NURS 453 test 1 Flashcards
(207 cards)
1
Q
COPD characterized by
A
airflow limitation, breathlessness, and exacerbation.
2
Q
COPD disease process os based mainly off of what concept
A
inflammation
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)
4
Q
pulmonary fibrosis
A
thickening of the tissue between the alveoli
5
Q
emphysema
A
damaged alveoli in which they trap air
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
7
Q
emphysema
A
abnormal permanent enlargement of the air spaces which causes a loss of lung elasticity and causes difficulty with exhaling
8
Q
Key preventative measure with COPD
A
smoking cessation to prevent and slo progression of disease
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.
10
Q
antitrypsin (AAT)
A
protects and inhibits lysis of the lung tissue during inflammation.
11
Q
elastin
A
gives elasticity and strength to the alveoli
12
Q
goals for medication during COPD
A
reduce dyspnea, improve exercise tolerance, and prevent complications
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,
14
Q
COPD causes a high risk for
A
depression due to quality of life decrease
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
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
17
Q
late clinical manifestations of COPD
A
clubbing and dyspnea at rest
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
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
20
Q
COPD diagnostics for chronic phase
A
pulmonary function test - determines COPD progression
echocardiogram - determines cor pulmonale
21
Q
characteristics of acute exacerbation of COPD
A
change or worsening of COPD symptoms such as increase in dyspnea, cough, and sputum
22
Q
what would put a acute exacerbation COPD pt Into the ICU
A
worsening hypoxemia, increasing hypercapnia, severe or worsening respiratory acidosis
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?)
24
Q
ABG findings in exacerbation
A
low PaO2 and SaO2
high PaCO2
normal or low PH
high HCO3
25
COPD meds for maintenance
anticholinergic agents (ipratropium)- long acting, steroid with LABA (Advair or Symbicort)
26
COPD meds for acute exacerbation
short acting beta 2 agonist (albuterol), antibiotic, steroid
27
bronchodilators
relaxes smooth muscles and improves lung ventilation
28
mucolytic agents
help thin secretions making them easier for the pt to expel
29
caution with beta blockers with COPD pts, why?
it can cause the bronchioles to constrict
30
types of breathing for COPD
pursed lip - prolongs exhalation
| diaphragmatic breathing - achieves maximum inhalation and decreased RR
31
Patient care goals in COPD
conserve energy, reduce fatigue, facilitate removal of secretions
32
Patient care goals in COPD
conserve energy, reduce fatigue, facilitate removal of secretions
33
smoking cessation strategies
pharmacological support and one to one counseling
34
pharmacological support for smoking cessation
Nicotine supplements, bupropion (wellbutrin, zyban), varenicline (chantix)
35
pulmonary hypertension
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.
36
pulmonary hypertension classic symptoms
dyspnea on exertion and fatigue due to low cardiac output
37
is pulmonary hypertension curable
no
38
#1 cause of pulmonary hypertension
COPD but there are a lot of reasons that can lead you to PH such as PE, HF, or medications
39
pulmonary hypertension labs
ABGs, CBC, electrolytes, BNP
40
diagnostic studies for pulmonary HTN
right cardiac Cath, 12 lead ECG, CT scan
41
right cardiac Cath
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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cor pulmonale
Enlargement of the right ventricle secondary to primary disorder or disease of the pulmonary system
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most common cause of cor pulmonale
COPD. pulmonary HTN is usually a preexisting condition but not always
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clinical manifestations of cor pulmonale
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
45
Right sided heart failure signs and symptoms
```
Peripheral Edema 3+
Weight Gain
JVD
Full, Bounding Pulse
Enlarged Liver
```
46
care for cor pulmonale
treat underlying condition, O2, palliative care procedures
47
goal of Pharm management of PH and Cor Pulmonale
promote vasodilation of pulm vasculature, RV overload, & reverse remodeling
48
meds for PH and cor pulmonale
calcium channel blocker, vasodilators, endothelial receptor antagonist, viagra, oxygen, diuretics, anticoagulants, inotropic agents
49
endothelial receptor antagonist
Given PO; binds to endothelin-1 receptors:↓ PA pressures, ↑ cardiac output
for PH and cor pulmonale
50
DVT is a concept of
inflammation
51
PE Is a concept of
perfusion that causes an issue of oxygenation and ventilation
52
pulmonary thromboembolism
Obstruction of one or more of the pulmonary arteries or one of it’s branches by a thrombus (VTE/DVT)
53
if PE is not treated what can happen to the patient
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
54
PE distrupts ____
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
55
Alveolar hypocarbia causes what to happen with the lungs?
low CO2 in alveolar = constriction in lungs
56
where do emboli originate
DVTs primarily LE but sometimes from UE
57
Virchow Triad for PE
Venous stasis
Vascular endothelium injury
Hypercoagulability
58
risk factor for PE
conditions of decreased venous return - Immobility!!
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most common symptom of PE
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
60
labs for pulmonary embolism
ABGs - oxygenation
D-Dimer - clotting in the body
BNP - cardiac ventricular stretch
troponin - how big it is
61
diagnostics for PE
spiral CT unless allergic to IV contrast them V/Q scan. also 12 lead ECG, echocardiogram
62
potential complications post PE
pulmonary infarction due to insufficient blood flow or
| pulmonary HTN due to chronic PE disease or chronic thromboses
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care for PE
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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sign of DVT
Deep calf pain, tenderness, warmth, or redness, unilateral edema
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Massive PE
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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Submassive PE
Acute PE w/ RV dysfunction
| Myocardial necrosis present
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Acute PE:
Signs and symptoms immediately after obstruction
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Thrombolytics
Fibrolytics (AKA Alteplase or tPA)
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Massive PE treatment
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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Submassive PE treatment
Thrombolytics considered on a case by case basis
71
Vitamin-K antagonist
warfarin - is main therapy with PE bridged w/ parenteral anti-coagulants but needs frequent monitoring of INR
72
Direct oral anticoagulants (DOACs)
can be used to treat PE - Examples: Xarelto, Pradaxa, Eliquist. more predictable and no lab monitoring
73
low molecular weight heparin example
enoxaparin sodium - no lab needed
74
warfarin INR goal
2-3
75
when pts are receiving anticoagulation therapy, priority is to
assess for bleeding and all associated signs and symptoms of a potential bleed
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Heparin lab
PTT (goal is 50-90)
77
bridge therapy
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)
78
hyperventilation
blowing off CO2 - vasoconstriction
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hypoventilation
keeping CO2 - vasodilation
80
two types of trauma
blunt force and penetrating
81
signs and symptoms of crush injury
petechiae in the whites of the eyes, cheeks, and face
82
pneumothorax
air in the pleural space resulting in partial collapse of lung - pressure goes from negative to positive
83
clinical manifestations of small pneumothorax
tachycardia and dyspnea
84
clinical manifestations of large pneumothorax
absent breath sounds. Respiratory Distress (shallow, rapid resps, dyspnea, air hunger, O2 desaturation); Chest pain, Cough with or without hemoptysis
85
spontaneous pneumo can happen in
also called a closed pnuemo can occur after rupture of blebs in COPD pt or in tall/thin male with marphans
86
Iatrogenic pnuemothorax
pnuemo that is caused from a medical procedure. This can be from mechanical ventilation or gastric tube and perforation of the esophagus
87
traumatic pneumothorax
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
Treatment of Open (traumatic) Pneumothorax
Should be covered with an occlusive, vented dressing. Allows air to escape and prevent a tension pneumo. Acts as one-way valve
89
Tension Pneumothorax
Rapid accumulation of air in pleural space without the ability to escape. (medical emergency) - respiratory and circulatory collapse
90
late sign of tension pneumothorax
tracheal deviation
91
Hemothorax
Accumulation of blood in the pleural space.
92
how much blood is too much during a hemothorax
250-300 ml of blood (unit of blood)
93
chylothorax
```
Lymphatic fluid in the
Pleural space due to a leak
in the thoracic duct.
-Causes: Trauma, Surgical
Procedures, and Malignancy
```
94
how much fluid is too much
1500-2400 ml.day
95
how to monitor hemodynamic stability
urine output and BP
96
treatment during hemothorax
preserve hemodynamic stability
97
subcutaneous emphysema
air leaking into the subcutaneous layer
98
chest tube should never be
clamped unless given the order to and never milk or strip because it can change the pressure and damager lung tissue
99
what to monitor in patients with chest tube
pain, drainage, that the tube still connected
100
complications of chest tubes
malposition, infection, pneumonia, frozen shoulder from pain
101
what should you do before the doctor removes a chest tube
pre-medicate
102
flail chest
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
sign of flail chest
paradoxical movement - breathing reverses this pattern, which means that during inspiration, the chest contracts, and during expiration, it expands.
104
pulmonary contusion
bruising of the lungs
105
cardiac tamponade
rapid collection of blood in the pericardial sac, reducing filling
106
s/s of cardiac tamponade
muffled, distant heart tones, decrease BP, jugular vein distention, and increase Central venous pressure
107
treatment of cardiac tamponade
it is a medical emergency and a pericardiocentesis or surgical repair needs to occur
108
respiratory failure
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
what causes respiratory failure
abnormalities in any component of the respiratory system
110
what is often present with respiratory failure
hypo perfusion secondary to shock (oxygenation problem)
111
respiratory failure is a major threat of
organ failure, metabolic acidosis, and cellular death
112
two types of respiratory failure
hypoxemic (oxygenation failure) or hypercapnic (ventilatory failure) both can be either chronic or acute
113
hypoxemia
insufficient O2 transferred to the blood - PaO2 less than 60
114
hypercapnia
inadequate CO2 elimination (not breathing fast enough) Co2 above 45 with academia
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causes of hypoxemic respiratory failure
V/Q mismatch, shunt, diffusion limitation, alveolar hypoventilation
116
causes of hypercapnic respiratory failure
abnormal chest wall movement, CNS issue, airways and alveoli
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symptoms of hypoxemic respiratory failure
low SaO2, low PaO2 showing with tachycardia and tachypnea, increased RR, and as a late sign changes in level of consciousness
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ventilation vs perfusion in upper zone of the lungs
greater ventilation
119
ventilation vs perfusion in middle zone of the lungs
equal
120
ventilation vs perfusion in lower zone of the lungs
greater perfusion
121
normal state of ventilation/perfusion
Ideal gas exchange, blood flow and ventilation match
122
abnormal state of ventilation/perfusion
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
perfusion without ventilation
shunt v/q=0
124
normal v/q
=0.8
125
ventilation without perfusion
dead space v/q = infinity (pulmonary embolism)
126
shunt
blood exits heart without having participated in gas exchange
127
anatomic shunt
ventricular/septal defect
128
intrapulmonary shunt
alveoli filled with fluid - ARDS, pneumonia, pulmonary edema
129
diffusion limitation
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
alveolar hypoventilation
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
examples of alveolar hypoventilation
CNS disease, chest wall dysfunction, obesity..
132
specific Manifestations of Hypoxemic Respiratory Failure
Dyspnea, tachypnea, Prolonged I:E time (1:3); nasal flaring, intercostal muscle retraction, use of accessory muscles, abnormal chest wall movement, CYANOSIS (LATE)
133
nonspecific Manifestations of Hypoxemic Respiratory Failure
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
Causes of Hypercapnic Respiratory Failure
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
Initial signs and symptoms of ventilation failure (aka hypercapnic respiratory failure
```
Changes in LOC
↑ HR
↑ RR (initial response)
HTN
Associated to high circulating catecholamines
```
136
Hypercapnic Respiratory FailureABG trends
↓ 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
Specific respiratory manifestations of hypercapnic respiratory failure:
Dyspnea (remember this is a patient complaint), tripod positioning, pursed lip breathing, ↓ tidal volume (or volume of breath), ↓ RR or ↑ RR and shallow
138
Nonspecific manifestations of hypercapnic respiratory failure
Morning headache , confusion, agitation, progressive somnolence, bounding pulse, muscle weakness, ↓ DTRs, DYSRTHMIAS, TREMORS/SEIZURES (both LATE)
139
labs for acute respiratory failure
determine the cause of it! BNP, D-dimer, troponin, CBC< sputum/blood culture, lactic acids, CMP, clotting studies
140
diagnostics for acute respiratory failure
Chest x-ray, consider spiral CT, MRI, VQ scan
12 lead ECG – get for MI, Afib, …
Pulmonary artery catheter (rarely utilized)
141
management of acute respiratory failure
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
oxygen therapy
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
Mobilization of secretions
Hydration and humidification
Chest physiotherapy (CPT)
Airway suctioning
Effective coughing and positioning
144
medications used for acute respiratory failure
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
PH
7.35-7.45
146
PaCO2
35-45
147
PaO2
80-100 - less than 60 is hypoxemia
148
HCO3
22-26
149
Bi-PAP
bi-level positive airway pressure - less invasive than mechanical ventilation so want to try before mechanical ventilation
150
what do you want to do before intubating patient
administer a paralytic and sedative because it is a very invasive procedure. This is not indicated on comatose or cardiac arrest patients
151
what to do following intubation
confirm placement, watch skin around tube, monitor labs (especially WBC)
152
Mechanical Ventilation indications
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
Positive pressure ventilation (PPV)
Used primarily in acutely ill patients
Pushes air into lungs under positive pressure during inspiration
Expiration occurs passively
154
Positive end-expiratory pressure (PEEP)
type of positive pressure ventilation: normal 2-5 – to keep a little pressure to keep alveoli popped open
155
complications of PPV (positive pressure ventilation)
↑ 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
Ventilator-associated pneumonia (VAP)
Pneumonia that occurs 48 hours or more after ET intubation
157
Guidelines to prevent VAP (Ventilator-associated pneumonia)
ORAL CARE!!!!!!!
HOB elevation at least 30 to 45 degrees unless medically contraindicated
No routine changes of ventilator circuit tubing
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artificial airways management
watch skin around tube, monitor labs, assess for aspiration, prevent unplanned extubation
159
indication for a tracheostomy
Prolonged intubations with unsuccessful weaning, management of bronchial hygiene, obstruction of the upper airway (head & neck trauma), and airway protection
160
advantages to tracheostomy over mechanical ventilation
```
Less risk of long-term damage to airway
Increased comfort
Patient can eat (potential)
Speaking (potential)
Increased mobility because tube is more secure
```
161
ARDS
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
ARDS is characterized by
```
Severe dyspnea/Tachypnea
Hypoxia/Hypoxemia
Decreased lung compliance
Alveolar Collapse
Diffuse pulmonary infiltrates
```
163
ARDs can develop from
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
how can pancreatitis cause ARDS
diaphragm tenses up because of the pancreatic juices – lung space decreases because the tense diaphragm.
165
phases of ARDs
exudative phase, reparative or proliferative phase, and fibrotic or chronic/late phase
166
ARDS exudative phase
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
reparative or proliferative phase in ARDs
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
Fibrotic or chronic/late phase in ARDs
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
pt in Fibrotic or chronic/late phase of ARDs may have
isolation, depression, suicidal, at home with O2, not able to do activities anymore
170
ABGs with ARDS
initial - hypoxemia and respiratory alkalosis secondary to hyperventilation. then respiratory acidosis and O2 keeps decreasing despite the amount of O2 they are receiving
171
what labs do you want for ARDS
rainbow lab - everything
172
treatment for ARDS
No definitive treatment currently exists but positioning to prone seems to help. PEEP and nitric oxide (dilator)
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when to stop prone position with ARDS
if there is no response within 48 hours
174
what could go wrong with prone position in ARDS
```
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
concepts important with burns
fluids and electrolytes and inflammation
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burns are injury to the tissue caused by
heat, chemical, electrical current, or radiation
177
what occurs after a burn
Local and systemic inflammatory reaction
| An immediate shift of intravascular fluid into the surrounding interstitial space
178
most common type of burn
thermal burn - Caused by flame, flash, scald or contact with hot objects
179
smoke or inhalation burn predictor of mortality
the injuries within the airways
180
assessment clues in smoke and inhalation burns
facial burns, singed nasal hair, hoarseness, painful swallowing, darkened oral mucosa and nasal membranes
181
associated injuries with smoke or inhalation burn
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
chemical burns
Contact with:
Acids: hydrochloric
Alkali: drain cleaners
Organic compounds: phenols (chemical disinfectants)
183
chemical burn treatment
remove chemical, then clothing, flush with copious amounts of water
184
iceberg effect
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
electrical burn patients are at high risk for
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
pain from cold thermal injury can last
for weeks to years.
187
two types of burn injury classification
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
which burn injury classification is more accurate
lund-browder chart
189
severity of burn is determined by
```
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
depth of the burn
superficial partial thickness, deep partial thickness, or full thickness
191
Superficial Partial thickness
epidermis to dermis
more painful then deep partial thickness and full thickness
Sunburn
192
Deep partial thickness
deep dermis including sweat & oil glands)
193
Full thickness
All layers of the skin & beyond including bone & muscles
Release of myoglobin and hemoglobin
194
burns put patients at risk for
hypovolemic shock (greatest initial threat)
195
hypovolemic shock
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
emergent phase for burn pts
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
priorities during emergent phase for burn pts
Assess & re-assessment of ABC’s;
Perfusion and oxygenation
VS and cardiac rhythm
LOC
198
acute phase in burn pts
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
rehabilitation phase for burn pts
Healed, patient can perform self care
↑ risk for contractures & scar tissue
Emotional support, self esteem issues
200
Management for Burns
```
airway management
Fluids:
Large bore IVs or central Line
Crystalloids, colloids; combo
Weight specific.
pain meds
wound care
```
201
Goal of urine output for burn patients
30-50 ml/hr
202
Partial-thickness burn assessment
pink or cherry red, wet & shiny w/ serous exudate (may or may not have blisters) & painful to touch or exposed to air
203
Full thickness burns assessment
dry & waxy white to dark brown or black and minor/localized sensation. See Grafting
204
Debridement
necrotic tissue is removed (Bedside, tub or OR)
205
Open method to wound care
burn covered in topical antimicrobial and no dressing over the wound
206
closed method to would care
sterile gauze laid over topical antimicrobials
| Changed Q12-24hr depending on product
207
Fasciotomies & Escharotomies
surgical procedure where the fascia is cut to relieve tension or pressure
Utilized for respiratory or vascular compromise
