Respiratory

Question 1

3 consequences of pathophysiology of ARDS

Answer 1

1. Impaired Gas exchange 2: Decreased lung compliance 3. Pulmonary hypertension

Question 2

ARDS predisposing factors

Answer 2

Sepsis Pneumonia Trauma Massive transufsion Pancreatitis Drug OD Near drowning Cardiopulmoary bypass

Question 3

Causes of massive hempotysis

Answer 3

Vascular: PE/infarct, mitral valve diease, LVF,
Infection: TB; pneumonia; abscess
Trauma
Autoimmune: vascuiltides- wegeners
Iatrogenic: SGC placement; intubation; broncoscopy
Neoplasm:
bleeding diatheses

Question 4

Causes of upper airway obstruction

Answer 4

Functional:
CNS: head injury; stroke; cardiac/resp arrest; hypoxia, drug OD, metabolic encephalopathies; encephalitis
neuromuscular: recurrent laryngeal n. palsy, OSA, laryngospasm, GBS, myasthenia gravis,

Mechanical:
ludwigs angina; epiglotitis; laryngobronchitis; hemmorhage; hematoma; trauma; burns; foreign body; neoplasm

Question 5

complications of NIV

Answer 5

agitation/intolerance claustrophiba aspiration pressure sore imparied nutrition impaired communication gastric distension oronasal dryness hypotension

Question 6

Contraindications to NIV

Answer 6

Facial trauma/deformity decreased LOC aspiration risk unable to clear secretions claustrphobic/ inability to co-operate resp/cardiac arrest significant hemydynamic instability

Question 7

Define ventilator associated pneumonia

Answer 7

No gold standard definition CDC uses: development of pneumonia in person who has been mechanically ventilated in 48 hr period preceeding development of infection

Question 8

Definition of ARDS

Answer 8

Berlin definition 2012: 1.symptoms begin within 1 week of clinical insult 2. bilaterla pulmonary infiltrates on CXR, not fully explained by caridiogenic pulmonary oedema or alterante causes 3. respirator failure not fully explained by cardiac failure orfluid overload (will need objective assessment if no ARDS risjk factors) 4. moderate to severe impairment of oxygenation must be present mild 200< PaO2/FiO2 < 200 - with PEEP 5 severe PaO2/FiO2<100 PEEP 5

Question 9

Factors contributing to failure to wean

Answer 9

Often multifactorial, consider: 1. increased ventilatory demand (fever, sepsis; metabolic acidosis; pain; delerium; agitation) 2. decreased neuromuscular respiratroy capacity (cortical; bainstem; spinal; neuroapthy; NMJ; myopathy) 3. increased resistance: (bronchspasm; sputum; PEEPi; circuit) 4. decreased compliance (pulm oedema; ARDs; effusions; consolidation; atelectasis, PTX; abdominal hypertension; obesity) 5. decreased ventilatory drive: sedatives; encephalopathies; obesity; metabolic alkalosis; 6. cardia dysfunction (LVF; ischemia)

Question 10

How do calculate ideal body weight?

Answer 10

Male: 50 + 0.9 (height - 152.4) Female 45 + 0.9( height- 152.4)

Question 11

mechanisms of ventilator associated lung injury

Answer 11

volutrauma- trasnpulmonary pressures above 30 cm H2O, disrupt basement membrane barotraumua: trnaspulmonary pressures greater than 50 cm H20 disrupt basement membrane biotrauma- volutrauma and barotrauma lead to upregulation of cytokines and infiltration with inflammatroy mediators de-rectuiment/re-recruitment- alveolar collapse of oedematous lungs and assocaited shear stress of re-opening alveoli high FiO2 prolonged

Question 12

methods of gas exchange in HFOV

Answer 12

Pendelufft mixing- mixing between lung units due to differing impedance Augmuented diffusion- gas mixing within alveolar units Taylor dispersion - movement of molecues beyond bulk flow front Coaxial flow pattern- net flow through the centre on the way in, on the outside on the way out Cardiogenic mixing - agitation of surrounding lung tissue with molecular diffusion

Question 13

Outline measures to prevent VAP

Answer 13

1.Prevent colonization of upper respiratroy tract and GI tract (mouthcare; stress ulcer prophylaxis when indicated (avoid SDD) 2. Prevent aspiration (head up; subglottic secretion drainage, ETT cuff 20-30 cm H20 3. Minimize duration of mechanical ventilation (early mobilization; early tracheostomy) 4. Endotracheal circuit care: (humidification; suction) 5. general measures to decrease spread of infection (hand hygiene; PPE; surveillance and audit)

Question 14

potential indications for NIV

Answer 14

COPD Cardiogenic pulmonary oedema (CPAP better than BiPAP) weaning COPD from MV OSA ?Asthma

Question 15

Prognosis in ARDS

Answer 15

High mortality: 30-60% (due to underlying causes and assoicated complications of ARDS- i.e. VAP) Ris factors for mortality- Age; degree of hypoexmia; positive fluid balance; steroids prior; Morbidity is also high with significant physcial, psychological and cognitive dysfunction for monthsto years Little improvement in mortality for ARDS over last 30 years. (change in definition; diffuse eitiologies; new therapies introduced; )

Question 16

Risk factors for post extubation stridor

Answer 16

intubation >5 days
traumatic/ difficult intubation
multiple intubation attempts
over inflated cuff
high BMI
female
trauma, surgery, infectin of upper airway
histroy of agitation

Question 17

Titraiton of CO2 parameters on HFOV

Answer 17

I:E ratio
oscillator frequency: 4-15 Hz (usually 4-7Hz in kids)
oscillator amplitude usually 90cm H2O

Question 18

What is a safe rapid shallow breathing index to extubate from?

Answer 18

Generally taken as less than 105. RSBI= RR/Vt (in L).

Question 19

Whatis the pathophysiology of ARDS

Answer 19

A diffuse, inflammatory acute lung kunry, leading to increased capillary permeability and alveolar damage with the release of pro-inflammatory cytokines and proteinaceous fluid filling the airspaces Phases: 1. Injury 2. Exudative phase: alveolar damage and capillary membrane disruption and high protein exudate 3. Proliferative phase (7-10days): resoution og pulmonary oedema and infiltration with type II pneumocytesand fibroblasts 3. Fibrotic phase: slow and incomplete repair with fibrosis and obliteration of normal architecture