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MRCS B - Critical Care (Kanani and Lammy) > Breathing > Flashcards

Breathing Flashcards

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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
What are the normal respiratory defence mechanisms?
``` Nasal humidification of air Nascociliary action Intact cough reflex Alveolar macrophages Secretory IgA ```
26
RF's for nosocomial pneumonia when intubated?
``` Breakdown of anatomical barriers Impaired cough reflex Re-intubation Colonisation of instruments Staff hygiene Aspiration of gastric contents Epithelial trauma due to airway / suction ```
27
What risk factors predispose the stomach to bacterial colonisation?
pH <4: PPIs or H blockers Continuous gastric feeding Chronic atrophic gastritis = achlorydia
28
How can pneumonia be prevented?
``` Isolate high risk patients Staff hygiene Suctioning subglottic secretions Controlled ABx use = no resistance Use of sucralfate for prophylaxis of stress ulcers ```
29
Complications of bacterial pneumonia?
``` Respiratory failure - T1RF = hypoxaemic Effusions Empyema and abscess Metastatic abscess Sepsis ```
30
3 types of pneumothorax?
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
Causes of pneumothorax?
Primary = idiopathic bursting of apical bled Secondary: Spontaneous = pre-existing lung disease Traumatic - blunt and penetrating iatrogenic - pleural aspiration, central line, barotrauma
32
How can pneumothorax be recognised in a ventilated patient?
Sudden increase In inflation pressure Sudden hypoxia / hypotension Raised JVP Development of new cardiac arrhythmia
33
Management of pneumothorax?
``` 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
What is the definition of lung compliance?
Lung compliance is the volume change of lung per unit pressure applied i.e. the ease with which the lung inflates
35
What is surfactant and what purpose does it serve?
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
Definition of ARDS? Diagnostic criteria?
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
How does ARDS relate to ALI and SIRS?
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
Causes of ARDS?
Direct insult = pneumonia, aspiration, contusion, inhalation injury Indirect = Sepsis, DIC, massive transfusion, pancreatitis
39
Describe the pathology of ARDS...
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
Management of ARDS?
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
Prognosis of ARDS?
Poor - mortality 30-60% | If sepsis present mortality as high as 90%
42
How does NO work?
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
What are the defining features of flail chest?
> 3 ribs broken, in > 2 places
44
Implications of flail chest?
Marker of severity - high impact force Likely co-existing injuries Early complications = respiratory failure, pneumo/haemothorax Late complications = sepsis, atelectasis and pneumonia
45
Pathophysiological changes to the respiratory system in flail chest?
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
Management of flail chest?
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
What is a sucking chest wound?
Open pneumothorax | Wound size must be > 2/3rds diameter of the trachea for air to preferentially enter via open wound
48
PE - Risk factors?
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
Where do DVTs commonly form?
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
Clinical signs of DVT?
Swollen painful calf Phlegasmia alba Dolens = oedema, pain and white blanching skin Phlegasmia cerulean Dolens = oedema, cyanotic and painful
51
Pathophysiology of PE?
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
How may PE present?
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
Common ECG changes in PE?
Sinus Tachy Tall p waves lead 2 RAD RBBB TWI anterior leads
54
Management of PE/DVT?
LMWH, the start them on DOAC If unstable thrombolysis If contraindications for thrombolysis = IR pulmonary catheterisation or surgical embolectomy
55
How can PE's and DVTs be prevented?
TEDs / IPC LMWH Stop procoagulants 4 weeks pre-op e.g. OCP Early mobilisation
56
What are normal ranges of Pa02 and PC02?
Pa02 = 10.6 - 13.3 kPA PC02 = 4.7 - 6.0 kPa
57
What is best measure of ventilation?
Measuring CO2 is key using capnography PaCO2 x alveolar ventilation = volume of CO2 exhaled in 1 minute
58
Definition of respiratory failure?
T1RF = Hypoxic <8kPa T2RF = Hypoxic + PC02 >6.7
59
T1RF vs T2RF? Causes of each?
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
Mx of respiratory failure?
ABCDE approach Adequate ventilation - may need high flow oxygen or NIV Serial ABGs Treat underlying cause
61
Purpose of a chest drain?
Diagnostic - Samples of pleural effusions - transudate or exudate Therapeutic: - effusions - Pneumothorax - Haemothroax - Chylothroax - Empyema - Post op in thoracic, cardiac, oesophagectomy
62
Pre-procedure check prior to chest drain?
Lab: PT Platelets CXR
63
Outline steps in chest drain insertion?
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
Investigations post chest drain?
CXR
65
Chest drain complications?
Early = malpositioned, haemothorax ion hit bundle under rib, pulmonary trauma, abdominal injury Late: Blocked drain Drain failure Pneumothorax following removal
66
Indications for removal of chest drain?
Re-expansion successful Drain no longer works Air and fluid ceased to drain - no further swinging / bubbling

MRCS B - Critical Care (Kanani and Lammy) (6 decks)

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