Lung Diseases Flashcards

1
Q

What are the causes of hypoxaemia

A
V/Q mismatch
Alveolar hypoventilation
Impaired diffusion: pulmonary fibrosis
Low partial pressure of inspired oxygen
Anatomical R-L shunt: PAVM lobar pneumonia - deoyxgenated bypassing capillary bed of lung - won't respond well to O2 therpay
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2
Q

What is the PaO2 for hypoxaemia

A

Less than 8kPa

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3
Q

What is the most common cause of arterial hypoxaemia

A

V/Q mismatch. Ventilation and perfusion must be exactlymatched

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4
Q

What happens in regions of high ventialtion

A

High blood flow i.e. base of lungs

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5
Q

What happens in regions of low ventilation

A

Low blood flow

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6
Q

What is a shunt alveolar unit

A

Va/Q = 0

Alveolar that are perfused but not ventilated. Q>V. Wasted perfusion

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7
Q

What is dead space

A

No perfusion. Gas makeup in alveolar same as room air - ventilation but no perfusion. Q

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8
Q

What is hypercapnia

A

PaCO2>6 kPa

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9
Q

What is alveolar respiration determined by

A

RR and tidal volume

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10
Q

What is T1 resp failure

A

Normal CO2 with hypoxaemia

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11
Q

What is T2 resp failure

A

Hypoxaemia and hypercapnia

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12
Q

How is alveolar respiration calculate

A

Va=Ve-VD

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13
Q

What are the two responses to O2 therapy

A

PaCO2 and clinical state may improve or px may become drowsy

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14
Q

What is the classical teach of what happens when px with COPD is given O2

A

Px with COPD rely on their hypoxia ventilatory drive due to blunted sensitivity to CO2 and H+
Hypercapnia results from a suppression of hypoxic ventilatory drive causing alveolar hypoventilation

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15
Q

What may actually happen when px with COPD is given O2

A

Worsened Va/Q matching due to attenuation of hypoxic pulmonary vasoconstriction - directs blood to areas of lung that are better ventilated. Giving O2 increase partial pressure and releases vasoconstriction, but not does increase ventilation. Decreased binding affinity of haemoglobin or CO2. Decreased Ve

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16
Q

What is hypercapnic respiratory failure caused by

A

Acute (on chronic) imbalance in load-capacity-drive
relationship
Caused by defect in each area or combination

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17
Q

What are examples of drive failure

A

Drive failure: cortical and brain stem lesion (encephalitis, ischaemia, haemorrhage), drugs (sedative, opioids), metabolic alkalosis (loop diuretics - reduces threshold of CO2 needed)

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18
Q

What are examples of load impedance

A

Elastic load - pulmonary infection, alveolar oedema, pleural effusion
Resistive load - bronchospasm, UAO, OSA

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19
Q

What is auto intrinsic PEEP

A

Incomplete expiration prior to the initiation of the next breath causes progressive air trapping (hyperinflation). This accumulation of air increases alveolar pressure at the end of expiration.

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20
Q

What are underlying conditions of resp failure

A

COPD, pneumonia, pulmonary oedema (cardiogenic, non-cardiogenic), pulmonary embolism, pulmonary fibrosis, asthma

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21
Q

How is resp failure assessed

A

ABC
Assess vital signs
Oxy-haemoglobin sats (>92% excludes hypoxia unless CO poisoning)
ABG analysis - asses for hypercapnia (hypoventilation from Duchenne’s)
If pH of venous gas is greater than 7.34, very unlikely to have resp failure (no need for ABGs)

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22
Q

How is resp failure managed

A

Treat underlying condition
Hypoxia kills - titrated oxygen
Non benefit from oxygen if not hypoxic - stroke, MI
Oxygen may worsen hypercapnia (tissue injuries are delivered by free radicals, increasing O2 increases free radicals. High O2 can cause vasoconstriction of the coronary and cerebral vessels)
Oxygen is not ventilation

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23
Q

What are the four types of resp support

A

Oxygen
Non-invasive ventilation (NIV)
Invasive mechanical ventilation (IMV)
Extra-Corporeal Membrane Oxygentation (ECMO)

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24
Q

What are the clinical features of resp failure

A

– Confusion
– Cyanosis
– Dyspnoea
– Somnolence / drowsiness

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25
Q

What are the benefits of NIV

A

Patient remains conscious
Maintains structural host defence system
Level 2 support
Positive pressure ventilators used more often

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26
Q

What are the benefits of invasive ventialtion

A

Greater control of ventilation
Secure ventilatory delivery
Level 3 support
Gold 3 standard treatment

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27
Q

What is given in severe resp failure

A

ECMO, VA for paeds

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28
Q

What is the pleura

A

Lung lining - parietal and visceral

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29
Q

What is pleural effusion

A

Fluid falls to bottom of pleural space usually
Decreased expansion on side of fluid
Mediastinum shifted away from side of fluid and trachea)

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30
Q

What are the signs of pleural effusion

A

Stony dull percussion
Breath sounds reduced - bronchial breathing at level of effusion
Vocal resonance reduced

31
Q

Where is thoracentesis and where is it performed

A

An invasive procedure to remove fluid or air from the pleural space for diagnostic or therapeutic purposes.
Go above rib to avoid neuromuscular bundle

32
Q

What is an exudate

A

Thick fluid - over 35g/L

33
Q

What is a transudate

A

Thin fluid - less than 25g

34
Q

What is pleural fluid protein is between 25-35

A
Use Light's criteria:
Exudate if one or more:
Pleural protein/serum protein over 0.5
Pleural LDH/serum LDH is >0.6
Pleural LDH is 2/3 upper limit of lab normal LDH
35
Q

What are the causes of transudates

A
Systemic failures:
Left ventricular failure, liver cirrhosis
Hypoalbuminaemia
Peritoneal dialysis
Hypothyroidism
Nephrotic syndrome
Mitral stenosis
36
Q

What are the causes of exudates

A
Problems local to lungs:
Malignancy, parapneumonic effusions, TB
PE
Rheumatoid arthritis
Other autoimmune pleuritis
37
Q

What should pleural pH be

A

Around 7.2. Less than 7.2 - complicated paraneumonic effusion. Indication for tube drainage

38
Q

What is empyema

A

Collection of pus in the pleural cavity

39
Q

What can strep milleri cause

A

Grows on teeth - can cause bacterial endocarditis

40
Q

What are malignant pleural effusions

A

Lung, breast, ovarian cancer
Lymphoma
Medial survival 4-6 motnhs

41
Q

Describe spontaenous pneumothorax

A

Can be primary (absence of underlying lung pathology) or secondary (due to presence of underlying lung pathology)

42
Q

What is tension pneumothorax

A

Forms due to one way valve where air can enter the pleural space upon inspiration, but not lave. Should have contralateral tracheal deviation, hypotension, tachy, hypoxia, increased JVp

43
Q

What is restrictive lung disease

A

Clinical syndrome, reduced lung compliance, reduced lung volume

44
Q

Describe normal respiration

A

Diaphragm and inspiratory muscle contract -> thorax expands -> Intrapleural pressure becomes subatmospheric -> increase in trans-pulmonary pressure -> lungs expand -> Alveolar pressure becomes subatmoshperic -> air flows into alveoli

45
Q

What are the four types of interstitial lung disease

A

ILD of known association
Idiopathic interstitial pneumonia
Granulomatous ILD
Miscellaneous ILD

46
Q

Describe granulomatous ILD

A

Sarcoidosis:
Multisystem granulomatous disease
Pulmonary most commonly affect organ
Range of pulmonary involvement including lung fibrosis

47
Q

Describe idiopathic interstitial fibrosis

A

Usually interstitial pneumonia histologically
Male predominance, progressive disease
Associated with finger clubbing

48
Q

What is hypersensitivity pneumonitis

A

Reaction to exposure including bacteria, fungi, avian proteins, animal proteins

49
Q

What is pneumonconiosis

A

Occupational lung disesae - coal workers pneumoconiosis, silicosis, berylliosis, asbestosis

50
Q

What is acute respiratory distress syndrome

A

Acute lung injury - sepsis, toxic inhalation, trauma, drugs, pancreatitis

51
Q

What are the symptoms of restrictive lung disease

A

Breathlessness: others due to underlying disease, but may include
Dry cough, wheeze, chest pain, haemoptysis, fever, myalgia, weight loss, weakness

52
Q

What are the signs of restrictive lung disease

A

General - tachypnoea, use of accessory muscle, cyanosis

Other signs - chest or spine deformity, obesity, reduced chest expansion, crackles (fibrosis), wheeze

53
Q

What investigations need to be carried out

A

Spirometry - FEV1/VC ratio unchanged

Flow volume loop - inspiratory moves to the left. Shape remains the shame

54
Q

What is the management step for restrictive lung disease

A

Conservative, pharmacological, oxygen, surgery, ventilatory support

55
Q

What is spirometry

A

Measurement of expire and inspired flows and volumes

56
Q

What is FVC

A

Forced vital capacity

57
Q

What is VC

A

Total volume of gas exhaled after breathing in total lung capacity

58
Q

What is normal ratio

A

FVC should be same as VC

59
Q

What if FVC

A

Airflow obstruction

60
Q

How is reversibility defined

A

Increase in FEV1
following BD of >12% from baseline → significant
reversibility

61
Q

What does increase in residual volume indicate

A

Gas trapping - can be due to airway collapse

62
Q

What is above horizontal axis in flow volume loop

A

Expiratory

63
Q

What is below horizontal axis in flow volume loop

A

Inspiratory

64
Q

What does obstructive lung disease look like on flow volume loop

A

Scooping of expiratory curve

65
Q

What does restrictive lung disease look like on flow volume loop

A

Miniature version of normal volume

66
Q

What is the gold standard of lung volume measurement

A

Body phethymosgraph - gold standard

Inert gas dilution - method underestimates volumes in px with airflow obstruction

67
Q

What causes an increase in FRC and RV

A

Intrapulmonary - airway obstruction

Extra pulmonary - expiratory muscle weakness

68
Q

What causes increased TLC

A

Emphysema

69
Q

What causes decreased TLC

A

Intrapulmonary: pneumonectomy, collapsed lung, consolidation, oedema, fibrosis
Extra pulmonary: pleural disease, rib cage deformity, respiratory muscle weakness

70
Q

How to measure gas exchange

A

CO - Measure of gas diffusion from lung to blood AND the combination of gas with Hb.

71
Q

What is TLCO

A

Reflects the ability of the lung to transfer gas from lung to blood

72
Q

What is normal for standardised residual

A

Between -1.64 to +1.65

73
Q

What is bronchiolitis obliterans

A

Inflammatory obstruction of the lung’s tinniest airways