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CSB335 > Respiratory assessment and SOB > Flashcards

Respiratory assessment and SOB Flashcards

1
Q

What does PO2 measure?

A

The amount of dissolved oxygen in the blood

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2
Q

What is the definition of hypoxia?

A

Lack of oxygen at the tissue level

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3
Q

What is hypoventilation?

A

Slow resp rate and/or low tidal volume

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4
Q

How much oxygen in a full B size cylinder?

A

200L

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5
Q

How much oxygen in a full C size cylinder?

A

400-490L

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6
Q

How much oxygen in a full D size cylinder?

A

1500L

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7
Q

Hudsen face masks with a reservoir bag are used for which patients?

A

Patients with spontaneous breathing who are acutely hypoxic and require high concentrations of oxygen

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8
Q

Normal PO2 in the blood should be between ____ and ____.

A

80 and 100mmHg

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9
Q

What are some things that can cause false PO2 readings?

A
  • Carbon monoxide poisoning
  • Hypothermia
  • Excessive ambient light
  • Vasoconstriction
  • Pt movement
  • Nail polish
  • Hypotension
  • Jaundice
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10
Q

What SPO2 range is a suitable goal with a stable COPD patient?

A

88 to 92%

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11
Q

What SPO2 range is a suitable goal with a stable patient?

A

94 to 98%

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12
Q

What is asthma?

A

A chronic inflammatory disorder of the airway characterised by recurring episodes of wheezing/breathlessness/chest tightness/coughing/mucous production

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13
Q

What are the risk factors for asthma?

A
  • Family hx
  • Smoking
  • Allergen exposure
  • Recurrent respiratory infections
  • Living in urban areas
  • Air pollution
  • Hygiene hypothesis (controversial)
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14
Q

What is the pathophysiology of asthma?

A

Hyper-responsiveness of the airway to inflammatory mediators

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15
Q

What are the two types of asthma triggers?

A

Allergens and irritants

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16
Q

Inflammatory mediator release causes what in asthma?

A
  • Bronchial smooth muscle spasm
  • Oedema
  • Thick mucous production
  • Thickening of the airway wall
  • Further hyper-responsiveness of the airway
  • Neuropeptide release
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17
Q

Mediators and immune cells lead to…

A

Cell damage and further airway obstruction

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18
Q

What are the two main syndromes of COPD/COAD?

A

Emphysema and chronic obstructive bronchitis

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19
Q

What are the differences between asthma and COPD?

A
  • COPD is not fully reversible

- COPD is progressive

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20
Q

What are the risk factors for COPD?

A
  • Active or passive smoking
  • Occupational exposure
  • Air pollution
  • Genetics
21
Q

What is the definition of chronic obstructive bronchitis?

A

Hyper-excretion of mucous and chronic productive cough for at least three months of the year for two consecutive years

22
Q

Describe some pathophysiology points of chronic obstructive bronchitis

A
  • Irritants cause airway inflammation
  • Thick mucous is secreted
  • Bronchial infiltration by neutrophils, macrophages, and lymphocytes
  • Airway defence mechanisms are compromised, increasing the likelihood of pulmonary infections leading to bronchospasm and productive cough
  • Continuous inflammation causes oedema
  • Starts with bronchi and progresses to bronchioles
  • Mucous glands and goblet cells increase in size and number, progressively narrowing the airway causing expiratory obstruction
23
Q

What is the definition of emphysema?

A

Abnormal permanent enlargement of gas exchange airways accompanied by destruction of the alveoli walls and associated capillary network

24
Q

Describe the pathophysiology of emphysema

A
  • Inhaled oxidants induces inflammation
  • Inflammation over time causes alveolar destruction and loss of compliance
  • Loss of surface area and capillaries causes V/Q mismatch
  • Expiration becomes difficult as alveoli stiffen
  • Air trapping results in a barrel chest
  • Significant energy put into breathing
25
Q

What are the most common causes of acute respiratory distress syndrome (ARDS)?

A

Sepsis and multi-system trauma

26
Q

What is ARDS?

A

A life-threatening condition involving lung inflammation and alveolar capillary damage

27
Q

What are some other causes of ARDS?

A
  • Pneumonia
  • Burns
  • Aspiration
  • Pancreatitis
  • Blood transfusions
  • Drug overdose
  • DIC
28
Q

Describe the pathophysiology of ARDS

A
  • Inflammation damages alveoli and capillaries
  • Severe pulmonary oedema and hypoxaemia follow
  • Fluids, proteins, and WBCs leak into the interstitial space
  • Interpleural shunting occurs
  • Epithelial cell damage due to inflammation causes platelet aggregation and thrombus formation
29
Q

True or false: damage in ARDS can be direct or indirect

A

True

30
Q

In what time frame will the clinical manifestation of ARDS be seen after the initial insult?

A

Within 24 hours

31
Q

What are the signs/symptoms of ARDS?

A
  • Severe dyspnoea
  • Rapid shallow breathing
  • Inspiratory crackles
  • Reduced compliance
  • Hypoxaemia unresponsive to O2 therapy
32
Q

What is pneumonia?

A

Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites

33
Q

What are the risk factors for pneumonia?

A
  • Old age
  • Immunosuppression
  • Underlying disease
  • Alcoholism
  • Smoking
  • Malnutrition
  • Immobilisation
34
Q

What are some common causes of pneumonia?

A
  • Bacteria (streptococcus pneumoniae)
  • Influenza
  • Legionella’s disease
35
Q

Should you always expect to hear crackles on auscultation of pneumonia patients?

A

No

36
Q

Describe the pathophysiology of pneumonia

A
  • Aspiration of oropharyngeal secretions
  • Inhalation of microorganisms
  • Bacteria infiltration of lungs via blood
  • Large concentrations of bacteria/viruses overwhelm the alveolar macrophages
  • Immune mediator release causing damage to bronchial mucous membranes and alveoli and associated capillaries
  • Bronchioles fill up with infectious debris and exudate causing V/Q inequality
37
Q

What are the clinical manifestations of pneumonia?

A
  • Usually preceded by an URTI
  • Fever
  • Chills
  • Productive cough
  • Malaise
  • Pleural pain
  • Dyspnoea
  • Haemoptysis
  • Inspiratory crackles
38
Q

Describe the pathophysiology of tuberculosis

A
  • Mycobacterium tuberculosis (transmitted through airborne droplets)
  • Microorganisms lodge in upper lung lobes
  • Bacteria multiplies causing inflammation
  • Bacteria infiltrate lymphocytes
  • Macrophages and neutrophils seal off bacterial colonies, forming tubercules
  • Infected tissue in tubercules dies
  • Scar tissue forms around tubercules
  • Tubercules remain dormant until immune system weakens or bacteria escapes
39
Q

Describe the clinical manifestations of tuberculosis

A
  • Fatigue
  • Weight loss
  • Lethargy
  • Loss of appetite
  • Chest pain
  • Low grade fever
  • Purulent cough
  • Night sweats
  • Dyspnoea
  • Haemoptysis
40
Q

What is acute bronchitis?

A

Infection of the bronchi

  • Self limiting
  • Usually viral
  • Purulent sputum may occur
41
Q

Does influenza trigger an immune response?

A

Yes (mediators -> airway oedema -> excess mucous production)

42
Q

What is a pneumothorax?

A

Presence of free air in the interpleural space

43
Q

What are the different types of pneumothorax?

A
  • Traumatic
  • Spontaneous
  • Iatrogenic
  • Secondary
44
Q

What causes iatrogenic pneumothorax?

A

Clinical procedures (central lines or decompression of a non-tension pneumothorax)

45
Q

What are the clinical features of pneumothorax?

A
  • Occurs suddenly
  • May be associated with sneezing, coughing, hyperventilation, or breathing deeply
  • 90% cases have chest pain on the affected side which may be dull, sharp, and may radiate to back/neck
  • 80% cases complain of dyspnoea
  • Reduced breath sounds on affected side
  • Reduced chest movement of affected side
  • Subcutaneous emphysema may occur
46
Q

What are the signs of a tension pneumothorax?

A

Signs of a pneumothorax, plus:

  • Decreased respiratory function
  • Decreased cardiovascular function
  • Increased JVP
  • Tachycardia
  • Tracheal deviation (late sign, always away from site of injury)
47
Q

What is the leading cause of lung cancer?

A

Smoking (90%)

48
Q

What are the risk factors for lung cancer?

A
  • Amount smoked per day
  • Years of smoking
  • Advanced age
  • COPD
49
Q

Describe the pathophysiology of lung cancer

A

Carcinogens in tobacco cause genetic mutations in cells, leading to carcinomas. Progression of carcinomas leads to invasion of surrounding tissue. Metastasis develop and travel thoughout the body.

CSB335 (12 decks)

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