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BNKN602 Exam > Week 2 - Respiratory > Flashcards

Week 2 - Respiratory Flashcards

1
Q

Define Hypoxia

A
  • Less than normal levels of 02 in the body tissues
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2
Q

Define Hypoxemia

A
  • Less than normal levels of 02 in the blood
    - Pa02<80mmHg
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3
Q

Define Hypercapnia

A
  • Greater than normal levels of C02
    - PaC02 > 45mmHg
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4
Q

Define Hypocapnia

A
  • Less than normal levels of C02
    - PaC02 < 35mmHg
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5
Q

What is the normal range of PaC02?

A

35-45mmHg

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6
Q

What is the normal range of Pa02 levels?

A

75-100mmHg

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7
Q

What is the normal range of Arterial Oxygen?

A

75-100mmHg

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8
Q

What are 12 signs and symptoms of hypoxaemia?

A
  1. Changes in the colour of your skin
  2. Confusion
  3. Restlessness
  4. Anxiety
  5. Increased heart rate
  6. Increased respiration rate
  7. Shortness of breath
  8. Sweating
  9. Wheezing
  10. Use of Accessory muscles
  11. Flaring of nostrils or pursed lips
  12. Decreased oxygen saturation levels
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9
Q

What are 8 clinical manifestations that a person would experience with COPD?

A
  1. Frequent chest infections
  2. Persistent wheezing
  3. Persistent chesty cough which can be dry or with sputum
  4. Difficulty breathing
  5. Dyspnea
  6. Decreased energy levels
  7. Tightness of the chest
  8. Swelling in the lower extermities
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10
Q

What is efficient gas exchange dependent on?

A

Adequate Ventilation and Perfusion

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11
Q

What is shunting?

A

When blood flow can be redirected from poorly ventilate alveolus (one air sac) to a well-ventilated alveolus through vasoconstriction

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12
Q

What is a dead space?

A

Poor perfusion and a well ventilated alveolus

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13
Q

What is a silent unit?

A

Poor ventilation AND Poor perfusion (no air moving through the lungs)

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14
Q

What are the two areas of Gas Exchange Insufficiency?

A

Mechanical
Functional

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15
Q

What are the three areas of Mechanical Insufficiency of gas exchange?

A
  • Structural damage
  • Airway obstruction
  • Medication
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16
Q

Describe how structural damage impacts on gas exchange

A
  • Nervous system (spinal injury high up, anything that impacts the nerve pathways)
  • Intercostal Muscles
  • Diaphragm (injury which impacts taking a deep breath to expel CO2 effectively, or on
    inspiration with the intake of O2)
  • Abdominal muscles (Pushing diaphragm out to push the air out)
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17
Q

Describe airway obstruction for gas exchange

A
  • Physiological and foreign objects (asthma, mucous)
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18
Q

Describe how medication can impact on gas exchange

A
  • CNS Depressants (Alcohol, benzodiazepines, sedatives. Anything which effects the
    respiration rate)
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19
Q

What functional factors can impact on gas exchange?

A
  • Cardiac Compromise (Poor venous return)
  • Pulmonary Embolism (Block off blood vessels and lungs - ventilated but not perfused)
  • Tumour (blockage which effects perfusion)
  • Hb (Haemoglobin) (Not enough Haemogolbin = not enough red blood cells to carry
    enough oxygen as Haemogolbin has 4 oxygen particles)
  • Infection (pus, anything in the lungs which block the perfusion in the lungs)
  • COPD
  • Compliance (the ability for the lungs to inflate and recoil)
  • Resistance
  • Surface area (hold the alveolus open, if you lose this, the alveoli might collapse more
    easily as the surface area will be reduced - smoking)
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20
Q

What are 4 problems with ventilation (air in/out)?

A
  • Inflammation of Bronchial walls causing epithelial oedema = decrease air entry, decrease gas exchange
  • Exudate in lower airways causing obstruction to air flow = decrease air entry, decrease gas exchange
  • Exudate in alveoli causing increased diffusion distance = decrease gas exchange
  • Inflammation in alveolar wall causing increased diffusion distance = decreased gas exchange
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21
Q

What are 2 problems with perfusion (blood to lungs and body)?

A
  • Partial or complete obstruction to pulmonary artery (could be a clot and partially close off the artery) causing reduced blood flow = decreased gas exchange
  • Ineffective functioning alveoli (from exudate or oedema) causing vasoconstriction of surrounding pulmonary capillaries = further decrease gas exchange
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22
Q

What clinical presentations are we observing with the respiratory rate?

A
  • Tachypnoea/bradypnoea (fast and slow breathing)
    • Orthopnoea (have trouble breathing lying down, but can breathe normally when sitting up
      heart not pumping efficiently)
    • Dyspnoea (subjective feeling of breathing, reporting they are struggling to breath)
    • Rhythm and depth (are they breathing in a normal rhythm? Gasping? Breathing shallow?)
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23
Q

What clinical presentations are we observing with breath sounds?

A
  • Wheeze
    • Crackles
    • Stridor (usually on inspiration, sounds like a barking type sound. Inflammation or
      obstruction of the airway)
    • Reduced Air entry
    • Cough
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24
Q

What accessory muscles are we observing for within the clinical presentation?

A
  • Sternocleidomastoid
    • Scalenes
    • Trapezius
    • Pectoralis minor/major
    • Abdominals (on expiration)
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25
Q

What clinical presentation are we observing for the patient’s positioning?

A
  • Upright
    • Tripod (leaning forward, supporting upper body with hands on knees/similar)
    • Chest symmetry
26
Q

What clinical presentation are we observing for with Neurological changes?

A
  • Anxiety
    • Agitation
    • Confusion
    • Drowsiness
    • Pain
27
Q

What clinical presentations are we observing for with the skin?

A
  • Diaphoresis
    • Pallor
    • Cyanosis (blue tinge, think about peripheral (capillary refit test.) Looking around the lip,
      face and sternum)
    • Flushing
    • Digital clubbing
28
Q

Define Diaphoresis

A

Clammy all over, dripping with sweat - feel cool and pale, associated with increased metabolic effort, also, hypocapnia can cause this. Not getting enough oxygen in then CO2 levels rise

29
Q

What clinical presentations are we observing for with sputum?

A
  • Colour
    • Odour
    • Haemoptysis (any blood?)
30
Q

What are the 6 signs of respiratory distress?

A
  • Diaphoresis
  • Hypoxia (body is trying to increase reparation rate by increasing chest expansion to get
    oxygen in to the cells and tissues)
  • Respiratory rate (>24)
  • Gasping (associated with running out of energy, RR high, using muscles to keep up with
    breathing, there respiration rate is dropping, turning the rhythm of gasping)
  • Accessory muscle use
  • Symmetry of chest movements
31
Q

What can you measure within a clinical presentation?

A
  • RR, depth and pattern
  • WOB
  • Peak flow measurement
32
Q

How do you measure work of breathing (WOB)?

A
  • Accessory muscle use
    - Nasal flaring/pursed lip breathing
    - Speaking long/short sentences, single words only, not speaking
    - Intercostal undraping
33
Q

How do you measure the Peak Flow?

A
  • Measurement of maximum forced exhaled air flow (L/min)
    - Baseline and to measure the effectiveness of interventions
    - It is useful for people with asthma to see how well they are able to expire air. A guide
    for medication
34
Q

What are some partial obstructions?

A
  • Tongue
    • Vomit
    • Epiglottis
    • Uvulitis
    • Secretions
    • Inflammation
    • Neurological impairment
    • Foreign body
35
Q

What is Emphysema (air or gas trapping)?

A
  • Loss of elasticity allows the alveoli to expand with inspiration but reduces its ability to recoil
    in expiration
    • Results in CO2 being ‘trapped’ increasing the alveolar PCO2 (partial pressure of carbon
      dioxide)
    • Bronchiole constriction also contributes to air/gas ‘trapping’
    • A rise in alveolar PCO2 means CO2 cannot diffuse readily from pulmonary capillaries,
      causing a build up in arterial blood = hypercapnia (increase of partial Pressure of carbon
      dioxide)
36
Q

What is Emphysema (Damaged Alveolar walls)?

A
  • Accumulation of damage causes large air spaces to develop
    • The surface area is reduced, reducing gas exchange between alveoli and pulmonary
      capillaries = hyperaemia (increased blood flow to a part of the body) and hypercapnia
37
Q

How is oxygen potentially harmful?

A
  • Giving too much O2 (hyperoxia) fools the arteries into thinking that everything is okay so
    they perfuse everywhere rather then concentrating on the few airways with good gaseous
    exchange surface areas, thus worsening hypoxia
38
Q

How would you treat asthma?

A
  • Bronchodilators (inhaler/nebuliser)
  • Corticosteroids (oral/IV/Inhaled)
  • Metered dose inhaler (MDI)/spacer/nebuliser use
  • Oxygen therapy
  • Positioning (sit upright)
  • Reassurance to decrease anxiety which reduced Sympathetic nervous system response
39
Q

What are the two types of Bronchodilators: B2-agonists and what does each one do?

A
  • Short-acting (SABAs) = relieve the effects
  • Long-acting (LABA) = controllers
40
Q

How do Short-Acting (SABAs) work?

A
  • Provide relief for 4-6 hours
    • Rapid onset of action - 5-10 mins
    • Can be used in an acute asthma attack (usually blue inhalers)
41
Q

How do Long-Acting (LABAs) work?

A
  • Long duration of action (12hrs)
    • Slow onset of action
    • Not to be used to relieve acute symptoms
42
Q

What are Inhaled Corticosteroids - ICS (preventers) and how do they work?

A
  • Potent anti-inflammatory agents
  • Given via inhalation route greatly reduced systemic adverse effects
  • EG. Fluticasone (Flixotide), Beclomethasone (Beclazone)
  • Reduce the hyper-responsiveness of the bronchial smooth muscle to irritants
43
Q

Inhaler VS Spacers VS Nebulisers for Asthma? - What are the differences and how do these work separately?

A
  • INHALER: Pushes out a pre-measured spray of asthma medicine
  • SPACER: A spacer is a specially designed plastic tube for use with an inhaler. A spacer used with a puffer delivers more medication into the lungs than using a puffer on it’s own
  • NEBULISER: A machine that converts liquid medication into a fine mist, which is inhaled through a mask or mouthpiece
44
Q

What does poor gas exchange indicate?

A

Hypercapnia (Greater than normal levels of C02) and Hypoxaemia (Less than normal levels of 02 in the blood)

45
Q

Effects of Hypercapnia?

A
  • Tachypnoea (Increased Respiratory rate) to “blow off” excess CO2
    • Use of accessory muscles to increase chest expansion and help with forced exhalation to
      expel CO2 and recruit 02
46
Q

Effects of hypoxaemia?

A
  • Tachypnoea once PO2 < 60mmHg to recruit more 02
    • Activation of sympathetic nervous system response (increase Heart rate, Blood pressure)
      to increase 02 circulation to tissues
    • Peripheral vasoconstriction (poor peripheral perfusion) to prevent O2 for vital organs
47
Q

What is the aim of oxygen therapy?

A

The reversal of Hypoxaemia and Hypoxia

48
Q

How would you administer oxygen therapy?

A
  • NASAL PRONGS:
    • Used when low to medium concentration of 02 is required
    • Greater than 4L/min may dry out nasal mucosa
    • Useful when the patient is eating and cannot use a face mask
  • SIMPLE FACE MASK (may also be called a Hudson Mask):
    • Inspired oxygen concentration varies with litre flow, rate and depth of reparations
    • There are other types of masks I.e. patient disease-specific
49
Q

How would you evaluate whether oxygen therapy has been effective?

A
  • Decreased respiratory rate
  • Increase in depth of respirations
  • Increase tissue oxygenation (mucous membranes, not just Sp02)
  • Decrease work of breathing/accessory muscle use
  • Decrease work of myocardium in patients with cardiac disease
  • Increased Sp02 levels
50
Q

What is the patho of asthma?

A
  1. An inflammatory response is triggered by allergens = mucous secretion that occludes small airways and bronchial hyper-reactivity
  2. Airway inflammation = swelling or oedema of the membranes that line the bronchi and bronchioles
  3. Mast cells, when activated, release several chemicals called mediators which cause an inflammatory response, leading to increased blood flow and movement of white blood cells to the area, and bronchoconstriction
  4. Alveoli in areas distal to airway obstruction become hyper-inflated
  5. Air trapping within the alveoli causes increased pressure that decreases alveolar perfusion causing a ventilation/perfusion (V/Q) mismatch. This will initially cause hypoxaemia and eventually cause hypercapnia leading to asthma symptoms.
51
Q

What is the aetiology of asthma?

A

Combination of genetic and environmental factors. This includes
1. Exercise-induced asthma can worsen when air is cold or dry
2. Occupational asthma, triggered by worplace irritants such as chemicals, fumes, gases or dust.
3. Allergy-induced asthma, triggered by airborne substances such as pollen, smoke, tobacco, pet fur

52
Q

What are some signs and symptoms of asthma?

A
  • Chest pain/tightness
  • Dyspnoea
  • Increased RR
  • Use of accessory muscles
  • Cough
  • SOB
  • Increased HR
  • Audible wheeze
  • Decreased Sp02
  • Fatigue
  • Diaphoresis
53
Q

What are some nursing interventions for asthma?

A
  • Administer bronchodilators as prescribed through nebuliser or spacers
  • Administer oxygen as prescribed
  • Sit pt upright to maximise air entry
  • Reassure pt to decrease anxiety and sympathetic NS response
  • Educate pt on spacer and prevention puffs
54
Q

What is the patho for COPD?

A

An irritant causes an abnormal inflammatory response
↓
Epithelium becomes chronically inflamed - cilia are destroyed and the ability to remove mucus is impaired.
↓
When activated by chronic inflammation, proteinases and other substances may be released, damaging the parenchyma of the lung.
↓
Cytokines (neutrophils, macrophages, lymphocytes) are released
↓
Ongoing bronchial irritation and inflammation
↓
Leaky capillaries – protein rich fluid seeps into alveoli
Mucous gland hypertrophy - Mucous production increased - Viscosity of mucus increases
↓
The attachments that support the walls of the small airways apply radial traction. When radial traction is reduced, small airways collapse causing air trapping and increased work of breathing
↓
Smooth muscle becomes thickened and contracted resulting in bronchconstriction
↓
Protease/antiprotease imbalance
decreased elasticity of airways
↓
Destruction of alveoli
↓
Smaller alveolar sacs merge to become larger inelastic ones
this results in reduced surface area of the alveolar membrane causing impaired gas exchange. Alveoli become solid due to fluid = consolidation
↓
Expiration is difficult due to loss of elastic recoil - impaired gas exchange ↓O2 ↑CO2 Ventilation perfusion imbalance

55
Q

What is the aetiology of COPD?

A

Tobacco smoking, Indoor + outdoor pollutants, Genetics, Occupational dust and chemicals

56
Q

What are some signs and symptoms of COPD?

A
  • SOBOE
  • Chronic cough
  • Fatigue
  • Sputum production
  • Increased frequency of chest infections
  • Dizziness
  • Tripod positioning
  • Clammy skin/diaphoresis
57
Q

What are some nursing interventions for COPD?

A
  • Encourage fluids to moisten secretions and encourage regular use of nebuliser to aid airway clearance of secretions
  • Sit pt upright to maximise air entry to the lungs
  • Education on breathing techniques (pursed lip breathing, DBE)
  • Suctioning or clearance of secretions
  • Administer 02 as required to reverse hypoxaemia
  • Administer bronchodilators or corticosteroids as prescribed for relaxation of smooth muscle in the airway to facilitate gas exchange
58
Q

What is the patho of Pneumonia?

A
  1. Bacteria invades spaces between cells and alveoli
  2. Inflammatory response + alveolar macrophages try to control infection
  3. Fluid and mucous build up in the lungs
  4. Impaired gas exchange and circulation
  5. Ventilation exceeds pulmonary perfusion (V/Q mismatch)
59
Q

What is the aetiology of Pneumonia?

A

Caused by bacteria, virus, fungi in the air.

Risk factors can be advanced age, immunocompromised, underlying lung disease, alcoholism, altered consciousness, smoking, malnutrition

60
Q

What are the signs and symptoms of pneumonia?

A
  • SOB
  • Increased RR
  • Decreased Sp02
  • Increased HR
  • Fever
  • Chills
  • Wheeze
  • Crackles on inspiration
  • Cough
  • Dullness on percussion
61
Q

What are some nursing interventions for pneumonia?

A
  • Administer prescribed antibiotics to treat infection
  • Encourage fluid intake and prescribed IV fluids to prevent dehydration and fever, thins the secretions in the lungs
  • Encourage mobilisation as required to reduce atelectasis
  • Encourage coughing techniques to help bring up sputum
  • Cooling cares to reduce fever
  • Position pt upright to maximise air entry

BNKN602 Exam (17 decks)

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