Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NPTE Study > 4.2 - CVP - PPT CVP DDX (Pulmonary Section) > Flashcards

4.2 - CVP - PPT CVP DDX (Pulmonary Section) Flashcards

Week 4, Tuesday

1
Q

Describe the muscles of inspiration

A

Diaphragm

External intercostals (elevates ribs)
SCM (elevates sternum)
Pec Minor (pull ribs outwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe muscles of expiration

A

Relaxation of diaphragm

Internal intercostals (pull ribs down)
Abdominals
QL (pulls ribs down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe how each of the following would deviate the trachea

Tension pneumothorax
Pleural effusion
Space-occupying lesion
Pneumectomy
Pleural fibrosis
Atelectasis (collapse of part / all of lung)

A

Space-occupying lesion -> pushes trachea away
Collapse of lung -> pull trachea towards it

Contralateral:
- Tension pneumothorax
- Pleural effusion
- Space-occupying lesion

Ipsilateral:
- Pneumonectomy
- Pleural fibrosis
- Atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the normal respiratory rate for adults & children

A

Adults 12-20
Children 18-30
Newborns 30-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is hyperpnea? Hypopnea?

A

Hyperpnea - increased breathing rate

Hypopnea - decreased breathing rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe a Kussmaul breathing pattern

What causes it?

A

Occurs in response to acidosis (Diabetic ketoacidosis)
- When hyperglycemia >300 mL

Increased tidal volume -> to expel CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe Cheyne-Stokes respiration

When does this typically occur?

A

End of life

Crescendo-decresecndo breathing w/ pauses between these cycles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are vesicular breath sounds?

A

Normal breath sounds

“gentle breeze”, “wind in leaves”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the following adventitious breath sounds & potential causes

Crackles (rales)
Wheezes
Rhonchi
Stridor

A

Crackles (rales) - fluid / air bubbles in the alveoli
- Pulmonary edema, pulmonary fibrosis, infection, CHF

Wheezes - high-pitched wheezing
- Asthma

Rhonchi - continuous, low-pitched; comes from copious secretions; “snoring, gurgling, rumbling” (“snoring rhino”)
- Pneumonia, bronchitis, cystic fibrosis, COPD

Stridor - high-pitched whistling; upper airway blockage / object
- Tracheal stenosis, object obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does pneumonia often show up on a chest x-ray?

A

Radioopaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How many lobes does each lung have?

A

R) 3 lobes
L) 2 lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe atelectasis vs pneuomothorax

A

Atelectasis - partial lung collapse (due to interference w/ natural forces that promote lung expansion)
- treatment: a) Deep breathing exs; b) Chest PT - postural drainage, percussion, vibration; c) time

Pneumothorax - whole lung collapse (due to collection of air or gas in intrapleural space
- Treatment: chest tube

(Jobst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does pulse oximetry measure?

Describe the normal range

What can cause inaccuracies with pulse ox?

A

Measurement of arterial oxygen saturation

Normal range: 94-100%

Inaccuracies: nail polish, anemia, low perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the recommendation for SpO2 during exercise

A

Want to maintain SpO2 >90% during exercise

If <90%, titrate oxygen according to hospital guidelines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can be used to increase SpO2?

A

Position change, deep breathing, pursed-lip breathing, supplemental O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can anemia affect pulse oximetry readings?

A

Even though patient has low Hb, pulseOx only reading % of that Hb that has oxygen

May have high SpO2, but have very little O2 in blood due to deficiency in RBC or Hb

(Jobst)

17
Q

Describe restrictive lung disease vs obstructive lung disease

Examples of each

A

Restrictive lung disease
- “Volume problem”
- Reduced expansion of lung
- Decreased total lung capacity
- Decreased forced vital capacity
- FEV1/FVC ratio is normal (“you mobilize all your air, but just don’t have much of it”)

Ex: SCI, scoliosis, pulmonary fibrosis

Obstructive Lung Disease
- “Flow problem”
- Normal total lung capacity, forced vital capacity
- Decreased FEV1/FVC ratio

Ex: COPD, chronic bronchitis, emphysema, asthma

18
Q

Describe the FEV1/FVC ratio is restrictive vs obstructive lung disease

A

Restrictive: FEV1/FVC = normal
- Flow is fine, but less volume

Obstructive: FEV1/FVC = <0.8
- Flow is impaired

19
Q

Describe each of the following lung volumes

Tidal Volume
TLC
VC
RV
ERV
IRV
FRC

A

Tidal volume - amount of air expired w/ each breath during quiet breathing (~500 mL)

TLC - total amount of air in lunges after maximum inspiration

VC - maximum amount of air that can be exhaled after maximum inhalation

RV - volume of air remaining in lungs after maximum expiration

ERV - additional air that can be exhaled after normal TV

IRV - additional air that can be inhaled after normal TV is inhaled

FRC - amount of air remaining in lungs after normal tidal expiration

20
Q

Describe how the lung volumes / capacities change w/ restrictive & obstructive lung diseases

A

Restrictive - reduce lung volumes & capacities

Obstructed - “hyperinflated” lung volumes & capacities
(problem is with flow / expiration, not volume)

21
Q

What is COPD?

A

Chronic airflow limitation caused by a mixture of small airway disease and parenchymal destruction

22
Q

Describe the pathogenesis of COPD

A

Chronic inflammation of lung tissue –> small airway disease & parenchymal destruction –> progressive airflow limitation

Small airway disease:
- Airway inflammation
- Airway fibrosis
- Increased airway resistance

Parenchymal destruction:
- Loss of alveolar attachments
- Decreased elastic recoil

23
Q

Describe the mechanisms of airflow obstruction in COPD

A
  • Inflammation (w/in airways narrow lumen)
  • Mucus (obstructs small airways)
  • Scarring (in small airways)
  • Collapse of airways (due to lung parenchyma no longer holding them open)
24
Q

Describe the clinical presentation of COPD

A

Productive cough
Dyspnea on exertion (progresses to dyspnea at rest)
Hyperinflation (“barrel chest”)
Cyanosis
Nail clubbing
Difficulty w/ expiration
Hypoxemia, hypercapnia

CXR:
- Hyperinflated lungs
- Flattened diaphragms

25
Q

Describe the FEV1/FVC in those w/ COPD

A

Clinical diagnosis of COPD: post-bronchodilator FEV1/FVC <0.70
- confirms persistent airflow limitation

26
Q

What are the 2 primary subtypes of COPD?

A

1) Emphysema
- “Pink puffers”

2) Chronic bronchitis
- “Blue bloaters”

27
Q

Describe emphysema

Describe the clinical presentation

Describe treatment

A

Permanent enlargement of air spaces in the alveoli, loss of elasticity
Lungs become hyperinflated

“Pink puffer”
Hyperventilation
Severe dyspnea
Accessory muscle use for breathing
Cachexic appearance (mm wasting bc using lots of energy to breathe)
Tachypnea
Barrel chest (lungs lose elastic ability)

Treatment:
- Teach energy conservation
- Teach breath control - do NOT encourage “deep breaths (they don’t have a problem getting air in); prolong exhalation phase (pursed lip breathing); pause at top of inhalation
- Infection control

28
Q

Describe chronic bronchitis

Clinical presentation

Treatment

A

Chronic inflammation of bronchi & bronchioles; increased tracheobronchial mucus production

Clinical Presentation
- Pallor
- Cyanosis (sign of deoxygenation)
- Bloating (result of edema)
- Lots of sputum
- Dyspnea
- Recurrent infections

Treatment:
- Hydration (makes mucus thinner)
- Airway clearance techniques
- Smoking cession
- Prevent infection

29
Q

What is Pancoast’s tumor?

Describe the clinical presentation

A

Apical tumor of lung

Clinical Presentation
Mimics thoracic outlet syndrome!
- Horner’s syndrome (sympathetic damage) - miosis, ptosis, enophthalmos
- Sharp shoulder pain, axilla, subscapular areas
- Pulmonary symptoms - dyspnea, cough, hemoptysis

PULMONARY SYMPTOMS w/ TOS or shoulder pain should be a RED FLAG

30
Q

Describe asthma

Clinical presentation
Treatment

A

Bronchoconstriction
Obstructs passage of air through the bronchi and bronchioles
- Increased responsiveness of airway smooth muscle to various stimuli

Stimulus triggers cascade of inflammatory cells –> “Spasm, swelling, secretions”
- Bronchial muscle spasm
- Inflammation of mucosa
- Mucus overproduction

Clinical Presentation:
- Increased work of breathing
- Tachypnea
- Wheezing
- Dry cough
- Chest tightness

Treatment:
- Stop activity
- Use rescue inhaler (short-acting bronchodilator)
- Sit up

If inhaler isn’t working –> call 911 (keep using inhaler until ambulance arrives)

Asthma medications:
- Bronchodilators (beta-agonists)
- Albuterol inhaler

31
Q

Describe potential side effects of bronchodilators

A

Bronchodilators = beta-agonists

Boosts sympathetic NS
- Bronchodilation
- Increased HR
- Increased BP

32
Q

Describe potential triggers for exercise-induced bronchospasms (asthma)

A

Hyperventilation (due to exercise itself)
Cold air
Dry air

33
Q

Prevention of EIB

A
  • Good control of asthma
  • Pre-exercise prevention (short-acting bronchodilator 20-30 min before exs)
  • Gentle, intermittent warm-up
  • Promote nasal breathing
  • Incorporate proper cool-down of at least 10 min
  • Exs in warm, humid envt

NPTE Study (49 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions