Respiratory Part 1 Flashcards
(215 cards)
1
Q
Acid-Base Balance
A
The process of regulatingthe pH, bicarbonateconcentration, and partialpressure of carbon dioxideof the body fluids
Regulated through respiratory and renal functions
2
Q
Gas Exchange
A
oxygen is transported to the cells and carbon dioxide is transported from the cells
3
Q
Perfusion
A
flow of blood through arteries and capillaries delivering nutrients and oxygen to cells and removing cellular wastes
4
Q
Upper Respiratory Tract anatomy
A
Nasopharynx
Oropharynx
Laryngopharynx
5
Q
Lower Respiratory Tract anatomy
A
Bronchioles (Trachea)
R and L lung
- alveolar ducts
- alveoli
6
Q
What the different airway obstructions?
A
- blockage from alveolar compromise (Pulmonaryedema)
- collapsed lungs (Atelectasis)
7
Q
Pulmonary edema (cardiogenic) caused by
A
backup of fluid that the heart cannot clear
8
Q
Non-cardiogenic PE caused by
A
inflammation from injury and/or infection
ARDS (trauma to the lungs causing redness and swelling)
9
Q
Atelectasis is caused by
A
collection of air or blood outside the lung but within the pleural cavity - a portion of the lung collapses
- Pneumothorax
- Hemothorax
10
Q
Pulmonary embolism occurs when
A
blood clot that is lodged in a blood vessel in the lungs blocking blood flow to part of the lung.
- Surgical pts, clotting disorders prone
11
Q
Perfusion obstruction includes
A
pulmonary embolism
12
Q
Tidal volume
A
the volume of air exchanged with each breath
13
Q
6-8mL/kg is approximately what in mL of tidal volume
A
400-500
14
Q
FiO2 is
A
fraction of % of inspired O2
15
Q
RA FiO2
A
21%
16
Q
Nasal Cannula 4-6L FiO2
A
37-45%
17
Q
High Flow 60L/min FiO2
A
100%
18
Q
MAP normal
A
> 65 mmHg (perfuse organs)
19
Q
If the MAP is extremely high, what is happening
A
no perfusion
- no cap refill, mottling
20
Q
What is the formula for MAP?
A
SBP + 2 (DBP) / 3
21
Q
MAP shows
A
how much Oxygen is being perfused in the tissues
22
Q
ABGs is used to
A
maintain homeostasis
- Respiratory CO2
- Metabolic HCO3
23
Q
pH normal
A
7.35-7.45
24
Q
< 7.35 pH
A
acidic
25
> 7.45 pH
alkalosis
26
PaO2 normal
80-100 (how much O2 is in arterial blood)
27
SaO2 normal
>95%
28
PaCO2 normal
35-45 mmHg
29
<35 PaCO2
hypercapnic
30
>45 PaCO2
hypercapnic (retaining too much
31
HCO3 normal
22-26
32
CO2 is the
ACID component of our blood
- lungs regulate the CO2 levels within minutes
33
To compensate for acidosis
RR and depth will increase to blow off CO2
34
To compensate for alkalosis
the RR and depth will decrease to retain CO2
35
PaO2/FiO2 Ratio is used to determine
determine lung injury
36
Normal Lung ratio
300-500
37
Acute lung injury ratio:
200-300
38
ARDS: < 200
very significant injury
39
ARDS: <100
severe injury with high mortality
40
Acute lung injury is like ARDS but has
less of a shunt resulting in hypoxemia
41
Normal lungs require
little outside O2 to maintain a normal PaO2
- 21%
42
As lungs become injured, they require
higher concentrations of supplemental O2
43
Lung injury formula
PaO2 (arterial O2) divided by FiO2 (oxygen %)
44
V/Q is the
ventilation to perfusion ratio
45
(V)
air moving in & out of the lung
- bringing oxygen in to /removing CO2 from the alveoli
46
(Q)
blood circulating to areas of the lung
- removing O2 from the alveoli and adding CO2 so the Co2 can be blown off by the lungs
47
In the lungs normally, V and Q are
the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical
48
Why is the V/Q ratio important?
the ratio between the ventilation and the perfusion is one of the major factors affecting the alveolar (and therefore arterial) levels of oxygen and carbon dioxide
49
If the V and Q are imbalanced, the patient will develop
hypoxemia on RA
- providing O2 will correct until the true cause can be addressed
50
A clot in the vascular or perfusion side prevents blood from circulating effectively in the pulmonary capillary in that area where some of the alveoli are, so even if the alveoli bring in O2 the blood stream cannot pick it up in that area – it is a _________ issue.
perfusion
51
If pneumonia secretions are sitting in the alveoli preventing breathed in oxygen to reach the pulmonary capillary of those alveoli the blood rushes by but is unable to pick up oxygen in that area – it is a ____________ issue.
These situations create a VQ mismatch and in these cases cause a respiratory failure event.
ventilation
52
Hypoxemia Respiratory Failure
decreased O2 gas exchange
- **V/Q mismatch or impaired diffusion at alveolar level**
- ventilation or perfusion failure
53
Early hypoxemia PaO2
<80
54
Late hypoxemia PaO2
<60
55
Hypoxemia leads to
Inadequate alveolar ventilation causing hypoventilation
56
Inadequate alveolar ventilation causing hypoventilation
- alveolar blockage
- perfusion blockage
- airway obstruction
- respiratory depression
57
Alveolar blockage includes
pulmonary edema
pneumonia
ARDS
cystic fibrosis
58
Perfusion blockage
pulmonary embolism
59
Airway obstruction
Asthma
COPD
Anaphylaxis
Atelectasis
Bronchospasm
60
Respiratory depression
opioids overdose
61
Hypercapnia
decreased CO2 removal
- causes ventilation failure
62
Late hypercapnia PaCO2
>50
63
Early hypercapnia PaCO2
>45
64
Hypercapnia can lead to
inadequate alveolar ventilation causes hypoventilation and CO2 retention
65
Hypoventilation and CO2 retention caused by
- CNS (spinal cord injury and opioid overdose)
- Neuromuscular (MS and ALS)
- Barrel chest, kyphosis, trauma - open thorax wound
- COPD and Cystic fibrosis
66
Hypoxia is the 1stsign of
hypoxemia ...
67
Hypoxia is the
reduction of O2 at the tissue level (SaO2)
68
Hypoxemia is the
reduction of arterial oxygen tension or partial pressure of oxygen PaO2
69
S/S of hypoxemia respiratory failure
Dyspnea
Tachypnea & tachycardia
Coughing
Wheezing
Confusion
Cyanosis (Bluish/purplish) color in skin, fingernails, and lips
70
Hypercapnic respiratory failure is also known as
ventilatory failure
- decreased ventilation or CO2 removal
71
COPD patients typically have a higher rate of
CO2
72
S/S of Hypercapnic
Hypoventilation (dyspnea) – unable to remove CO2 from body
Tachycardia
Diaphoresis
Headache
Restlessness
Change in consciousness – CO2 sedates – so very lethargic
73
Consequences of hypercapnia
slow changes in CO2 allow for compensation (tolerate high CO2 better than low O2)
- TX PRIMARY CAUSE BEFORE THEY DETERIORATE
74
When CO2 levels cannot be maintained within normal limits by the respiratory system, one of two primary problems exists:
(1) an increase in CO2 production
(2) a decrease in alveolar ventilation.
75
Hypoventilation caused by
Blockage in alveoli
Airway obstruction
Perfusion blockage
Issues with mechanical movement of thorax
76
What happens in hypoxemia or hypercapnia?
Diffusion limitation
Shunting
Alveolar hypoventilation
77
Shunting
blood exits the heart without taking part in gas exchange as this is a perfusion issue:
- i.e. cardiac-like septal defect, cardiogenic pulmonary edema
- PE is not going to be perfused
78
Diffusion limitation occurs when
gas exchange across the alveolar-capillary membrane is compromised by either the destruction of the alveoli or blockage within the pulmonary capillaries
SO EITHER PERFUSION AND/OR VENT ISSUES: i.e., ARDS, pulmonary edema
79
Alveolar hypoventilation
decrease in ventilation that causes hypercapnia and hypoxemia which is typically caused by vent issues:
- i.e. CNS conditions, acute asthma, chest wall dysfunction (respiratory paralysis, flail chest)
80
S/S of early respiratory failure
mental status changes (confusion)
dyspnea
tachypnea
tachycardia
hypotension
refusal to take oral fluids
decreased urination (concentration)
wheezing
persistent cough
81
Late s/s of respiratory failure
bradycardia
bradypnea
increased CO2 **HA morning, decreased LOC and RR**
lethargic
unresponsive
cyanosis (PaO2 is < 45)
82
What does cyanosis look like in darker skin tones?
purple (lips, oral mucous, clubbing
pallor (hands, conjuctivia)
83
ARDS is
pulmonary edema due to trauma or infection
84
Causes of ARDS
Aspiration of gastric contents
Near drowning
MVC
Chemical Inhalation (paints etc.) – need to wear a mask
**Sepsis**
COVID-19
**Viral pneumonia, fat emboli, decreased surfactant production, fluid overload, and shock**
85
S/S of ARDS
Changes in LOC
Severe dyspnea and coughing
Tachypnea and shallow
**Inspiratory crackles – Rice Krispies**
**Hypoxemia unresponsive to O2**
Tachycardia
Cyanosis
Orthopnea – can’t breathe when lying down (sit them up)
increased WBC
respiratory distress
86
These s/s of ARDS cn lead to what intervention
- Profound dyspnea,
hypoxemia,
increased WOB
respiratory distress
endotracheal intubation
87
A chest x-ray of ARDS shows
white out and plural effusions
88
ARDS can lead to
severe hypoxemia
hypercapnia
metabolic acidosis
organ dysfunction
89
ARDS phases
Exudative
Proliferative
Fibrotic
90
ARDS Exudative phase
Cell injury and inflammation
Alveolar edema decreases ventilation > hypoventilation occurs
- Low PaO2 and elevated PaCO2
- Whiteout on chest xray
Respiratory failure
- Classic sign >**refractory hypoxemia (PaO2 < 60 mmHg)**
Assisted ventilation needed
91
ARDS Proliferative phase
Edema fluid resorption
Recovery phase
92
ARDS Fibrotic phase
Fibrosis of lungs
Ventilator dependent breathing
93
Nursing interventions for ARDS
Assess respiratory rate, depth, and vitals
Administer oxygen
Fowler’s position (45 degrees)
Mobility – passive ROM, TCDB, turn the whole body (turn on the good side (good lung) to cause secretions)
Restrict fluid intake (Daily wts and I&Os)
Breathing treatments (AIMS)
Administer diuretics and/or glucocorticoid steroids (Furosemide and K
Prepare for intubation and mechanical ventilation if the patient declines
94
What position should a patient with ARDS lay on
the good side to get rid of secretions
95
What respiratory secretions are Rx to ARDS patients?
AIMS
- 1st Albuterol
- Inhaled and IV steroids
96
Blood sugar does what on steroids
goes up
97
If K is low
dysrhythmias and muscle weakness
98
Atelectasis causes
Pneumos: VALI (Ventilator Induced Lung Injury) – high PEEP and/or Tidal Volumes on vents
Either: Trauma
– MVC, gunshot wound,
99
Pneumothorax
open/closed wound causing air to enter chest wall
100
Hemothorax
blood in the pleural space causing atelectasis
101
S/S of Atelectasis
Tachycardia
Hypotension
Tachypnea
Shallow breathing
Hypoxia
Chest pain
Tension Pneumo = tracheal deviation
102
Pneumothorax causes
blunt or penetrating chest injury, certain medical procedures (high tidal volumes on mechanical vents), or lung disease
103
VALI
(Ventilator Induced Lung Injury) caused by high PEEP levels and/or Tidal Volume too high on ventilator; car crash with rib fractures causing either pneumo and/or hemo.
104
PEEP
Positive End-Expiratory Pressure
105
On a dry suction chest tube, the orange bellow means
connection to suction
106
Dry chest tube suction
stays at the suction on the dial regardless of the suction on the wall
107
Bubbling in the wet chest tubes suction chamber intervention
nothing normal (expected)
108
The water seal chamber should not
constantly bubble
= air leak
109
If pneumothorax in the water seal chamber bubbles
occasionally okay not constant
**on expiration**
110
If the chest tube becomes dislodged then
place in sterile water and place a 3 sided dressing on the incision site
111
What type of pressure is the chest tube restoring
negative pressure with releasing air or blood
112
Pneumothorax chest tubes are placed in
upper portion
113
Hemothorax chest tubes are placed in
placed in the lower portion
114
Nurses should assess for what in atelectasis patients
- Absent breath sounds on the affected side
- Cyanosis
- Dyspnea
- Decreased chest expansion unilaterally
- Hypotension
- Sharp chest pain
- Subcutaneous emphysema – CO2 or air leaking into the skin causing crepitus (crackling) feeling in skin
- Tracheal deviation to the unaffected side with a tension pneumo
=Tension pneumos seen with closed pneumos from closed-chest wounds or mechanical ventilation
=Creates a “one way” valve which allows air out of the lung, but not out of the pleural space creating a tracheal deviation
- Monitor skin around insertion site
- Keep patient moving by turning frequently
- Keep sterile gauze at the bedside to place over site if the tube becomes dislodged
115
Mobility for atelectasis patients
ROM
TCDB
Turn frequently
116
Care of chest tubes
Dislodged from patient
Sterile dressing over site, taped on 3 sides, and call the physician immediately
System breaks
Insert tube into sterile water or saline
Milking, stripping or clamping
NOT recommended
117
The drainage chamber is marked each
shift for output
118
If the drainage chamber is full,
chnage out system with a new one
119
Miking, clamping, striping could cause increase of
pneumo or cause a pneumo if the patient has a hemo
120
What to do if chest tube becomes dislodged?
Cover the site with a sterile dressing, and tape on three sides (this allows air to escape and prevent tension pneumothorax) and notify physician immediately.
121
What do you do if the System breaks?
Insert the tube 1 inch into a bottle of sterile water or sterile normal saline and obtain a new system.
122
Milking or stripping tubing?
Not recommended anymore because it creates too much negative pressure (always follow hospital policies)
123
Clamping tubing?
Increase risk of patient developing a tension pneumothorax. Never do it without an order and follow hospital policies.
124
Wet system type of chest tube
suction control uses water for the pressure
125
Dry system type of chest tube
suction control has a bellow (orange) for the pressure.
126
If the patient has a pneumothorax, the drainage chamber will have
nothing to monitor
127
Wet system suction chamber
needs water to suction
- refill PRN to Rx pressure as it evaporates overtime
- continuous bubbling noted as expected in wet system
- connect to suction
128
Dry system suction chamber
connected to suction and the orange bellow needs to be seen in the suction control window.
- There is no water in the suction control chamber with a dry system
129
Water seal chamber (wet and dry)
continuous bubbling = leak in system
- normal for tidaling (water move up and down) with inspiration
130
How do you identify crepitus?
Palpate around chest tube insertion site
- air leaking under the skin
131
Pulmonary embolism
Embolus lodged within the pulmonary system
132
PE causes
DVT (common), cancer, fat emboli (trauma – pelvic fx)
133
PE s/s
Severe dyspnea, tachypnea
Hypoxemia unresponsive to oxygen therapy
Chest pain
Tachycardia, diaphoresis
Changes in mental status
**Syncope
Cyanosis
Pallor**
134
How do you dx PE?
D Dimer lab – elevated levels from proteins that break down blood clots
CT Scan (1st)
135
What drugs combined can cause DVT - PE?
Dextromethorphan (Niquil) contraindicated with antidepressants
- Straddle
136
PE nursing interventions
Assess respiratory rate, depth, and vitals (1st)
Elevate HOB
**Oxygen
Heparin therapy (PT, black stools-GI and stomach)**
Warfarin (takes several days)
Mobility - cautious (ROM, TCDB, frequent turning)
Nutrition - deficits, calories, tube feedings, oral eating
Teaching about anticoagulant therapy
137
Coumadin (Warfarin) needs to limit
Vitamin K (moderation)
- green leafy veggies
138
Everything involving respiratory nursing mgmt
Assessment (VS, lung sounds, rate and depth of breaths, work of breathing)
Positioning (HOB, aspiration = side-lying, unilateral/bilateral
O2 Therapy (PaO2 > 60, SaO2 >95%)
Dx (CBC = WBC, RBC, **H&H**, platelets, ABG (sedative - retaining too much CO2)
- Chest Xrays = infiltrations, confirm chest tube placements (Hemothorax if white at the bottom)
Pharmacologic therapy and reassessments
Nutritional therapy
Mobility
sleep
pt education
139
If the patient is on a ventilator, then the patient should be
prone to move secretions
140
ARDS has a fluid
restriction
141
COPD patients with CO2
rely on the hypoxic drive to breathe.
- chemoreceptors that recognize CO2 are less sensitive to Co2.
- lack of oxygen that causes them to breathe.
-too much oxygen, they might become severely hypoxic because their drive to breathe is high CO2 and not high O2 levels.
But remember, **never withhold oxygen from a hypoxic patient**
142
O2 Delegation
cannot be delegated to UAP unless it is already in place.
RNs must assess and evaluate the patient before delegation**
143
When should you start enteral feedings with a respiratory/ventilator?
within 48 hours to keep gut working
144
Verify OG or HG tube with
xray confirmation prior to using it
145
What type of diet will a repsiratory patient eat
high protein promote healing
146
Parenteral feedings are through a
central line
147
Turn the pateint every
2 hours if tolerated
148
ROM or PROM should be done
every shift
149
If the patient is not vented then encourage
ambulation (early)
150
Sleep deprivation decreases
healing
151
T/F: Paralytic patients can still hear
yes
152
Pt edu for patient with respiratory problems
Labs and what they mean – understand what they are for so you can pass this along to your patients and their families
Oral care for vented patients
Medications – what are they for? What side effects?
Mobility – Incentive spirometer, ambulation
Sleep – importance of rest
153
Respiratory Meds - Bronchodilators
Beta blockers (1st albuterol)
Anticholinergic (2nd Ipratropium)
Methylxanthines
BAM and SLaM
154
Respiratory Meds - Anti-inflammatory
Steroids (Beclomethasone and Flutaxaxone – inhaled steroids)
Leukotriene inhibitors –(Montelukast)
Mast Cell stabilizers
155
Beta 2 Agonist
Albuterol 1st line for ashtma attack
- dilate bronchodilators
- immediate action
156
What are the expected s/s of Beta 2 agonists?
wheezing to diminish and hearing clear breath sounds
157
Anticholinergics med type
(Ipratropium – 2nd)
158
What are the expected s/s of Anticholinergics
– dry mucous membranes, tachycardia, hot/dry skin
159
Methylxanthines MOA
Bronchodilator and stimulatory effects
- LONG TERM CONTROL OF ASHTMA
caffeine
160
1st and 2nd Ashtma attack meds
**Albuterol – 1st line used for asthma attack
Ipatropium – 2nd line for asthma attack**
161
How to take bronchodilators?
Shake it before you take it
Breathe out, then inhale puffs
2-4 puffs every 20 mins
162
Nebulizer Bronchodilators if not effective after
3 doses = call HCP
163
Which inhaler goes first?
Bronchodilator
steroid inhalers
164
Nebulizer Bronchodilators are effective if
decrease in RR and O2 sats increased >90%
165
Nebulizer bronchodilator side effects (expected)
Tachycardia, Tremors, and insomnia (feels like adrenaline rush)
166
Steroids med types
(Beclomethasone and Flutaxaxone – inhaled steroids)
167
Steroids onset
Slow onset so not used as first line for asthma attack.
168
Inhaled steroids
need to rinse mouth or perform oral care – **DO NOT SWALLOW WATER - as these can cause thrush**
- swish and spit
169
Inhaled steroids on BG
not affect blood sugar, only IV (prednisone) does
170
Leukotriene inhibitors med type
Montelukast
171
Leukotriene inhibitors onset
Slow onset (1-2 weeks) but opens airway
- not a rescue drug
172
What is expected with Leukotriene inhibitors?
cough, sore throat, fatigue, headache
173
Mast Cell Stabilizers onset
Acts fast but is not rescue inhaler
174
Take Mast Cell Stabilizers 15 minutes before
exercise to reduce exercise induced asthma
175
DO NOT USE _______________ or _____________ as a primary for an asthma attack.
Salmeterol or Fluticasone
- long term inflammatory control of the bronchioles
176
How do I know if respiratory drugs are working?
Lung sounds, go down on FiO2 and stats go up, regular, rate
177
After an inhaled steroid on a ventilator patient, what needs to be done?
oral care
178
What diuretics could help respiratory illnesses?
furosemide, hydrochlorothiazide, bumetanide
spironolactone
179
What anticoagulants could help respiratory illnesses?
Injection: heparin, enoxaparin
Oral: warfarin, apixaban, rivaroxaban
180
What anti-inflammatory steroids could help respiratory illnesses?
Oral: prednisone
Oral or injection: methylprednisolone, dexamethasone, betamethasone
Inhaled: beclomethasone, fluticasone
181
Diuretics decrease
BP, decrease fluid (causing increased urination), and dehydrate
182
Furosemide or HCTZ: potassium
wasting
183
Spironolactone potassium
sparing
184
Nutrition education for Furosemide and HCTZ
encourage high potassium foods
Bananas, Oranges, Green leafy vegetables, Liver, avocado
185
Hypokalemia ECG
> flat T waves, prolonged QT, ST depression, U waves
186
ICU patients K needs to be
4-5
187
Spirinolactone nutrition
avoid K
188
Hyperkalemia ECG
peaked T waves, maybe ST elevation, P wave
Hyperkalemia KILLS
189
Anticoagulants do what
decrease the body’s ability to clot and prevent clots from forming allowing the body time to reabsorb and break down clots in the body already. They do not break down clots
**prevnt forming new clots and growth of existing clots
190
Heparins MONITOR
platelets (do not give if less than 100,000 mcL
191
Heparin Labs
PTT 46-70
192
Antidote for Heparin
Protamine Sulfate
193
Actions if PTT >70 or signs of bleeding from Heparin
STOP the heparin gtt and notify provider
Prepare antidote
Reassess labs in 1 hour
194
Warfarin Labs
INR levels for warfarin- therapeutic levels 2-3
195
Antidote for Warfarin
Vitamin K
196
Actions if INR > 4 in Warfarin
Assess for bleeding
Prepare Vitamin K
197
Actions if INR > 2 in Warfarin
Give warfarin to increase INR to 2.5
198
Which anti-coagulant is fast acting?
Heparin
199
Which anti-coagulant is slow-acting?
Warfarin
- 5 days therapeutic levels
200
PE patients in the hospital should be started on
Warfarin
- unless apixaban is Rx
201
Apixaban and rivaroxaban begin working within
few hours of taking so they can start after the heparin therapy. Can start on discharge. Does not require INR testing.
202
Nutrition education for anticoagulants
consistent levels of leafy green vegetables or liver which are high in Vitamin K. They do not have to avoid these but keep it in moderation.
203
ASA and clopidogrel
antiplatelets
204
Glucocorticoids used to
suppress immune responses like inflammation.
205
Prednisone and prednisolone are intermediate acting and have a half life up
36 hours
206
Dexamethasone and betamethasone are longer acting and have a half life up to
50 hours
207
Which glucocorticoid is only give orally?
prednisone
208
Side effects of Glucocortoids
Hyperglycemia, infection, **insomnia**, polydipsia, polyphagia
- No need to report to HCP as this is an expected finding, but should be part of patient teaching
209
Hypokalemia can occur with what interaction cobination: glucocorticoid and
HCTZ and loop diuretics
210
Glucocorticoids can cause insomnia so take
early in the day
211
Patient with severe asthma presents to the ER with the following vital signs: HR 120 BPM, RR 32 BPM, O2 Sat 90% on room air and a Peak Expiratory flow of <40%. What medication would you give? Select all that apply
- Inhaled salmeterol
- Albuterol inhaler
- Nebulizer ipratropium
- IV Methamphetamines
- IV Methylprednisolone
- Albuterol inhaler
- Nebulizer ipratropium
- IV Methylprednisolone
Think AIM – albuterol, ipratropium, steroid
BAM and SLaM
212
The emergency department nurse is assessing a client who has sustained a blunt injury to the chest wall. Which finding would indicate the presence of a pneumothorax in this client?
1. A low respiratory rate
2. Diminished breath sounds
3. The presence of a barrel chest
4. A sucking sound at the site of injury
2. Diminished breath sounds
Rationale:
This client has sustained a blunt or closed-chest injury. Basic symptoms of a closed pneumothorax are shortness of breath and chest pain. A larger pneumothorax may cause tachypnea, cyanosis, diminished breath sounds, and subcutaneous emphysema. Hyperresonance also may occur on the affected side. A sucking sound at the site of injury would be noted with an open chest injury.
213
The nurse instructs a client to use the pursed-lip method of breathing and the client asks the nurse about the purpose of this type of breathing. The nurse responds, knowing that the primary purpose of pursed-lip breathing is to promote which outcome?
1. Promote oxygen intake
2. Strengthen the diaphragm
3. Strengthen the intercostal muscles
4. Promote carbon dioxide elimination
4. Promote carbon dioxide elimination
Rationale:
Pursed-lip breathing facilitates maximal expiration for clients with obstructive lung disease. This type of breathing allows better expiration by increasing airway pressure that keeps air passages open during exhalation. Options 1, 2, and 3 are not the purposes of this type of breathing.
214
The nurse is assessing a client with multiple trauma who is at risk for developing acute respiratory distress syndrome. The nurse should assess for which early sign of acute respiratory distress syndrome?
1. Bilateral wheezing
2. Inspiratory crackles
3. Intercostal retractions
4. Increased respiratory rate
4. Increased respiratory rate
Rationale:
The earliest detectable sign of acute respiratory distress syndrome is an increased respiratory rate, which can begin from 1 to 96 hours after the initial insult to the body. This is followed by increasing dyspnea, air hunger, retraction of accessory muscles, and cyanosis. Breath sounds may be clear or consist of fine inspiratory crackles or diffuse coarse crackles.
215
A client has experienced pulmonary embolism. The nurse should assess for which symptom?
1. Hot, flushed feeling
2. Sudden chills and fever
3. Chest pain that occurs suddenly
4. Dyspnea when deep breaths are taken
3. Chest pain that occurs suddenly
Rationale:
The most common initial symptom in pulmonary embolism is chest pain that is sudden in onset. The next most commonly reported symptom is dyspnea, which is accompanied by an increased respiratory rate. Other typical symptoms of pulmonary embolism include apprehension and restlessness, tachycardia, cough, and cyanosis.
