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Nursing school level 4 > NURS 453 test 1 > Flashcards

NURS 453 test 1 Flashcards

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1
Q

COPD characterized by

A

airflow limitation, breathlessness, and exacerbation.

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2
Q

COPD disease process os based mainly off of what concept

A

inflammation

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3
Q

process of COPD

A

inhaling noxious particles which releases inflammatory mediators. this causes damage to the tissue of the lungs and an increase in mucus. The lungs become more and more injured which leads to structural remodeling and an increase in scar tissue. the result is either pulmonary fibrosis or damage/destruction (emphysema)

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4
Q

pulmonary fibrosis

A

thickening of the tissue between the alveoli

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5
Q

emphysema

A

damaged alveoli in which they trap air

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6
Q

characteristic of chronic bronchitis

A

chronic, productive cough for more than 3 months over consecutive 2 years. it is inflammation of bronchi r/t chronic exposure

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7
Q

emphysema

A

abnormal permanent enlargement of the air spaces which causes a loss of lung elasticity and causes difficulty with exhaling

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8
Q

Key preventative measure with COPD

A

smoking cessation to prevent and slo progression of disease

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9
Q

antitrypsin (AAT) deficiency

A

genetic risk factor for COPD. Deficiency of AAT causes a breakdown of elastin in alveoli, and inability to make coagulation factors in the liver.

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10
Q

antitrypsin (AAT)

A

protects and inhibits lysis of the lung tissue during inflammation.

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11
Q

elastin

A

gives elasticity and strength to the alveoli

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12
Q

goals for medication during COPD

A

reduce dyspnea, improve exercise tolerance, and prevent complications

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13
Q

with what assessment findings is COPD considered

A

intermittent cough (usually in AM) or with exertion, sputum production, dyspnea, exposure to risk factors,

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14
Q

COPD causes a high risk for

A

depression due to quality of life decrease

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15
Q

early clinical manifestations of COPD

A

dyspnea with exertion every day, air hunger, gasping, increase effort of breathing, chronic cough or sputum production, fatigue

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16
Q

physical assessment of COPD

A

barrel chest, underweight, increase expiratory phase, wheezes, decrease breath sounds, tripod position, purse lip breathing, LE edema, polycythemia, cyanosis

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17
Q

late clinical manifestations of COPD

A

clubbing and dyspnea at rest

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18
Q

what labs do you want for COPD

A

WBC and sputum cultures- PNA or infection
Hgb/Hct - may be increased due to chronic low level of O2
ABGs - hypoxic
electrolytes - Na/K, BUN, glucose
trops - if MI caused acute exacerbation
BNP - if HF caused acute exacerbation
D-dimer - if PE caused acute exacerbation

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19
Q

COPD diagnostics for acute exacerbation

A

CXR - to determine PNA
echocardiogram - determines cor pulmonale
12 lead ECG - if from an MI
spiral CT - if from PE

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20
Q

COPD diagnostics for chronic phase

A

pulmonary function test - determines COPD progression

echocardiogram - determines cor pulmonale

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21
Q

characteristics of acute exacerbation of COPD

A

change or worsening of COPD symptoms such as increase in dyspnea, cough, and sputum

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22
Q

what would put a acute exacerbation COPD pt Into the ICU

A

worsening hypoxemia, increasing hypercapnia, severe or worsening respiratory acidosis

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23
Q

what do you need to think about with labs and diagnostics in acute exacerbation of COPD

A

what the cause is (PNA, MI, PE?)

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24
Q

ABG findings in exacerbation

A

low PaO2 and SaO2
high PaCO2
normal or low PH
high HCO3

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25
Q

COPD meds for maintenance

A

anticholinergic agents (ipratropium)- long acting, steroid with LABA (Advair or Symbicort)

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26
Q

COPD meds for acute exacerbation

A

short acting beta 2 agonist (albuterol), antibiotic, steroid

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27
Q

bronchodilators

A

relaxes smooth muscles and improves lung ventilation

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28
Q

mucolytic agents

A

help thin secretions making them easier for the pt to expel

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29
Q

caution with beta blockers with COPD pts, why?

A

it can cause the bronchioles to constrict

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30
Q

types of breathing for COPD

A

pursed lip - prolongs exhalation

diaphragmatic breathing - achieves maximum inhalation and decreased RR

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31
Q

Patient care goals in COPD

A

conserve energy, reduce fatigue, facilitate removal of secretions

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32
Q

Patient care goals in COPD

A

conserve energy, reduce fatigue, facilitate removal of secretions

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33
Q

smoking cessation strategies

A

pharmacological support and one to one counseling

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34
Q

pharmacological support for smoking cessation

A

Nicotine supplements, bupropion (wellbutrin, zyban), varenicline (chantix)

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35
Q

pulmonary hypertension

A

Chronic progressive disease of small pulmonary arteries (PA) leading to increase pressure in the arteries and vascular remodeling. This can lead to backflow into the right ventricle which puts extra work on it and can lead to failure.

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36
Q

pulmonary hypertension classic symptoms

A

dyspnea on exertion and fatigue due to low cardiac output

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37
Q

is pulmonary hypertension curable

A

no

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38
Q

1 cause of pulmonary hypertension

A

COPD but there are a lot of reasons that can lead you to PH such as PE, HF, or medications

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39
Q

pulmonary hypertension labs

A

ABGs, CBC, electrolytes, BNP

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40
Q

diagnostic studies for pulmonary HTN

A

right cardiac Cath, 12 lead ECG, CT scan

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41
Q

right cardiac Cath

A

Examines the right atrium, right ventricle and pulmonary pressures through vena cava. should see a increase in pulmonary artery and vascular pressure

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42
Q

cor pulmonale

A

Enlargement of the right ventricle secondary to primary disorder or disease of the pulmonary system

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43
Q

most common cause of cor pulmonale

A

COPD. pulmonary HTN is usually a preexisting condition but not always

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44
Q

clinical manifestations of cor pulmonale

A

Symptoms are subtle and masked by symptoms of the pulmonary condition, but should see exertional dyspnea, tachypnea, cough, fatigue
Also: RV hypertrophy, increased intensity of S2, chronic hypoxemia

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45
Q

Right sided heart failure signs and symptoms

A 
Peripheral Edema 3+ 
Weight Gain
JVD
Full, Bounding Pulse
Enlarged Liver
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46
Q

care for cor pulmonale

A

treat underlying condition, O2, palliative care procedures

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47
Q

goal of Pharm management of PH and Cor Pulmonale

A

promote vasodilation of pulm vasculature,  RV overload, & reverse remodeling

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48
Q

meds for PH and cor pulmonale

A

calcium channel blocker, vasodilators, endothelial receptor antagonist, viagra, oxygen, diuretics, anticoagulants, inotropic agents

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49
Q

endothelial receptor antagonist

A

Given PO; binds to endothelin-1 receptors:↓ PA pressures, ↑ cardiac output
for PH and cor pulmonale

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50
Q

DVT is a concept of

A

inflammation

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51
Q

PE Is a concept of

A

perfusion that causes an issue of oxygenation and ventilation

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52
Q

pulmonary thromboembolism

A

Obstruction of one or more of the pulmonary arteries or one of it’s branches by a thrombus (VTE/DVT)

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53
Q

if PE is not treated what can happen to the patient

A

the patent will go into shock due to right ventricular dysfunction (blood backing up into the ventricle and not able to keep up with demand). shock will lead to cardiac arrest and death

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54
Q

PE distrupts ____

A

blood flow to a region of the lungs. this causes:
Bronchoconstriction due to Alveolar hypocarbia
Shunting with risk of infection of lung tissue
↑ pulmonary vascular resistance
↑ RV workload

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55
Q

Alveolar hypocarbia causes what to happen with the lungs?

A

low CO2 in alveolar = constriction in lungs

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56
Q

where do emboli originate

A

DVTs primarily LE but sometimes from UE

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57
Q

Virchow Triad for PE

A

Venous stasis
Vascular endothelium injury
Hypercoagulability

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58
Q

risk factor for PE

A

conditions of decreased venous return - Immobility!!

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59
Q

most common symptom of PE

A

sudden onset of unexplained dyspnea but other s/s can be subtle they include: anxiety, tachypnea, tachycardia, Change in LOC secondary to hypoxemia, feeling of impending doom, hypotension, murmur

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60
Q

labs for pulmonary embolism

A

ABGs - oxygenation
D-Dimer - clotting in the body
BNP - cardiac ventricular stretch
troponin - how big it is

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61
Q

diagnostics for PE

A

spiral CT unless allergic to IV contrast them V/Q scan. also 12 lead ECG, echocardiogram

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62
Q

potential complications post PE

A

pulmonary infarction due to insufficient blood flow or

pulmonary HTN due to chronic PE disease or chronic thromboses

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63
Q

care for PE

A

prevent growth of thrombi, optimize oxygenation and ventilations with O2 therapy and turn cough deep breath, monitor for bleeding due to anticoagulants, pain relief

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64
Q

sign of DVT

A

Deep calf pain, tenderness, warmth, or redness, unilateral edema

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65
Q

Massive PE

A

Acute PE w/ sustained SPB <90 for greater than 15 mins
Need for inotropes (no other reason)
Signs of shock
10% of these patients die within the first hour

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66
Q

Submassive PE

A

Acute PE w/ RV dysfunction

Myocardial necrosis present

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67
Q

Acute PE:

A

Signs and symptoms immediately after obstruction

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68
Q

Thrombolytics

A

Fibrolytics (AKA Alteplase or tPA)

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69
Q

Massive PE treatment

A

Throbolytics/Fibrolytics: recommended for pts with a low to moderate risk of bleeding. Avoid patients at high risk to bleed: hx or current intracranial hemorrhage, cerebrovascular disease, neoplasm, suspected aortic dissection, w/in 3 months of ischemic cerebral vascular accident

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70
Q

Submassive PE treatment

A

Thrombolytics considered on a case by case basis

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71
Q

Vitamin-K antagonist

A

warfarin - is main therapy with PE bridged w/ parenteral anti-coagulants but needs frequent monitoring of INR

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72
Q

Direct oral anticoagulants (DOACs)

A

can be used to treat PE - Examples: Xarelto, Pradaxa, Eliquist. more predictable and no lab monitoring

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73
Q

low molecular weight heparin example

A

enoxaparin sodium - no lab needed

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74
Q

warfarin INR goal

A

2-3

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75
Q

when pts are receiving anticoagulation therapy, priority is to

A

assess for bleeding and all associated signs and symptoms of a potential bleed

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76
Q

Heparin lab

A

PTT (goal is 50-90)

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77
Q

bridge therapy

A

Initial treatment begins with heparin or LMWH.
Warfarin (least 5 days) or a DOAC (1-2 days) is started and continued with the heparin/LMWH until the designated time frame and then the heparin/LMWH is stopped
Warfarin/DOAC are PO and patients can take these long term at home (at least 3 months post PE)

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78
Q

hyperventilation

A

blowing off CO2 - vasoconstriction

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79
Q

hypoventilation

A

keeping CO2 - vasodilation

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80
Q

two types of trauma

A

blunt force and penetrating

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81
Q

signs and symptoms of crush injury

A

petechiae in the whites of the eyes, cheeks, and face

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82
Q

pneumothorax

A

air in the pleural space resulting in partial collapse of lung - pressure goes from negative to positive

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83
Q

clinical manifestations of small pneumothorax

A

tachycardia and dyspnea

84
Q

clinical manifestations of large pneumothorax

A

absent breath sounds. Respiratory Distress (shallow, rapid resps, dyspnea, air hunger, O2 desaturation); Chest pain, Cough with or without hemoptysis

85
Q

spontaneous pneumo can happen in

A

also called a closed pnuemo can occur after rupture of blebs in COPD pt or in tall/thin male with marphans

86
Q

Iatrogenic pnuemothorax

A

pnuemo that is caused from a medical procedure. This can be from mechanical ventilation or gastric tube and perforation of the esophagus

87
Q

traumatic pneumothorax

A

This is also known as a sucking chest wound. Occurs through an opening in the chest such as GSW, Stabbing, Surgical Thoracotomy. Sucks air in every time the pt takes a breath

88
Q

Treatment of Open (traumatic) Pneumothorax

A

Should be covered with an occlusive, vented dressing. Allows air to escape and prevent a tension pneumo. Acts as one-way valve

89
Q

Tension Pneumothorax

A

Rapid accumulation of air in pleural space without the ability to escape. (medical emergency) - respiratory and circulatory collapse

90
Q

late sign of tension pneumothorax

A

tracheal deviation

91
Q

Hemothorax

A

Accumulation of blood in the pleural space.

92
Q

how much blood is too much during a hemothorax

A

250-300 ml of blood (unit of blood)

93
Q

chylothorax

A 
Lymphatic fluid in the 
Pleural space due to a leak
in the thoracic duct.
-Causes: Trauma, Surgical
Procedures, and Malignancy
94
Q

how much fluid is too much

A

1500-2400 ml.day

95
Q

how to monitor hemodynamic stability

A

urine output and BP

96
Q

treatment during hemothorax

A

preserve hemodynamic stability

97
Q

subcutaneous emphysema

A

air leaking into the subcutaneous layer

98
Q

chest tube should never be

A

clamped unless given the order to and never milk or strip because it can change the pressure and damager lung tissue

99
Q

what to monitor in patients with chest tube

A

pain, drainage, that the tube still connected

100
Q

complications of chest tubes

A

malposition, infection, pneumonia, frozen shoulder from pain

101
Q

what should you do before the doctor removes a chest tube

A

pre-medicate

102
Q

flail chest

A

life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall.

103
Q

sign of flail chest

A

paradoxical movement - breathing reverses this pattern, which means that during inspiration, the chest contracts, and during expiration, it expands.

104
Q

pulmonary contusion

A

bruising of the lungs

105
Q

cardiac tamponade

A

rapid collection of blood in the pericardial sac, reducing filling

106
Q

s/s of cardiac tamponade

A

muffled, distant heart tones, decrease BP, jugular vein distention, and increase Central venous pressure

107
Q

treatment of cardiac tamponade

A

it is a medical emergency and a pericardiocentesis or surgical repair needs to occur

108
Q

respiratory failure

A

sudden and life threatening deterioration of one or both ventilation and oxygenation which causes issues with acid base balance, fluids and electrolytes and perfusion.

109
Q

what causes respiratory failure

A

abnormalities in any component of the respiratory system

110
Q

what is often present with respiratory failure

A

hypo perfusion secondary to shock (oxygenation problem)

111
Q

respiratory failure is a major threat of

A

organ failure, metabolic acidosis, and cellular death

112
Q

two types of respiratory failure

A

hypoxemic (oxygenation failure) or hypercapnic (ventilatory failure) both can be either chronic or acute

113
Q

hypoxemia

A

insufficient O2 transferred to the blood - PaO2 less than 60

114
Q

hypercapnia

A

inadequate CO2 elimination (not breathing fast enough) Co2 above 45 with academia

115
Q

causes of hypoxemic respiratory failure

A

V/Q mismatch, shunt, diffusion limitation, alveolar hypoventilation

116
Q

causes of hypercapnic respiratory failure

A

abnormal chest wall movement, CNS issue, airways and alveoli

117
Q

symptoms of hypoxemic respiratory failure

A

low SaO2, low PaO2 showing with tachycardia and tachypnea, increased RR, and as a late sign changes in level of consciousness

118
Q

ventilation vs perfusion in upper zone of the lungs

A

greater ventilation

119
Q

ventilation vs perfusion in middle zone of the lungs

A

equal

120
Q

ventilation vs perfusion in lower zone of the lungs

A

greater perfusion

121
Q

normal state of ventilation/perfusion

A

Ideal gas exchange, blood flow and ventilation match

122
Q

abnormal state of ventilation/perfusion

A

Volume of blood perfusing the lungs each minute (4-5L) fails to match the fresh gas reaches the alveoli. Most common cause of hypoxemic respiratory failure

123
Q

perfusion without ventilation

A

shunt v/q=0

124
Q

normal v/q

A

=0.8

125
Q

ventilation without perfusion

A

dead space v/q = infinity (pulmonary embolism)

126
Q

shunt

A

blood exits heart without having participated in gas exchange

127
Q

anatomic shunt

A

ventricular/septal defect

128
Q

intrapulmonary shunt

A

alveoli filled with fluid - ARDS, pneumonia, pulmonary edema

129
Q

diffusion limitation

A

Gas exchange is compromised or limited because a process has thickened or destroyed the alveolar membrane can happen from COPD, recurrent PE, pulmonary fibrosis, interstitial lung disease

130
Q

alveolar hypoventilation

A

Oxygen being brought into the alveoli is insufficient to meet metabolic needs of the body
↓ in ventilation = ↑ PaCO2 AND ↓ PaO2
problem on oxygen and ventilation

131
Q

examples of alveolar hypoventilation

A

CNS disease, chest wall dysfunction, obesity..

132
Q

specific Manifestations of Hypoxemic Respiratory Failure

A

Dyspnea, tachypnea, Prolonged I:E time (1:3); nasal flaring, intercostal muscle retraction, use of accessory muscles, abnormal chest wall movement, CYANOSIS (LATE)

133
Q

nonspecific Manifestations of Hypoxemic Respiratory Failure

A

TACHYCARDIA and HTN (EARLY)- heart compensating, agitation, disorientation, restlessness, delirium, confusion, change in LOC, cool/clammy skin, fatigue, inability to speak in complete sentences, COMA, DYSRTHYMIAS, HoTN (all LATE)

134
Q

Causes of Hypercapnic Respiratory Failure

A

Airways and alveoli:
obstruction of airflow and ↑ dead space
CNS issues:
suppressed drive to breathe (overdose, brainstem infarct, high level spinal cord injury)
Chest wall:
prevention of normal movement of chest wall (fractures, flail, restriction)
NM disease:
weakness of respiratory muscles (ALS, multiple sclerosis, Guillain Barre, paralytic medications)

135
Q

Initial signs and symptoms of ventilation failure (aka hypercapnic respiratory failure

A 
Changes in LOC
↑ HR
↑ RR (initial response)
HTN
Associated to high circulating catecholamines
136
Q

Hypercapnic Respiratory FailureABG trends

A

↓ pH: Acidosis
↑ PaCO2: carbon dioxide is an acid
↓ PaO2: (remember hypoxemia is at 60 or less)
↓ SaO2 : this can take a long time to change!!!
↓ RR: think retention of CO2
RR can also go up; more common for it to go down…

137
Q

Specific respiratory manifestations of hypercapnic respiratory failure:

A

Dyspnea (remember this is a patient complaint), tripod positioning, pursed lip breathing, ↓ tidal volume (or volume of breath), ↓ RR or ↑ RR and shallow

138
Q

Nonspecific manifestations of hypercapnic respiratory failure

A

Morning headache , confusion, agitation, progressive somnolence, bounding pulse, muscle weakness, ↓ DTRs, DYSRTHMIAS, TREMORS/SEIZURES (both LATE)

139
Q

labs for acute respiratory failure

A

determine the cause of it! BNP, D-dimer, troponin, CBC< sputum/blood culture, lactic acids, CMP, clotting studies

140
Q

diagnostics for acute respiratory failure

A

Chest x-ray, consider spiral CT, MRI, VQ scan
12 lead ECG – get for MI, Afib, …
Pulmonary artery catheter (rarely utilized)

141
Q

management of acute respiratory failure

A

identify what the cause is, O2, optimize oxygenation and ventilation using positioning, prevention of desaturation, Continuous monitoring for desaturation and decrease in ventilation, and Promoting secretion clearance (turn cough and deep breathe or TCD)

142
Q

oxygen therapy

A

Be tolerated by the patient
PaO2 at a minimum of 61 mmHg or more
SaO2 at 90% or more at the lowest O2 concentration possible
Low flow, high flow or positive pressure (CPAP or intubation)

143
Q

Mobilization of secretions

A

Hydration and humidification
Chest physiotherapy (CPT)
Airway suctioning
Effective coughing and positioning

144
Q

medications used for acute respiratory failure

A

Bronchodilators: relief of bronchospasm
Corticosteroids: reduction of airway inflammation
Diuretics and mucolytics: reduction of pulmonary congestion
Antibiotics: treatment of pulmonary infections
Benzodiazepines: sedation (increased risk for delirium)
Analgesics: pain management
Neuromuscular blocking agents (NMBA): optimize ventilation and decrease oxygen consumption (ex. ARDS)

145
Q

PH

A

7.35-7.45

146
Q

PaCO2

A

35-45

147
Q

PaO2

A

80-100 - less than 60 is hypoxemia

148
Q

HCO3

A

22-26

149
Q

Bi-PAP

A

bi-level positive airway pressure - less invasive than mechanical ventilation so want to try before mechanical ventilation

150
Q

what do you want to do before intubating patient

A

administer a paralytic and sedative because it is a very invasive procedure. This is not indicated on comatose or cardiac arrest patients

151
Q

what to do following intubation

A

confirm placement, watch skin around tube, monitor labs (especially WBC)

152
Q

Mechanical Ventilation indications

A

Respiratory muscle fatigue – so exhausted they cannot breath for themselves anymore
Apnea or impending inability to breathe
Acute respiratory failure
Severe hypoxia – below 60 besides some COPD who may live around 50

153
Q

Positive pressure ventilation (PPV)

A

Used primarily in acutely ill patients
Pushes air into lungs under positive pressure during inspiration
Expiration occurs passively

154
Q

Positive end-expiratory pressure (PEEP)

A

type of positive pressure ventilation: normal 2-5 – to keep a little pressure to keep alveoli popped open

155
Q

complications of PPV (positive pressure ventilation)

A

↑ Intrathoracic pressure compresses thoracic vessels
Air can escape into pleural space from alveoli or interstitium, accumulate, and become trapped and lead to pneumothorax
Ventilator-associated pneumonia (VAP)
gut filling with air from swallowing it
muscle atrophy from being in bed
fluid retention

156
Q

Ventilator-associated pneumonia (VAP)

A

Pneumonia that occurs 48 hours or more after ET intubation

157
Q

Guidelines to prevent VAP (Ventilator-associated pneumonia)

A

ORAL CARE!!!!!!!
HOB elevation at least 30 to 45 degrees unless medically contraindicated
No routine changes of ventilator circuit tubing

158
Q

artificial airways management

A

watch skin around tube, monitor labs, assess for aspiration, prevent unplanned extubation

159
Q

indication for a tracheostomy

A

Prolonged intubations with unsuccessful weaning, management of bronchial hygiene, obstruction of the upper airway (head & neck trauma), and airway protection

160
Q

advantages to tracheostomy over mechanical ventilation

A 
Less risk of long-term damage to airway
Increased comfort
Patient can eat (potential)
Speaking (potential)
Increased mobility because tube is more secure
161
Q

ARDS

A

Sudden failure of the respiratory system
Extensive lung inflammation and small blood vessel injury.
Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid
Alveoli fill with fluid

162
Q

ARDS is characterized by

A 
Severe dyspnea/Tachypnea
Hypoxia/Hypoxemia
Decreased lung compliance
Alveolar Collapse
Diffuse pulmonary infiltrates
163
Q

ARDs can develop from

A

from a variety of direct or indirect lung injuries:
direct mechanisms such as pneumonia, sepsis, and chest trauma
Indirect: Triggered from outside the lung through the release of tissue damaging inflammatory cytokines that travel to the lungs such as sepsis, trauma, pancreatitis

164
Q

how can pancreatitis cause ARDS

A

diaphragm tenses up because of the pancreatic juices – lung space decreases because the tense diaphragm.

165
Q

phases of ARDs

A

exudative phase, reparative or proliferative phase, and fibrotic or chronic/late phase

166
Q

ARDS exudative phase

A

usually 24-48 hours after lung injury. release of inflammatory mediators which causes permeability. increase permeability causes Damage to the alveolar capillary endothelial cells and alveolar epithelial cells. Begin collapsing.
Proteinaceous fld. Floods alveoli and inactivates surfactant.
Normal gas exchange is compromised triggering diffuse alveolar collapse. V/Q mismatch & Shunting
Worsening hypoxemia that doesn’t respond to supplemental O2.

167
Q

reparative or proliferative phase in ARDs

A

Last up to 1-2 weeks
Influx neuts, monos, & lymphs, & fibroblasts.
Marked by resolution of acute phase & initial repair of the lung OR pt worsens.
Severe Hypoxemia
A patient who reaches this phase may recover fully, or move on to the fibrotic phase.

168
Q

Fibrotic or chronic/late phase in ARDs

A

2-3 wks post initial insult. Fibrotic tissue replaces normal lung structure, scarring.
Causes progressive vascular occlusion & pulmonary hypertension
Require long-term support, mechanical ventilation & supplemental O2

169
Q

pt in Fibrotic or chronic/late phase of ARDs may have

A

isolation, depression, suicidal, at home with O2, not able to do activities anymore

170
Q

ABGs with ARDS

A

initial - hypoxemia and respiratory alkalosis secondary to hyperventilation. then respiratory acidosis and O2 keeps decreasing despite the amount of O2 they are receiving

171
Q

what labs do you want for ARDS

A

rainbow lab - everything

172
Q

treatment for ARDS

A

No definitive treatment currently exists but positioning to prone seems to help. PEEP and nitric oxide (dilator)

173
Q

when to stop prone position with ARDS

A

if there is no response within 48 hours

174
Q

what could go wrong with prone position in ARDS

A 
Kinking of ETT or lines
Gastric residual increase/abd pressure
Pressure ulcers
Brachial plexus injury from positioning
Hemodynamic instability. – watch BP and urinary output
175
Q

concepts important with burns

A

fluids and electrolytes and inflammation

176
Q

burns are injury to the tissue caused by

A

heat, chemical, electrical current, or radiation

177
Q

what occurs after a burn

A

Local and systemic inflammatory reaction

An immediate shift of intravascular fluid into the surrounding interstitial space

178
Q

most common type of burn

A

thermal burn - Caused by flame, flash, scald or contact with hot objects

179
Q

smoke or inhalation burn predictor of mortality

A

the injuries within the airways

180
Q

assessment clues in smoke and inhalation burns

A

facial burns, singed nasal hair, hoarseness, painful swallowing, darkened oral mucosa and nasal membranes

181
Q

associated injuries with smoke or inhalation burn

A
  1. Metabolic asphyxiation:
    Majority of deaths at scene
    Carbon Monoxide (CO) displaces O2 on Hgb leading to hypoxemia
    can occur in absence of burned skin
  2. Upper airway injury:
    Thermally produced; redness, blistering, edema; mechanical obstruction occurs quickly; not always “seen”
  3. Lower airway injury:
    Inhalation of toxic chemicals/smoke
    Clinical manifestations~12 -24 hrs may progress to ARDS
182
Q

chemical burns

A

Contact with:
Acids: hydrochloric
Alkali: drain cleaners
Organic compounds: phenols (chemical disinfectants)

183
Q

chemical burn treatment

A

remove chemical, then clothing, flush with copious amounts of water

184
Q

iceberg effect

A

occurs with electrical burns - majority of damage beneath the skin making it hard to determine extent of injury
Important to know point of contact

185
Q

electrical burn patients are at high risk for

A

Very high risk for fall injuries/fractures
- C-spine injuries
Dysrhythmias/cardiac arrest (v.fib/vtach), severe metabolic acidosis, myoglobinuria, acute tubular necrosis/acute kidney injury

186
Q

pain from cold thermal injury can last

A

for weeks to years.

187
Q

two types of burn injury classification

A
  1. Lund-Browder chart (more accurate)
    - Percentages = 100%
  2. Rule of Nines (adults)
    - Head & neck 9%
    - Arms 9% each
    - Ant trunk 18%
    - Post trunk 18%
    - Legs 18% each
    - Perineum 1%
188
Q

which burn injury classification is more accurate

A

lund-browder chart

189
Q

severity of burn is determined by

A 
Extent of burn
How much of the body
Depth of injury
Location of burn
Risk factors:
- Preexisting heart, lung, kidney disease has poorer prognosis; alcoholism, drug abuse, malnutrition, or other injuries sustained
190
Q

depth of the burn

A

superficial partial thickness, deep partial thickness, or full thickness

191
Q

Superficial Partial thickness

A

epidermis to dermis
more painful then deep partial thickness and full thickness
Sunburn

192
Q

Deep partial thickness

A

deep dermis including sweat & oil glands)

193
Q

Full thickness

A

All layers of the skin & beyond including bone & muscles
Release of myoglobin and hemoglobin

194
Q

burns put patients at risk for

A

hypovolemic shock (greatest initial threat)

195
Q

hypovolemic shock

A

Massive shift of fluids out of vascular space
Water, sodium and protein move into the interstitial spaces and potassium is released into the circulation (i.e. increased risk for cardiac dysrythmias). Significant 3rd spacing occurs during this time period…remember water loves salt! These patients also lose huge amounts of volume due to evaporation (burns are often HOT), and they are no longer able to control their body temperature, there is hemolysis of RBC’s. Due to the shifting of fluids and evaporation there is a significant decrease in blood flow to the kidneys putting them at risk for acute kidney injury, if their fluids and electrolytes are not fixed, death may result.

196
Q

emergent phase for burn pts

A

Resuscitation of the patient
~24-72 hrs. Always consider other injuries!
Primary concerns: Hypovolemic shock and edema
Perfusion, fluids & electrolytes, inflammation
Ends when fluid is resuscitation has mobilized and diuresis begin

197
Q

priorities during emergent phase for burn pts

A

Assess & re-assessment of ABC’s;
Perfusion and oxygenation
VS and cardiac rhythm
LOC

198
Q

acute phase in burn pts

A

Wound Healing…weeks to months
↓ edema, burns are more evident
Necrotic tissue begins to slough
Electrolyte abnormalities:
Hyponatremia or hypernatremia
Risk of: infection/sepsis, contractures, ileus, ↑ FSBS (stress), pain, psychosocial distress
Phase ends when burned area is covered by skin grafts or wounds are healed

199
Q

rehabilitation phase for burn pts

A

Healed, patient can perform self care
↑ risk for contractures & scar tissue
Emotional support, self esteem issues

200
Q

Management for Burns

A 
airway management 
Fluids:
Large bore IVs or central Line
Crystalloids, colloids; combo
Weight specific. 
pain meds 
wound care
201
Q

Goal of urine output for burn patients

A

30-50 ml/hr

202
Q

Partial-thickness burn assessment

A

pink or cherry red, wet & shiny w/ serous exudate (may or may not have blisters) & painful to touch or exposed to air

203
Q

Full thickness burns assessment

A

dry & waxy white to dark brown or black and minor/localized sensation. See Grafting

204
Q

Debridement

A

necrotic tissue is removed (Bedside, tub or OR)

205
Q

Open method to wound care

A

burn covered in topical antimicrobial and no dressing over the wound

206
Q

closed method to would care

A

sterile gauze laid over topical antimicrobials

Changed Q12-24hr depending on product

207
Q

Fasciotomies & Escharotomies

A

surgical procedure where the fascia is cut to relieve tension or pressure
Utilized for respiratory or vascular compromise

Nursing school level 4 (6 decks)

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