Breathing Flashcards

1
Q

what investigations should we use In assessing respiratory function?

A

NON-INVASIVE:
Peak flow, Pulse oximetry , Capnogrpahy, sputum sample

Spirometry - FEV1/FVC should be >80%

DLco = transfer factor = measures transfer of low carbon monoxide concentrations in inspired air to Hb
Kco = DLco corrected for alveolar volume

CXR, CT, Echo

INVASIVE:
ABG
Bronchoscopy - rigid or flexi 
Lung biopsy
Mediastinoscopy - if need tracheobronchial LNs
PET scan
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2
Q

Applications of flexible bronchoscopy?

A

Diagnostic = biopsy via direct sampling or brushings, visualising obstruction

Therapeutic = Removing obstruction, argon coagulation therapy, difficult intubations, stenting

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3
Q

Advantage ov rigid brocnhosocpy over flexible?

A

Rigid bronchoscope permits simultaneous instrumentation, good if need to suction or remove foreign body

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4
Q

Outline the measurable lung volumes?

A

TV = volume of inspired air - 500ml OR 7ml/kg

ERV = volume that can be forcibly expired after quiet expiration
- 1.3L

IRV = volume that can be forcibly inspired above TV
- 3L

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5
Q

What lung volumes are there that are non measurable with spirometry?

A

Anything that involves residual volume.

Residual volume = Volume in lung after maximal expiration
- 1.2-1.5L

Total lung volume = VC + RV

Functional residual capacity = ERV + RV = volume left after quiet expiration
2.5-3L

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6
Q

Equation for FRC, normal range, and what can increase it or decrease it?

A

FRC = Functional residual capacity = ERV + RV

normal range = 2.5-3L

Increased in:
Obstructive disorders e.g. COPD / asthma
PEEP e.g CPAP

Decreased with:
Age
Obesity
Pregnancy 
Factors limiting expansion = Effusions, abdo swelling, restrictive lung disease
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7
Q

Obstructive vs restrictive on spirometry?

A

Obstructive has reduced FEV1 = FEV1/FVC is low <0.8

Restrictive both are low but FVC is more low:
FEV1/FVC >0.8

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8
Q

What is atelectasis?

A

absence of gas from all or part of the lung

Plain CXR can be sub-segmental, segmental, lobar or pulmonary collapse

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9
Q

Causes of atelectasis?

A

Bronchial obstruction - sputum, FB or tumour

Alveolar hypoventilation leading to progressive airway collapse

Parenchymal compression due to oedema or effusions

Bronchial intubation collapses contralateral side

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10
Q

Why does airway obstruction cause atelectasis?

A

The gas trapped distally is absorbed as it has a higher partial pressure than the mixed venous blood = progressive collapse

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11
Q

Risk factors for post-op atelectasis?

A
Abdominal or thoracic surgery 
BMI > 27
Age >59
ASA >2
COPD
IPPV > 1 day
Smoking in the preceding 8 weeks
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12
Q

Management of post-op atelectasis?

A

Pre-op - breathing exercises

Intra-op:
Humidified air
Avoid unnecessarily high FiO2

Post-op:
Upright position and breathing exercises
Mobilise early
Adequate analgesia
CPAP
Bronchoscopy for mucus plugs / secretions
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13
Q

What is CPAP and its effect on respiratory system?

A

Continuous positive airway pressure

Has a valve with set pressure.
On inspiration and expiration positive pressure cannot fall below this set pressure, if it does then pressure given.

Improves ventilation by:
Opening of collapsed airways + prevention of collapsing on expiration
Increases FRC
Increases lung compliance
Decreases work of breathing 
Increases V/Q ratio = improved perfusion
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14
Q

Disadvantages of CPAP?

A

Tight uncomfortable mask - pressure sores
Risk of barotrauma
Gastric dilation due to swallowed air

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15
Q

What is bronchiectasis?

A

The irreversible dilation of bronchi due to chronic inflammatory processes

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16
Q

name the types of bronchiectasis?

A

Follicular = loss of bronchial elastic tissue + multiple lymphoid follicles

Atelectatic = localised dilation of airways, associated with parenchymal collapse

Saccular / cystic = patchy dilation of airways, with loss of bronchial subdivisions

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17
Q

Aetiology of bronchiectasis?

A

Congenital:
Ciliary dyskinesia e.g. Kartageners
Cystic fibrosis
Ig deficiencies (will see recurrent infections in infancy)

Acquired:
Post-infective bronchial damage e.g measles, pertussis, TB
Bronchial obstruction - tumour, FB, LN's
Immunodeficiency e.g. AIDS
Autoimmune - RA, UC
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18
Q

What bacteria may colonise bronchiectasis?

A

Haem. Influenzae
Staph aureus
Strep pneumo

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19
Q

Complications of untreated bronchiectasis?

A

Early =

  1. haemoptysis
  2. infections > abscess and empyema
  3. metastatic infection e.g. cerebral abscesses

Late:

  1. Cor pulmonale
  2. Respiratory failure
  3. Secondary amyloidosis with protein A deposition
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20
Q

Mx of bronchiectasis?

A

Manage reversible airway obstruction with neb and steroids

Chest physio

Treat underlying cause and treat any infection

Surgery - lung transplant in CF

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21
Q

What is pneumonia?

A

Inflammatory process of lung characterised by consolidation due to exudate in alveolar space

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22
Q

Types of pneumonia?

A

Lobar - confined to one lobe, linear demarcation.
Exudate forms in bronchioles and alveoli and spills over to adjacent segments via pore of Kohn.

Bronchopneumonia = starts at bronchioles and extends into alveoli > numerous foci of consolidation

Interstitial = chronic alveolar inflammation, not necessarily infective in origin - may be immune based

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23
Q

Pathological classes of pneumonia?

A

1 = acute congestion, day 1-2

  • lobe is heavy, dark and firm.
  • inflame exudate and cellular infiltrate including erythrocytes

2 = red hepatisation, day 2-4

  • lung is firm, red and consolidated
  • neutrophils fibrin and extravasated erythrocytes

3 = grey hepatisation, day 4-8

  • Heavy, consolidated and grey
  • Extensive fibrin network and degenerating erythrocytes

4 = resolution > day 8

  • Macrophage action liquefies exudate
  • can take 3 weeks
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24
Q

Organsims involed in ICU pneumonias?

A

Ventilator related

Within 1-4 days of intubation = early onset:
- Strep. pneumonia, s. aureus and h influenza

Lates onset >4 days = gram negative
- Pseudomonas, enterobacter, aeruginosa

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25
Q

What are the normal respiratory defence mechanisms?

A
Nasal humidification of air
Nascociliary action 
Intact cough reflex 
Alveolar macrophages 
Secretory IgA
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26
Q

RF’s for nosocomial pneumonia when intubated?

A
Breakdown of anatomical barriers
Impaired cough reflex
Re-intubation
Colonisation of instruments
Staff hygiene 
Aspiration of gastric contents 
Epithelial trauma due to airway / suction
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27
Q

What risk factors predispose the stomach to bacterial colonisation?

A

pH <4:
PPIs or H blockers
Continuous gastric feeding
Chronic atrophic gastritis = achlorydia

28
Q

How can pneumonia be prevented?

A
Isolate high risk patients
Staff hygiene
Suctioning subglottic secretions 
Controlled ABx use = no resistance 
Use of sucralfate for prophylaxis of stress ulcers
29
Q

Complications of bacterial pneumonia?

A
Respiratory failure - T1RF = hypoxaemic 
Effusions 
Empyema and abscess 
Metastatic abscess 
Sepsis
30
Q

3 types of pneumothorax?

A

Simple = two way valve, no CVS compromise

Tension = closed valve system, quick CVS compromise

Open = sucking chest wound, must be greater than 2/3rds diameter trachea

31
Q

Causes of pneumothorax?

A

Primary = idiopathic bursting of apical bled

Secondary:
Spontaneous = pre-existing lung disease
Traumatic - blunt and penetrating
iatrogenic - pleural aspiration, central line, barotrauma

32
Q

How can pneumothorax be recognised in a ventilated patient?

A

Sudden increase In inflation pressure
Sudden hypoxia / hypotension
Raised JVP
Development of new cardiac arrhythmia

33
Q

Management of pneumothorax?

A
Primary:
<2cm not SOB = home with OPD
>2cm with SOB > aspirate
success = home
failure = chest drain

Secondary:
> 2cm and SOB = chest drain
1-2cm = aspirate, if success and now <1cm = monitor, if failure = chest drain
<1cm = monitor for 24 hours

34
Q

What is the definition of lung compliance?

A

Lung compliance is the volume change of lung per unit pressure applied i.e. the ease with which the lung inflates

35
Q

What is surfactant and what purpose does it serve?

A

Surfactant is a phospholipid mixture, produce by type 2 pneumocytes

Acts to reduce surface tension of fluid lining alveoli = greater compliance:

  • Reduces work of breathing
  • Stabilises smaller alveoli preventing atelectasis
36
Q

Definition of ARDS?

Diagnostic criteria?

A

Acute onset respiratory failure with persistent inflammatory change in the lungs.

  1. Acute onset <1week
  2. Bilateral pulmonary opacities
  3. Pa02:Fi02 <26.6kPa (200mmHg)

Also must have pulmonary artery capillary wedge pressure < 18mmHg = excluding. cardiac cause

37
Q

How does ARDS relate to ALI and SIRS?

A

ARDS and ALI are on a spectrum. Acute Lung Injury is non-specific pathological changes in the lung due to a specific insult.

The changes are like ARDS but less severe

ARDS is the respiratory component of SIRS

38
Q

Causes of ARDS?

A

Direct insult = pneumonia, aspiration, contusion, inhalation injury

Indirect = Sepsis, DIC, massive transfusion, pancreatitis

39
Q

Describe the pathology of ARDS…

A

Initially during acute insult 3 things happen:

  1. Vasoactive mediators released
  2. Activation of neutrophils and macrophages
  3. Activation of complement and coag cascade

This then leads to other processes

Vasoactive mediators:
= pulmonary vasoconstriction = increase PVR = R heart strain

Activation complement and coag:
= Oedema:
- Vascular compression = increased PVR = RH strain
- V/Q mismatch = hypoxic = increased PVR = RH strain
- Increased secretion/retention = atelectasis / infection

Activation of neutrophils and macrophages:
= Free radicals, TNF, protease, collagenase:
- Oedema due to endothelial injury and capillary permeability
- Epithelial injury = reduced type 2 pneumocytes = reduced surfactant = atelectasis / infection

40
Q

Management of ARDS?

A

ABCDE
Manage initial insult

Careful fluid resuscitation due to oedema
Mechanical ventilation:
- High PEEP to keep airways open
- small tidal volumes show improved outcome, leads to a hypercarbia but is usually well tolerated
- Increasing inspiratory phase

Inhaled NO = pulmonary vasodilation and increase oxygenation. Effect on survival is equivocal.

41
Q

Prognosis of ARDS?

A

Poor - mortality 30-60%

If sepsis present mortality as high as 90%

42
Q

How does NO work?

A

NO is a vasodilator. Works by acting upon cytoplasmic enzyme guanylyl cyclase.

This increases intracellular cyclic guanosine monophosphate cGMP which stimulate a protein kinase.

This leads to relaxation of vascular smooth muscle cells

43
Q

What are the defining features of flail chest?

A

> 3 ribs broken, in > 2 places

44
Q

Implications of flail chest?

A

Marker of severity - high impact force
Likely co-existing injuries
Early complications = respiratory failure, pneumo/haemothorax
Late complications = sepsis, atelectasis and pneumonia

45
Q

Pathophysiological changes to the respiratory system in flail chest?

A

Reduced tidal volume:

  • Flail segment exhibits paradoxical motion. On inspiration moves in, due to negative intrapleural pressure.
  • Pain also reduces tidal volume

Retention of secretions due to reduced tidal volume and inefficient cough mechanism

Can lead to T1RF

46
Q

Management of flail chest?

A

ATLS principles

Mx flail itself and any underlying injuries

Most will be managed conservatively with observation, humidified air and analgesia

If deterioration can intubate

47
Q

What is a sucking chest wound?

A

Open pneumothorax

Wound size must be > 2/3rds diameter of the trachea for air to preferentially enter via open wound

48
Q

PE - Risk factors?

A

Based around virchows triad:
Venous stasis
Hyper-coagulability
Vessel lumen

Stasis = AF, trauma, surgery (specifically neurosurgery due to controversy with anticoags), immobility.

Hyper coagulable = Pregnancy, cancer, OCP, Chemo, thrombophilias

Vessel lumen = Atherosclerotic disease

49
Q

Where do DVTs commonly form?

A

Commonly form in deep venous system of calves or venous plexus in soleus
Specifically forms around valves.

Can form distally or more proximally, meaning higher risk of PE’s

50
Q

Clinical signs of DVT?

A

Swollen painful calf

Phlegasmia alba Dolens = oedema, pain and white blanching skin

Phlegasmia cerulean Dolens = oedema, cyanotic and painful

51
Q

Pathophysiology of PE?

A

Pulmonary artery obstruction as embolus is impacted past right ventricle outflow.

Activated platelets within the thrombus release vasoactive mediators = increase PVR = increased right ventricular afterload = RH strain and tachycardia

52
Q

How may PE present?

A

Small = SOB, tachy, pleuritic pain

Large = Above +:

  • Shock
  • Severe central chest pain
  • Signs of right ventricular strain = Wide splitting heart sound, tricuspid regurgitation, raised JVP, RV heave
53
Q

Common ECG changes in PE?

A

Sinus Tachy

Tall p waves lead 2
RAD
RBBB
TWI anterior leads

54
Q

Management of PE/DVT?

A

LMWH, the start them on DOAC

If unstable thrombolysis

If contraindications for thrombolysis = IR pulmonary catheterisation or surgical embolectomy

55
Q

How can PE’s and DVTs be prevented?

A

TEDs / IPC
LMWH
Stop procoagulants 4 weeks pre-op e.g. OCP
Early mobilisation

56
Q

What are normal ranges of Pa02 and PC02?

A

Pa02 = 10.6 - 13.3 kPA

PC02 = 4.7 - 6.0 kPa

57
Q

What is best measure of ventilation?

A

Measuring CO2 is key using capnography

PaCO2 x alveolar ventilation = volume of CO2 exhaled in 1 minute

58
Q

Definition of respiratory failure?

A

T1RF = Hypoxic <8kPa

T2RF = Hypoxic + PC02 >6.7

59
Q

T1RF vs T2RF?

Causes of each?

A

Type 1 RF is hypoxic only, PO2 <8.
Due to a V/Q mismatch - typically problems that affect oxygenation:
- Shunt e.g. Congenital heart disease
- V/Q mismatch in PE as not enough blood to absorb oxygen
- Mismatch in parenchymal disease as oxygen cannot get to blood e.g. ARDS, pneumonia,

Type 2 RF is hypoxic, as well as PC02 >6.7
It is due to alveolar hypoventilation:
- COPD, asthma
- cerebral lesions - tumour, head injury
- neuromuscular - MND, guillian barre
- Thoracic cage - e.g. flail chest.
60
Q

Mx of respiratory failure?

A

ABCDE approach

Adequate ventilation - may need high flow oxygen or NIV

Serial ABGs

Treat underlying cause

61
Q

Purpose of a chest drain?

A

Diagnostic - Samples of pleural effusions - transudate or exudate

Therapeutic:

  • effusions
  • Pneumothorax
  • Haemothroax
  • Chylothroax
  • Empyema
  • Post op in thoracic, cardiac, oesophagectomy
62
Q

Pre-procedure check prior to chest drain?

A

Lab:
PT
Platelets

CXR

63
Q

Outline steps in chest drain insertion?

A
  1. position = supine, arm abducted and hand being head
  2. Marking - 5th ICS MAL
  3. Scrub, clean area, drape
  4. Local anaesthetic to make wheal, then insert 10-15ml to subcutaneous layers
  5. Incision - 2-3cm transverse incision with size 11 blade
  6. Blunt dissection suing Roberts clamp to open muscular layers to parietal pleura
  7. Confirm position by entering needle and aspirate air / fluid
  8. Secure incision with two 0 silk mattress sutures
  9. Insert chest drain. 24 for pneumothorax, 32 for Haemo
    Clamp with Roberts forceps and insert and secure
  10. Closed system drainage
64
Q

Investigations post chest drain?

A

CXR

65
Q

Chest drain complications?

A

Early = malpositioned, haemothorax ion hit bundle under rib, pulmonary trauma, abdominal injury

Late:
Blocked drain
Drain failure
Pneumothorax following removal

66
Q

Indications for removal of chest drain?

A

Re-expansion successful
Drain no longer works
Air and fluid ceased to drain - no further swinging / bubbling