Unit 2 Flashcards
(159 cards)
1
Q
What is the patho for Acute Respiratory Distress Syndrome?
A
acute lung injury resulting from an unregulated systemic inflammatory response to acute injury or inflammation. damaged capillary membranes allows fluid to escape into the interstitial space, entering the alveolar membrane, diluting and inactivating surfactant. causing alveolar collapse and reducing gas exchange and compliance.
2
Q
What are conditions associated with the development of ARDS?
A
Shock - hemorrhagic or septic
inhalation injuries - aspiration, toxic gases, near-drowning
infections - sepsis, pneumonia, tb
drug overdose - heroin, methadone, propoxyphene, aspirin
trauma - burns, head injury, lung contusion, fat emboli
other- DIC, pancreatitis, uremia, multiple transfusions, open heart surgery with bypass.
3
Q
What is the rate of mortality with ARDS?
A
VERY high, 45%
4
Q
What are risk factors for ARDS?
A
indirect insults - sepsis, trauma, pancreatitis
direct insults - pulmonary infections, aspiration, pneumonia, drowning.
others - age >70, immunocompromised, smokers
5
Q
What are the clinical manifestations of ARDS?
A
Hypoxemia, Tachypnea, Dyspnea, anxiety, use of accessory muscles, intercostal retractions, cyanosis, adventitious breath sounds (crackles & rhonci), and mental status changes (agitations/confusion -> lethargy)
6
Q
What are the clinical manifestations for hypoxia?
A
dyspnea, tachypnea, intercostal retractions, tachycardia, cyanosis, atelectasis
7
Q
What are the clinical therapies for hypoxia?
A
bronchodilators, beta-agonists, corticosteroids. oxygen. monitoring pulmonary artery pressures and cardiac output. mechanical ventilation. CPAP, BiPAP, or PEEP. prone positioning. surfactant therapy.
8
Q
What are the clinical manifestations for nutritional imbalance?
A
confusion, F&E imbalance, weakness or fatigue
9
Q
What are the clinical therapies for nutritional imbalance?
A
fluid replacement. total parenteral/enteral nutrition or enteral feedings. Nutritional analysis.
10
Q
What are the clinical manifestations for activity intolerance?
A
irritability, fatigue, confusion, lethargy, and inability to maintain activities of daily living.
11
Q
What are the clinical therapies for activity intolerance?
A
care may need to be split to prevent overtaxing. assess level of consciousness. severe activity intolerance from significant hypoxia may require paralytics and sedation to reduce oxygen demands.
12
Q
What changes on a patients ABGs for ARDS?
A
decreased PO2 <60 decreased CO2 <35 pH >7.45 respiratory alkalosis r/t tachypnea progresses to respiratory and metabolic acidosis
13
Q
What diagnostic tests are used for ARDS?
A
Refractory Hypoxemia (ABGs)
Chest xray/CT
CBC/Chemistries/Cultures (blood & sputum)
14
Q
What is refractory hypoxemia?
A
hypoxemia that does not improve with O2 therapy.
is a hallmark sign of ARDS
15
Q
What is the pharmacologic therapies for ARDS?
A
No definitive drug therapy. nitric oxide - relaxes smooth muscle of pulm corticosteroids (methylprednisolone IV). surfactant therapy treatment of initial insult
16
Q
How do you manage a patient with ARDS?
A
identify and treat the cause. maintain the airway. provide adequate oxygenation. and support hemodynamic function.
17
Q
What is the main therapy with ARDS?
A
intubation and mechanical ventilation.
18
Q
What should the FIO2 setting be on a ventilator?
A
set at lowest level to maintain PO2 >60 and O2 sat >95.
19
Q
What is the purpose of PEEP?
A
to help maintain blood and tissue oxygenation and keep the alveoli open.
20
Q
What is the risk with PEEP?
A
decreases CO and increases the risk of barotrauma (lung injury r/t alveolar over distension)
21
Q
What are the five P’s of ARDS nonpharmacologic therapy?
A
Protective lung ventilation Perfusion Positioning Protocol weaning Preventing complications
22
Q
What level of FiO2 should you avoid and why?
A
greater than 50% to avoid toxicity
23
Q
When can a patient receive BiPAP or CPAP for mechanical ventilation?
A
when a patient can protect their own airway and doesn’t require an ETT.
24
Q
What are the modes of ventilation?
A
CPAP AC SIMV PEEP PSV
25
What is CPAP?
patient breathing on their own, just need pressure to keep open airway
26
What is AC (Assist Control)?
all breaths delivered at a specific set Tidal volume. ventilator will only initiate breaths if patient indicated rate falls below set rate
27
What is SIMV (Synchronized intermittent mandatory ventilation)?
No ventilator assistance between a set rate. patient will pull their own volume on breaths outside the set limit.
28
What is PEEP (Positive End Expiratory Pressure)?
must be intubated. given in addition to the previously described modes (AC, SIMV, PSV)
29
What is PSV (Pressure Support Ventilation)?
gives defined amount of pressure with patient initiated breaths. no ventilator initiated breath.
30
What are some ventilator complications?
hospital-acquired pneumonia (ventilator associated pneumonia)
barotrauma/pneumothorax
cardiovascular effects
gastrointestinal effects
31
What are S/S of ventilator associated pneumonia?
thick, tenacious secretions build up in lungs causing infection.
32
What are interventions to prevent VAP?
frequent, meticulous oral hygiene and strict asepsis used for suctioning and other respiratory procedures.
33
What are s/s of pneumothorax?
unequal chest expansion. sudden loss or significant decrease in in breath sounds on the affect side.
34
What are interventions for pneumothorax?
chest tube insertion
35
What are ventilator complications related to the cardiovascular system?
increased pressure in the chest decreases venous return and ventricular filling. decreases cardiac output. can cause hypo perfusion of liver and kidneys.
36
What are ventilator complications related to the gastrointestinal system?
stress ulcers, constipation, gastric distention.
37
What ventilator settings are used for ventilator weaning?
SIMV and PSV because the patient is initiating breaths.
38
What is a cause for a high pressure alarm on a ventilator?
patient biting tubing.
blockage from secretions.
ARDS
39
What causes a low pressure alarm on a ventilator?
an air leak. most often a piece of the tubing is disconnected.
40
How long can you keep an ETT in before needing to switch to a tracheostomy?
7 days
41
What are some therapies for ventilator patients?
prone positioning. chest PT. postural drainage. LMWH to prevent VTE/DIC
42
What are some nursing interventions for ARDS patients?
```
maintaining airway patency.
promoting spontaneous ventilation.
enhancing cardiac output.
monitor for ventilatory weaning.
anxiety/mentation.
```
43
What are some interventions for maintaining airway patency?
suction as needed.
obtain sputum for culture if purulent or odorous.
perform percussion, vibration, and postural drainage.
secure ETT or trach.
assess fluid balance and maintain adequate hydration.
44
What are some interventions for promoting spontaneous ventilation?
assess and document respiratory rate, vital signs, and oxygen saturation every 15-30 min.
promptly report worsening ABGs and oxygen sats.
administer oxygen as ordered
place in fowler or high-fowlers
minimize activities and energy expenditures
45
What are some interventions for enhancing cardiac output?
monitor and record vitals, including apical pulse, q2h
assess LOC q4h
assess heart and lung sounds frequently
daily weights
maintain IVF as ordered
administer analgesics, sedatives, and neuromuscular blockers
46
What are some interventions for monitoring ventilatory weaning response?
monitor vital signs every 15-30 minutes
place in high fowlers
assess for findings indicative of dysfunctional weaning such as dyspnea, decreased oxygen sats, cyanosis, pallor, diminished breath sounds.
slow reduction of ventilatory support
keep oxygen at bedside
provide pulmonary hygiene such as percussion and postural drainage
47
What are some interventions for relieving anxiety?
```
explain all monitors, procedures, unusual sounds, and machinery
provide simple means of communication
encourage family visits
provide distraction
reassure patient
```
48
What are spinal cord injuries secondary to?
trauma - MVC, Fall, GSW.
49
What is a spinal cord injury?
vertebra or other objects forced against the spinal cord, causing damage, preventing messages between brain and body parts.
50
What is the result of a spinal cord injury?
sensory info from the body to the brain or motor info from the brain to body may be impaired or even absent.
51
How do you know what is effected by a spinal cord injury?
the vertebra effected and everything below
52
What do the cervical spinal cord nerves control?
diaphragm, chest wall, muscles, arms, and shoulders
53
What do the thoracic spinal cord nerves control?
upper body, gastrointestinal function
54
What do the lumbar spinal cord nerves control?
lower body
55
What do the sacral spinal cord nerves control?
bowel, bladder, and sexual function.
56
What are the risk factors for spinal cord injuries?
ages 16-30
male gender
risky behaviors - diving into shallow pools, sports without gear, driving ATVs/MC
older adults more likely from fall (osteoporosis)
57
How do you prevent spinal cord injuries?
safe driving. wearing a seat belt. child safety seats. avoid diving into shallow water. wear appropriate gear for sports. fall prevention strategies. avoid areas of high crime.
58
What are emergency signs and symptoms of spinal cord injuries?
extreme pain/pressure in neck or back.
weakness/paralysis/lack of sensation or pins and needles. loss of bladder/bowel control. impaired breathing after injury. oddly positioned neck or back. muscle spasms.
59
what is spinal shock?
immediate temporary loss of total power, sensation, and reflexes below the level of injury.
60
What is the mechanism of spinal shock?
peripheral neurons become temporarily unresponsive to brain stimuli
61
What occurs to the body with spinal shock?
hypotension, bradycardia, absent bulbocavernosus reflex, and flaccid paralysis.
62
What occurs to the body with neurogenic shock?
hypotension, bradycardia, variable bulbocavernosus reflex. variable motor reflex.
63
What is the mechanism of neurogenic shock?
disruption of autonomic pathways -> loss of sympathetic tone and vasodilation.
64
When does spinal shock and neurogenic shock typically occur?
48-72 hours immediately following SCI
65
How do you classify spinal cord injuries?
complete or incomplete
66
What is a complete spinal cord injury?
total loss of all sensory and motor function below level of injury. damage is irreversible.
67
What is an incomplete spinal cord injury?
partial loss of sensory and motor function below level of injury. may have sensation but no motor, or movement with no sensation.
68
What are the signs and symptoms of autonomic dysreflexia?
above injury: vasodilation, increased sweating, decreased HR, distended neck veins, headache, increased bp, flushed face.
below level of injury: pale, cool, no sweating
69
Which spinal cord injuries are at risk for autonomic dysreflexia?
spinal cord injury at t6 or higher
70
What triggers autonomic dysreflexia?
triggered by sustained stimuli at t6 or below from restrictive clothing, full bladder or uti, pressure areas, or fecal impaction.
71
What are managed as SCIs until ruled out?
head trauma, unconscious patients, penetrating injuries near spine, fall, and MVC.
72
What is the priority with emergency care of an SCI?
maintain airway. (ABCs) and then immobilization of spine before transit.
73
What are the diagnostic tests for spinal cord injuries?
xray, CT or MRI. Myelogram.
Somatosensory Evoked Potential - neural response to stimulation.
ABGs - resp insuff or failure
H&H - r/o hemorrhage
74
What are the surgical interventions for spinal cord injuries?
decompression - removal of debris
| spinal stabilization/realignment - rods and screws
75
What meds are used for spinal cord injuries?
corticosteroids - high dose methylprednisolone IV
antispasmodics - baclofen, dantrolene
analgesics - opioids, NSAIDs, etc
vasopressors - norepinephrine, dopamine, dobutamine, etc.
anticoagulants - enoxaparin, heparin
stool softeners - docusate
76
What is some nursing management for spinal cord injuries?
administer O2 or intubate. pulmonary hygiene. immobilize spine. stabilize. monitor VS. bowel & bladder. skin care. DVT prophylaxis.
77
What is normal brain function?
```
A&O x3
pupils regular, brisk, and equal
eyes move in opposite direction of head movement
caloric testing produces nystagmus
purposeful movement
responds to commands
breathing is normal.
```
78
What occurs in the early progression or first stage of deteriorating brain function due to increased ICP?
responds to verbal stimuli, decreasing concentration, agitation, confusion, lethargy.
pupils small and reactive.
roving eye movements; dolls eyes present.
eye deviation away from cold caloric stimulus and toward warm stimulus.
purposeful movement in response to pain.
yawning, sighing respirations.
79
What occurs during the second stage of deteriorating brain function due to increased ICP?
requires continuous stimulation to arouse.
| decorticate posturing. Cheyne-stokes respirations
80
What occurs during the third stage of deteriorating brain function due to increased ICP?
displaces reflexive positioning to pain stimulus.
pupils fixed.
caloric testing produces nystagmus.
decerebrate posturing.
central neurogenic hyperventilation with rapid, regular, and deep respirations.; apneusitc breathing with prolonged inspiration and pauses at full inspiration.
81
What is the final stage of deteriorating brain function due to increased ICP?
no response to stimuli.
fixed pupils in midposiiton.
no spontaneous eye movement or nystagmus.
flaccidity.
cluster or ataxic breathing with irregular pattern and depth.
82
What is decorticate posturing?
elbows, wrists, and fingers flexed. legs extended and rotated inward. damage to the cerebrum/midbrain
83
What is decerebrate posturing?
head arched back, extended by the sides. legs/feet extended. damage to midbrain/brainstem.
84
What are some alterations in level of consciousness?
confusion, disorientation, obtunded (obtundation), stupor, semi comatose, coma, deep coma
85
What is confusion?
unable to think rapidly and clearly. easily bewildered, with poor memory and short attention span. misinterprets stimuli. judgement is impaired
86
What is disorientation?
not aware of or not oriented to time, place, or person
87
What is obtundation?
lethargic, somnolent. responsive to verbal or tactile stimuli but quickly drifts back to sleep.
88
What is stupor?
generally unresponsive. may be briefly aroused by vigorous, repeated, or painful stimuli. my shrink away from or grab at the source of stimuli.
89
What is semicomatose?
does not move spontaneously. unresponsive to stimuli, although vigorous or painful stimuli may result in stirring, moaning, or withdrawal from stimuli without actual arousal.
90
What is coma?
unarousable. will not stir or moan in response to any stimuli. may exhibit nonpurposeful response of area stimulated but makes not attempt to withdrawal.
91
What is deep coma?
completely unarousable and unresponsive to any kind of stimuli, including pain. absence of brainstem reflexes, corneal, papillary, and pharyngeal reflexes, and tendon and plantar reflexes.
92
What is the Glasgow Coma Scale?
assess patients level of consciousness
93
What is the best score you can get on the Glasgow Coma Scale?
15
94
What score is considered a significantly altered level of consciousness on the Glasgow Coma Scale?
<8
95
What is the worst score you can get on the Glasgow Coma Scale?
3
96
What are assess in the Glasgow Coma Scale?
eye opening, verbal response, motor reponse
97
What are the points for eye opening of the GCS?
spontaneous - 4
to loud voice - 3
to pain - 2
none - 1
98
What are the points for verbal response of the GCS?
```
oriented - 5
confused, disoriented - 4
inappropriate words - 3
incomprehensible sounds - 2
none - 1
```
99
What are the points for motor response of the GCS?
```
obeys - 6
localizes - 5
withdraws - 4
abnormal flexion posturing - 3
extension posturing - 2
none - 1
```
100
What is considered an increased ICP?
>15 mmHg
101
When does increased ICP require intervention?
>20 mmHg
102
What are factors that increase ICP?
coughing, bending, sneezing, and straining
103
What is the most frequent cause of increased ICP?
cerebral edema
104
What are some causes of increased ICP?
head injury, hydrocephalus, cerebral edema, excess CSF, or intracranial hemorrhage
105
What are some signs and symptoms of increased ICP?
decreased LOC, pupillary dysfunction, oculomotor dysfunction, drooping eyelids. visual abnormalities - blurred vision, diplopia. papilledema (late sign), motor impairment - hemiparesis or hemiplegia (early) or posturing/flaccidity (late). headache, worse in the mornings. projectile vomiting w/o nausea. Cushing's triad. altered respiratory pattern. elevated temp.
106
What are the most common respiratory patterns with increased ICP?
biot's and Cheyne-stokes
107
What is Biot's respiratory pattern?
rapid, deep respirations (gasps), with short pauses between sets
108
What is Cheyne-stokes respiratory pattern?
gradual increases and decreases in respirations with periods of apnea
109
What are the components of Cushing's Triad?
increased systolic BP/widening Bp
Bradypnea
Bradycardia
110
What is Cushing's Triad?
a late sign of increased intracranial pressure
111
What are the diagnostic tests for increased intracranial pressure?
CT/MRI
serum osmolality
ABGs
112
What diagnostic test is not to be done until increased ICP is ruled out?
Lumbar Puncture
113
What is a complication of Increased ICP?
diabetes insipidus
114
What is diabetes insipidus?
when the hypothalamus doesn't produce enough ADH causing profound diuresis of extremely dilute urine. (Specific gravity <1.010)
115
What are the results of diabetes insipidus?
hypernatremia and increased serum osmolarity
116
How do you treat diabetes insipidus?
hydration with 1/2 normal saline
117
What is the surgical management of increased ICP?
drainage catheters (ventriculostomy) and burr holes
118
What are used to monitor ICP?
intraventricular catheter, subarachnoid bolt or screw, or epidural probe.
119
Why do you monitor ICP?
identify increased ICP early. initiate appropriate treatment. continuous measurement of CPP. provide access to CSF for sampling/drainage. evaluate effectiveness of treatment
120
What is the biggest risk with ICP monitoring?
risk for infection
121
How do you calculate Cerebral Perfusion Pressure (CPP)?
CPP = MAP - ICP
122
What is a good CPP?
>70 mmHg
123
When is the CPP most damaging?
<50 mmHg
124
What should you remember when administering mannitol for increased ICP?
administer with a filter. observe for crystals. change tubing every shift.
125
What is the purpose of administering osmotic diuretics (mannitol) for increased ICP?
increases the osmolarity of the blood, drawing water out of edematous brain tissue and into the vascular system for elimination through the kidneys.
126
What is the purpose of administering loop diuretics (furosemide) for increased ICP?
inhibits sodium and chloride reabsorption. causes a reduction in the rate of CSF production, decreasing cerebral edema which decreases ICP.
127
What should you monitor for when administering furosemide?
hypokalemia/hyponatremia and hypotension
128
What is the purpose of administering anticonvulsants (phenytoin) for increased ICP?
to prevent seizures caused by the increase in ICP
129
What should you remember when administering phenytoin?
dilute medication, it is caustic to tissues. Monitor therapeutic drug levels and watch for toxicity.
130
What is the purpose of administering corticosteroids (dexamethasone) for increased ICP?
for its anti-inflammatory action to decrease cerebral edema which decreases ICP.
131
What is the purpose of administering Ca Channel Blockers (nimodipine) for increased ICP?
given for increased ICP due to hemorrhage. relaxes blood vessels which decrease vasospasms, increasing CPP.
132
What should you remember when administering nimodipine?
do not give if SBP <90
133
What is the purpose of administering Vasopressors (phenylephrine) for increased ICP?
keeps CPP good.
increases BP, increases MAP. which increases CPP.
monitor closely
134
What is the purpose of administering sedation (Propofol) for increased ICP?
to prevent further brain damage and decrease metabolic needs.
135
How is Propofol dosed?
titrated based on the RASS scale
136
What is the RASS scale?
used to measure the sedation level of a person
137
What are the RASS scale levels?
-5 to +4
138
What is a +4 on the RASS scale?
combative - violent, immediate danger to staff
139
What is a +3 on the RASS scale?
very agitated - pulls or removes tubes or catheters, aggressive.
140
What is a +2 on the RASS scale?
agitated - frequent, non-purposeful movement, fights ventilator
141
What is a +1 on the RASS scale?
restless - anxious, apprehensive but movements not aggressive or vigorous
142
What is a 0 on the RASS scale?
alert & calm
143
What is a -1 on the RASS scale?
drowsy- not fully alert, but as sustained awakening to voice >10 sec
144
What is a -2 on the RASS scale?
light sedation - briefly awakens to voice <10 sec
145
What is a -3 on the RASS scale?
moderate sedation - movement or eye-opening to voice but no eye contact
146
What is a -4 on the RASS scale?
deep sedation - no response to voice, but movement or eye opening to physical stimulation.
147
What is a -5 on the RASS scale?
unarousable - no response to voice or physical stimulation
148
What is the purpose of mechanical ventilation for patients with increased ICP?
respiratory management. maintains partial pressure of O2 (100) & CO2 (35)
149
What are some nursing interventions with increased ICP patients?
```
frequent neuro checks 15min - 1hr.
mechanical ventilation - preO2 and limit sx to 10 sec
prevent hypoxia and hypercapnia.
HOB 30 degrees or flat.
head/neck alignment
prevent bending of neck
monitor bladder and bowel
assist patient up in bed
do not cluster care
fluid restrictions/strict I&Os
decrease stimuli
avoid footboards and restraints
ICP monitor care
```
150
What is brain death?
cessation and irreversibility of all brain functions including the brain stem. no evidence of cerebral or brainstem function for 6-24 hours in a patient with a normal body temp and not affected by depressant drugs or alcohol poisoning
151
What are the clinical criteria for brain death?
unresponsive coma with absent motor and reflex movements.
no spontaneous respiration.
pupils fixed and dilated.
absent ocular responses.
flat EEG and no cerebral blood circulation on angiogram.
persistence of these manifestations for 30 minutes to 1 hour and for six hours after onset of coma nd apnea.
152
What is the apnea test?
bring temp >97 SBP >90. normal PCO2 >40 mmHg, and normal PO2.
Disconnect ventilator and give O2 down ETT.
watch for respiratory movement and draw ABGs after 8 minutes, and then reconnect ventilator.
153
What would the ABGs be for positive brain death on the apnea test?
respiratory movement is absent.
| PCO2 >60 or there is a 20mmHg increase over baseline
154
What is the iced water caloric test?
tests oculovestibular reflex.
intact tympanic membrane required. HOB >30 degrees. MD instills ice water into the ear canal and observes for eye movement
155
What response is for positive brain death on the iced water caloric test?
no eye movement
156
What are some other confirmatory tests for brain death?
angiography, EEG, and technetium 99 brain scan.
157
When should lifeNet be called?
patient has a GCS of 4 or less
158
Who approaches the family about organ donation and when?
LifeNet approaches the family to discuss organ donation once the patient is declared brain dead
159
What organs can be donated?
heart & lungs, kidneys, pancreas, liver, intestines, bone & tissue, eyes, & skin
