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BRS YEAR 2 > Respiratory Failure > Flashcards

Respiratory Failure Flashcards

1
Q

what is respiratory failure?

A

Inadequate gas exchange due to dysfunction of one or more components of resp system

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2
Q

main classifications?

A

Acute
Chronic
Acute on chronic

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3
Q

Acute subsets

A

Pulmonary and extra pulmonary

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4
Q

Chronic subsets

A

Pulmonary/airways
Muskoskeletal

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5
Q

Possible causes of acute on chronic

A

infective exacerbation, myasthenic crisis, post-op

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6
Q

What components of the resp system can fail for resp disease to occur

A

nervous system (CNS, peripheral, neuromuscular junction)

respiratory muscle (diaphragm, thoracic muscles)

pulmonary (airway disease, alveolar/capillary issues, circulation)

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7
Q

Risk factors for chronic respiratory failure

A

COPD, pollution, recurrent pneumonia, cystic/pulmonary fibrosis, neuromuscular disease,

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8
Q

Risk factors for acute respiratory failure

A

Infection,aspiration,trauma,pancreatitis,transfusions,primary

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9
Q

Where in the lung is perfusion greatest and why

A

Bottom due to higher Intravascular pressure due to effect of gravity
Causes more recruitment less resistance and higher flow rate

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10
Q

Where in the lung is ventilation greatest and why

A

Bottom as less transmural pressure difference,smaller and more compliant alveoli

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11
Q

O2 saturation of blood before and after gas exchange?

A

before → 75%

after → close to 100%

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12
Q

pressure pO2 change?

A

5.3 kPa to 13.1 kPa

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13
Q

Approx pulmonary transit time

A

0.75 seconds

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14
Q

Gas exchange time

A

0.25 seconds

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15
Q

Where in the lung is alveolar pressure highest

A

Top

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16
Q

hierarchies of alveolar, arterial, venous pressures in top/middle/bottom?

A

top: alv > art > ven

middle: art > alv > ven

bottom: art > ven > alv
V/Q is highest at apex (~3)as ventilation greater and lower in the bottom (~0.6)as perfusion is greater

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17
Q

Structural properties of lung tissue

A

Compliance:v/p
Elastance:p/v

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18
Q

difference between lung volumes and lung capacities?

A

Volume-discrete
Capacities-sum if volumes

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19
Q

Tidal volume

A

Difference between min and max volume during relaxed breathing

20
Q

Inspiratory reserve volume

A

Difference between max in tidal and max possible

21
Q

Expiratory reserve volume

A

Difference between min tidal and min forced

22
Q

Residual volume

A

difference between min forced and 0 (residual air that can’t be exhaled)

23
Q

Type 1 resp failure

A

Hypoxemic
pO2 < 60 mmHg = 8 kPa

failure of oxygen exchange due to alveolar flooding ,increased shunting,hypoxadmia refractory to supplemental oxygen (as large right to left shunt. There’s a V/Q mismatch (low perfusion). Blood bypasses the lungs so deoxygenated blood enters circulation
for eg collapse, aspiration,pulmonary odema,fibrosis,pulmonary embolism,pulmonary hypertension

24
Q

Type 2 resp failure

A

Hypercapnic

failure to exchange/remove CO2

CO2 pressure > 45

decreased alveolar minute ventilation and dead space ventilation

due to nervous system,neuromusclar,muscle failure,airway obstruction,chest wall deformity

25
Q

Type 3 resp failure

A

Perioperative
Increased atelectasis due to low functional residual capacity with normal abdominal wall mechanics
can be hypoxaemia or hypercapnia, essentially due to low functional residual capacity from pressure collapsing lung

prevention-anaesthetic or operative technique,posture,incentive spirometry,analgesia,attempts to lower intra abdominal pressure

26
Q

Type 4 resp failure

A

Shock
On ventilation/intubation during shock (septic/cardiogenic/neurologic)

optimise ventilation by improving gas exchange, lower oxygen consumption to unload resp muscles

27
Q

What is ARDS

A

acute respiratory distress syndrome → alveoli fill with fluid and make breathing less effective
heterogenous disease presentation

28
Q

Components driving ARDS Pathophysiology

A

leukocyte recruitment, inflammation

29
Q

Consequences of ARDS

A

leaky endothelium in alveolar capillaries, edema fluid in alveoli, necrosis and fibrosis in alveolar cells

30
Q

Examples of causes of ARDS

A

pulmonary → aspiration, trauma, drug toxicity,surgery,burns:inhalation

extrapulmonary → pancreatitis, transfusion, bone marrow transplant,trauma,burns,drug toxicity,pancreatitis

both: infection !!

31
Q

Effect on gas exchange for ARDS

A

distance for gas to exchange across increases due to inflammation and capillary damage

gas exchange becomes less efficient

32
Q

especially relevant pathways, processes and leukocytes?

A

TNF signalling implicated

alveolar macrophage and neutrophil recruitment both involved

DAMP release (HMGB1 and RAGE), cytokine release (IL-6,8,IL-1B.IFN-Y)

cell death-necrosis in lung biopsies and apoptotic mediators (FAS,FAS-I,BCI-2)

33
Q
  • what does management involve?
A

treat underlying disease:
Inhaled therapies such as bronchodilator or pulmonary vasodilator,steroids,abx,anti virals,drugs (pyridostigamine,plasma exchange,IViG,rituximab

resp support:physio,oxygen,nebulisers,high flow oxygen,non invasive ventilation,extra corporeal support,mechanical ventilation

multiple organ support:fluids,vasopressors,inotropes,pulmonary vasodilators,haemofiltration,haemodialysis,plasma exchange,convalescent plasma

34
Q

what does respiratory support involve?

A

low volume ventilation, conservative fluid management

moderate to severe → prone positioning, increased PEEP, neuromuscular blockade, inhaled vasodilators, extracorporeal membrane oxygen

35
Q

consideration for ventilation in ARDS?

A

compliance is less in injured lung → same pressure yields less volume

36
Q

what are upper and lower inflection points?

A

upper → above this pressure, more alveolar recruitment requires disproportionate pressure increase

lower → minimum baseline pressure for optimal alveolar recruitment

37
Q

potential points for consideration in ventilation?

A

pCO2 control → good minute ventilation

alveolar recruitment → monitor PEEP (positive end expiratory pressure)

V/Q mismatch ventilation without gas exchange

ventilation induced lung injury

38
Q

who to treat?

A

severe resp failure, non cardiac cause (murray score 3+)

positive pressure ventilation not appropriate (eg significant tracheal injury)

39
Q

acute on chronic

A

infective exacerbation
copd/cf,myasthic crises,post operative

40
Q

what are the ventilatory affects on the right and left heart for type 4 shock

A

reduced afterload which is good for LV
increased preload which is bad for RV

41
Q

Pharmacological intervention

A

Tried-steroids,salbutamol,surfactant,n-acetylcysteine,neutrophil esterase inhibitor,GM-CSF,statins

trials-mesecnhymal stem cells (ex vivo benefit),keratinocyte growth factor,microvesicles,steroids,ECCO2R

42
Q

Murray score

A

0=normal
1-2.5=mild
2.5=severe
3=ECMO

43
Q

Exclusion criteria

A

Contraindications to continue active treatment
Significant co morbidity dependent to ECMO support
Significant life limiting co morbidity

44
Q

Evidence for ECMO

A

Statistically no significant difference
RBH survival 79%
Issues with time to access,referral system
Technical to obtain access of IJV,subclavian,femoral,circuit,haemodynamics,clotting/bleeding

45
Q

ARDS sequele

A

Poor gas exchange
Inadequate oxygenation
Poor perfusion
Hypercapneoa
Infection-sepsis
Inflammation
Systemic affects

BRS YEAR 2 (42 decks)

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