one is worse?

Meningitis is an acute infection and inflammation of meninges.

A

Differentiate by CSF analysis w/ lumbar puncture

Bacterial meningitis is an acute, life threatening emergency.

Good prognosis for viral meningitis.

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9
Q

What type of precautions is used for meningitis?

A

droplet

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10
Q

Clinical Presentation of Meningitis

A

-Headache like they have never felt before
-Nuchal rigidity, back of the neck is stiff
-Nausea/vomiting
-Photophobia: eye discomfort due to exposure to light
-Brudzinski Sign: flexion of the neck elicits flexion of hips and knees
-Kernig Sign: bilateral hamstring pain prevents straightening of the leg

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11
Q

What is the most important thing to monitor for meningitis?

A

level of consciousness

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12
Q

What do we do stat with bacterial meningitis?

A

Requires STAT LP followed by immediate IV antibiotics.

Do not give antibiotics before the LP, can skew the results.

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13
Q

What do we do for viral meningitis?

A

supportive care- antipyretics, hydration, and rest

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14
Q

What is the priority assessment post craniotomy?

A

-Monitor for and prevent increased ICP is the PRIORITY

Followed by:
-Observe dressing
-Prevent infection (handwashing)
-Monitor neurological status
-Monitor fluid and electrolytes
-Monitor for diabetes insipidus: during surgery the pituitary gland be affected
-Prevent complications of immobility: DVT prophylaxis, skin breakdown

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15
Q

What is the drug of choice for cerebral edema?

A

Dexamethasone (Decadron)

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16
Q

What is the difference between a primary spinal cord injury and a secondary injury?

A

Primary Injury: Initial disruption of cord.

Secondary injury: on-going damage from ischemia, inflammation, toxic metabolites, and edema.

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17
Q

What types of shock should you look out for w/ spinal cord injuries?

A

Neurogenic- damage to the nerves themselves

Hypovolemic- fluid loss

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18
Q

What is our priority with cervical spinal injuries?

A

Above C4 requires mechanical ventilation

C3, 4, & 5 keep the diaphragm alive.

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19
Q

All cervical injuries cause respiratory insufficiency meaning the pt will have

A

-Decreased cough
-Decreased vital capacity
-High risk of atelectasis and pneumonia

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20
Q

What do we see in spinal shock?

Due to acute spinal injury

A

Loss of motor, sensory and reflex activity at the level of injury and below:

-Flaccid paralysis
-Flaccid bladder
-Paralytic ileus- gut is going to slow down or stop
-Loss of sensation
-Decreased or absent reflexes

Can last days to months. Spasticity may emerge after spinal shock resolves.

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21
Q

Who has the highest risk of developing neurogenic shock?

A

High risk w/ injury above T6

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22
Q

What sets neurogenic shock apart from spinal shock?

A

hemodynamic phenomenon

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23
Q

What are the three critical features of neurogenic shock?

A

Hypotension
Bradycardia
Poikilothermia

All other shocks have hypotension and TACHYcardia

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24
Q

What is the cause of autonomic hyperreflexia?

A

distended bladder and fecal impaction

We need to dis-impact them or drain their bladder or their BP will continue to go through the roof.

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25
Q

What are the priority symptoms of autonomic hyperreflexia?

A

Severe, life-threatening hypertensive crisis.

Other sx include: HA, blurred vision, diaphoresis, & flushing

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26
Q

What is the nursing care for autonomic hyperreflexia?

A

-Elevate HOB to help reduce BP (PRIORITY)
-Monitor BP
-Remove noxious stimuli
-If BP remains elevated administer BP medication
-Close neuro assessment

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27
Q

Immediate Post- Spinal Cord Injury

A

-Immobilize injury w/ backboard & neck brace
-Prioritize ABCs
-Comprehensive neuro assessment (touch, pain, muscle strength)
-Methylprednisolone (Solu-Medrol) can help w/ inflammation
-Maintain MAP between 80-90 (may require dopamine)
-NG tube for ileus
-Stress ulcer prophylaxis with a PPI
-DVT prophylaxis (SCDs & Lovenox)

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28
Q

What is the formula to calculate MAP?

A

(SBP + 2DBP) / 3

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29
Q

What is a Transient Ischemic Attack (TIA)?

A

“Mini-stroke”

Reversible cerebral ischemia. Usually precedes thrombotic stroke: “Warning sign”. Commonly caused by carotid stenosis.

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30
Q

What is the ABCD assessment tool for stroke risk?

A

Age of at least 60 years
BP of at least 140/90 (either SBP, DBP, or combination)
Clinical TIA features
Duration of symptoms

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31
Q

What is the medication management for TIA?

A

Antiplatelets drugs such as aspirin or Plavix

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32
Q

What are other management techniques for TIA?

A

ABCS of stroke management

-Blood pressure management
-Controlling diabetes, if necessary
-Lifestyle changes: smoking cessation, encouraging physical activity, dietary management

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33
Q

What are the two types stroke?

A

Ischemic (occlusive) and Hemorrhagic (bleeding)

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34
Q

What are the two types of ischemic strokes? What is the main cause of each type?

A

-Thrombotic –> Atherosclerosis
-Embolic –> A-Fib

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35
Q

What are the 4 types of hemorrhagic strokes? What is the main cause if each type?

A

-Intracerebral hemorrhage –> severe or sustained HTN

-Subarachnoid hemorrhage –> ruptured aneurysm or AVM rupture

-Aneurysm

-Arteriovenous malformation (AVM) –> congenital abnormality

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36
Q

What is FAST?

A

Facial dropping, arm pain, slurred speech, & time=brain

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37
Q

Interventions for cerebral aneurysms

A

clipping and coiling

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38
Q

Thunder clap headache

A

Subarachnoid hemorrhage

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39
Q

What are the hallmark signs/sx of a stroke?

A

-Sudden weakness
-Difficulty talking
-Difficulty understanding
-Severe headache with no known cause

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40
Q

What is the first priority for stroke patient?

A

Ensure pt is transported to a stroke center.

Complete focused/rapid assessment. Remember that there is always a risk that LOC will change.

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41
Q

Broca’s aphasia vs Wernicke’s aphasia

A

difficulty talking vs difficulty understanding

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42
Q

Emergent Care Stroke

A

-Assess ABCs
-Provide oxygen (this is an ischemic issue)
-2 Large bore IVs
-Take blood samples and blood glucose
-Perform NIH Stroke Scale
-Order a non-contrast CT- must be read within 45 minutes
-Obtain 12-lead to look for A-fib
-Do not delay CT to get ECG

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43
Q

Within 45 minutes of the patient’s arrival, the specialist must decide, based on the CT scan, if a hemorrhage is present.

Take these actions if a hemorrhage is present:

A

-Note that the patient is not a candidate for fibrinolytics.
-Arrange for a consultation with a neurologist/neurosurgeon.
-Consider transfer, if available.

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44
Q

If it is hemorrhagic you need to get a

A

neurosurgeon consult ASAP

45
Q

Within 45 minutes of the patient’s arrival, the specialist must decide, based on the CT scan, if a hemorrhage is present.

Take these actions if a hemorrhage is NOT present:

A

-Decide if the patient is a candidate for fibrinolytic therapy.
-Review criteria for IV fibrinolytic therapy
-Repeat the neurological exam (NIHSS)

46
Q

If ischemic- assess criteria for tPA

What is the criteria?

A

Period of time between symptom onset and arrival time to the stroke center.

FDA approves use of tPA within 3 hours of stroke symptom onset.

The American Stroke Association endorses 4.5 hours, if no exclusion criteria are present.

47
Q

Exclusion criteria for tPA

A

Age older than 80 years
Anticoagulation therapy
Baseline NIHSS score greater than 25
History of both stroke and diabetes
Evidence of active bleeding
BP greater than 185 systolic or 110 diastolic
History of cerebral bleed
Elevated PT/INR

48
Q

If they are not a candidate for tPA, what is next?

Endovascular interventions

A

Mechanical embolectomy- MERCI Retrieval System

Intra-arterial thrombolysis: tPA is delivered directly to the thrombus within 6 hrs of symptom onset

Carotid artery angioplasty with stenting

Carotid Endarterectomy (CEA)

49
Q

Mechanical embolectomy- MERCI Retrieval System is for patients that do not qualify for tPA or fail tPA therapy. Has to be completed

A

within 8 hours of stroke onset

50
Q

If we do a carotid endarterectomy, what do we watch for?

A

swelling in the airway

51
Q

Nursing Care for Stroke

A

-FALL PRECAUTIONS
-Transfer to the strong side
-Place objects in their visual field and approach them from the unaffected side
-NPO until swallow study
-Sit up 90 degrees
-Assess gag reflex

52
Q

Concussion

What is second impact syndrome?

A

A second concussion that occurs before the brain can completely recover from the first.

Can result in massive cerebral edema.

53
Q

What are the clinical manifestations of an epidural hematoma?

Arterial bleeding into the space between the skull and the dura. Faster bleed.

A

-Immediate post-traumatic unconsciousness, followed by “lucid interval”
-Rapid deterioration in LOC may follow, up to and including death
-Ipsilateral pupil enlargement
-Increasing headache
-Seizures
-Motor weakness

54
Q

What do we do for an epidural hematoma?

A

Requires emergent surgical evacuation

55
Q

Is a subdural hematoma emergent or nonemergent?

A

nonemergent, but can be fatal.

Sx are less severe and is a slower bleed.

56
Q

What are the three components of ICP?

Normal ICP is 10-15 mm Hg

A

-Brain tissue
-Blood
-Cerebrospinal fluid (CSF)

57
Q

How do we calculate Cerebral Perfusion Pressure (CPP) and what does it mean?

A

MAP-ICP= CPP

Pressure needed to ensure adequate perfusion of brain

58
Q

CPP ranges

A

CPP 70-100 normal

CPP 50-60 minimum required for adequate cerebral perfusion

CPP < 50 brain ischemia, neuronal death

CPP <30 incompatible with life

59
Q

What are the clinical manifestations of increased ICP?

A

-Change in level of consciousness (LOC)
-Headache and projectile vomiting.
-Compression of CN III Oculomotor (“blown pupil”)
-Cushing’s Triad (systolic hypertension, widened pulse pressure, bradycardia)
-Decorticate & Decerebrate posturing
-Brain stem herniation
-Death

60
Q

ICP Management

Priority is to manage ICP

A

*Mechanical ventilation to maintain PO2 > 100
*Maintain SBP between 100-160
*Maintain CPP > 70 (70-100 is normal)
*Osmotic Diuretic (Mannitol)- treats cerebral edema, takes swelling out of the brain by pulling water out of the
extracellular space decreasing brain edema
*Loop Diuretics
*Anticonvulsants- increased ICP= increased risk for seizures
*Fentanyl may be used to help manage agitation when patients are ventilated
*HOB elevated to 30 degrees and head midline
*Limit suctioning and stimulation

61
Q

Eye Trauma Priorities

A

-Assess peripheral vision
-Antibiotics can be given to prevent infection
-NEVER TAKE OUT THE FOREIGN BODY
-MRI is contraindicated because it can pull out the object and the eye

62
Q

Eye Trauma – Foreign Bodies

Particles may come in contact with the conjunctiva or cornea
Patient complaints:
Blurry vision; feeling like something is in the eye
Sensory perception is assesses prior to treatment
Irrigate with 0.9% NS
Eye dressing or patch may be applied after foreign body is removed

What is the RN’s priority?

A

Priority is to assess peripheral vision!

To prevent infection, antibiotics are provided. Visual acuity in the affected eye cannot be assessed. The patient may or may not need enucleation. The object is only removed by the ophthalmologist.

63
Q

Name COPD complications

A

Hypoxemia
Acidosis
Respiratory infections
Right sided HF
Cardiac dysrhythmias
Respiratory failure

64
Q

What would a chest x-ray look like for a COPD pt?

A

Often hyperinflation > flattened diaphragm + widely spaced ribs

65
Q

Oxygen therapy for COPD

  • SPO2 levels *
A

All hypoxic patients, including patients with COPD and hypercarbia, should receive oxygen therapy at rates appropriate to reduce hypoxia and bring SPO2 levels between 88-92%.

Anything above that can decrease respiratory drive.

66
Q

What type of medications do we use for COPD pts?

A

Beta-adrenergic agents
Cholinergic antagonists
Methylxanthines
Corticosteroids
NSAIDs
Mucolytics

67
Q

What type of breathing technique can we teach COPD pts?

A

pursed lip breathing

68
Q

What is the diet for a COPD patient?

A

high protein & high calorie

69
Q

Seasonal influenza is a highly contagious acute viral respiratory infection. Sx include:

A

Rapid onset of severe headache, muscle ache, fever, chills, fatigue, weakness, anorexia.

70
Q

What is the time limit for antiviral agents when treating seasonal influenza?

  • Drugs end in -ivir *
A

24-48 hours

Not effective after 48 hours

71
Q

When is seasonal influenza contagious?

A

Contagious between 24 hours before symptoms occur – 5 days after symptoms begin.

Isolation is key to prevent spread

72
Q

What are the complications associated with seasonal influenza?

A

pneumonia & death

73
Q

Supportive care for seasonal influenza

A

-Rest
-Increase fluid intake (take precautions with fluid restrictions)
-Saline gargles to reduce throat pain
-Antihistamines for rhinorrhea

74
Q

Rapid influenza diagnostic test has high false-negative rates. Do you retest?

A

No, provide supportive care based on sx.

75
Q

Prevalent among animals and birds. Virus can mutate and become infectious to humans.

Examples: H1N1 (swine flu), H5N1 (bird flu), MERS, SARS, COVID-19

Strict isolation precautions- contact and airborne until specific type of pandemic influenza is identified w/ routes of transmission known

A

Pandemic influenza

76
Q

Pandemic influenza tx includes:

A

Treatment is often supportive:
-recover at home and avoid exposures
-encourage rest and fluids
-acetaminophen for myalgias

Antiviral drugs can be started within the first 48 hrs of symptom onset
*Oseltamivir (Tamiflu), zanamivir (Relenza)

77
Q

Pneumonia is caused by excess fluid in lungs resulting from inflammatory process.

What are some symptoms?

A

purulent sputum, fever, pleuritic chest pain

other sx: increased RR/dyspnea, hypoxemia, cough

78
Q

What should we see on a chest x-ray for pneumonia pt?

A

consolidation in lobes

79
Q

What should we always monitor for pneumonia pts?

A

always monitor pulse ox and vital signs

80
Q

Nursing care for pneumonia

A

Improve gas exchange
-Oxygen therapy, incentive spirometry

Prevent airway obstruction
-Cough and deep breathing exercises Q2 hours
-Fluid promotion to thin secretions
-Bronchodilators for bronchospasms
-Inhaled or IV steroids for inflammations
-Expectorants (guaifenesin)

Prevent sepsis
-Anti-infectives for bacterial sources
-Prevent aspiration

Prevent/manage empyema
-Antibiotic management
-Chest tube may be needed to promote lung expansion and drainage

81
Q

What are two ways we can prevent pneumonia?

A

smoking cessation and immunization

82
Q

What is the most common substance to cause Pulmonary Embolus (PE)?

Collection of particulate matter—solids, liquids, air—that enters venous circulation and lodges in pulmonary vessels usually occurs when a blood clot from a venous thromboembolism in leg or pelvic vein breaks off and travels through the vena cava into the right side of the heart.

A

blood clots

83
Q

Sx of PE

A

sense of impending doom, dyspnea, coughing up blood (hemoptysis), syncope, distended neck veins

84
Q

Risk factors for PE

A

prolonged immobilization, central venous catheters, surgery, pregnancy, obesity, advancing age, conditions that increase blood clotting, hx of thromboembolism, other causes- Air, amniotic fluid and fetal debris, foreign objects, injected particles, fat, and infected clots.

85
Q

Health Promotion & Maintenance Lifestyle changes for PE

A

No smoking, weight reduction, increased physical activity, DO NOT massage leg muscles

  • If traveling, drink plenty of water, change positions often, avoid crossing legs, and get up from sitting position 5 minutes of each hour.
86
Q

PE Treatment includes

A

-Oxygen, elevate HOB, comfort patient
-Anticoags/fibrinolytic
-IV fluids for hypotension –> vasopressors used if it persists
-Surgical management may be necessary

87
Q

Acute Respiratory Failure

What is the problem with ventilatory (hypercapnic) failure?

A

-Physical problem of lungs or chest wall
-Defect in respiratory control center in brain
-Poor function of respiratory muscles, especially diaphragm

88
Q

Acute Respiratory Failure

What causes ventilatory (hypercapnic) failure?

A

CNS depression, neuromuscular disorders​

89
Q

Acute Respiratory Failure

What is the problem with oxygenation (gas exchange) failure?

A

-Insufficient oxygenation of pulmonary blood at alveolar level
-Ventilation normal, lung perfusion decreased
-Right to left shunting of blood
-Ventilation/perfusion (V/Q)mismatch
-Low partial pressure of O2
-Abnormal hemoglobin

90
Q

Acute Respiratory Failure

What causes oxygenation (gas exchange) failure?

A

Pneumonia, ARDS, pulmonary edema​

91
Q

Can you have combined? If so, what causes it?

A

yes, often occurs in patients with lung disease: Chronic bronchitis, Emphysema, asthma

Diseased bronchioles and alveoli cause oxygenation failure; work of breathing increases; respiratory muscles unable to function effectively.

92
Q

Acute Respiratory Failure symptoms include:

A

*restlessness, irritability, and agitation
*Dyspnea
*Decreased responsiveness
*Confusion
*Increased dyspnea or decreased effort (especially in hypercapnic failure in patients with COPD)

93
Q

What is refractory hypoxemia?

A

hypoxemia that persists even when 100% oxygen is given

94
Q

What do we see on a chest X-ray in ARDS pt?

A

Dense pulmonary infiltrates on chest x-ray

95
Q

What is the main site of injury in ARDS?

A

Alveolar-capillary membrane is main site on injury

-Increased permeability to larger molecules (debris, protein and fluid). Lungs are going to get stiff.
-Thick exudate inhibits gas exchange

96
Q

What will vital signs shows in ARDS pt?

A

HTN, tachycardia, & dysrhythmias

97
Q

ARDS pts require intubation and PEEP. What is PEEP?

A

Positive end-expiratory pressure, is a pressure applied by the ventilator at the end of each breath to ensure that the alveoli are not prone to collapse.

98
Q

What are the three phases of ARDS?

A

Exudative phase
Fibrosing alveolitis phase
Resolution phase

99
Q

What do we see during the Exudative phase?

A

Pulmonary shunting and atelectasis (alveoli becoming fluid filled). Appears as lung infiltrates on CXR. Pulmonary edema in the absence of heart failure. Inactivation of surfactant.

Presentation:
Acute onset
Dyspnea
Restlessness and confusion
Tachycardia
Diffuse crackles
Dry cough

100
Q

What do we see during the Fibrosing alveolitis phase?

What complication are they at risk for?

A

Increased lung injury > pulmonary HTN and fibrosis. Decreased gas exchange and oxygenation.

MODS

101
Q

What is happening during the Resolution phase?

A

Usually occurs after 14 days

Resolution of injury may occur or damage has resulted in chronic lung disease

Mortality rate very high if patient reached this phase

102
Q

What happens if the pt is bucking the vent?

A

sedate pt

103
Q

What is the VAP Bundle?

A

-Elevation of the HOB between 30 and 45 degrees
-Oral care per facility policy (including antimicrobial rinse)
-Preventing aspiration
-Peptic ulcer disease prophylaxis
-Pulmonary hygiene (chest physiotherapy, postural drainage, turning and repositioning)

104
Q

Pulmonary Contusion occurs after chest trauma & inhibits gas exchange. Sx include:

A

Bloody sputum, decreased breath sounds, crackles, wheezes

105
Q

How do we treat a pulmonary contusion?

A

Maintenance of ventilation and oxygenation

106
Q

Rib fractures are often caused by direct blunt trauma to the chest. Chest usually not splinted by tape or other materials.
Uncomplicated rib fractures reunite spontaneously.

Focus is on pain management, why?

A

Decrease pain so that adequate ventilation is maintained

Encourage incentive spirometer

107
Q

Flail Chest is r/t two or more rib fractures causing the chest wall to destabilize.

What will you see on assessment with flail chest?

A

Paradoxical chest movement—“Sucking inward” of loose chest area during inspiration, “puffing out” of same area during expiration.

108
Q

What will you see on the assessment of tension pneumothorax?

A

-Asymmetry of thorax
-Tracheal movement away from midline toward unaffected side
-Respiratory distress
-Absence of breath sounds on one side
-Distended neck veins (r/t increase in central venous pressure)
-Cyanosis
-Hypertympanic sound on percussion

109
Q

How do we treat tension pneumothorax?

A

chest tube to decompress the area and help lung expand

CH2 (8 decks)

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