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BRS YEAR 2 > Resp - Resp Failure > Flashcards

Resp - Resp Failure Flashcards

1
Q

What is respiratory failure

A

Syndrome of inadequate gas exchange due to dysfunction of one or more of the components for the respiratory system

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2
Q

What systems can cause respiratory failure

A

Nervous system
Respiratory musculature
Pulmonary

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3
Q

What in the nervous system can cause resp failure

A

CNS/Brainstem
Peripheral nervous system
NMJ

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4
Q

What in the muscles can cause resp failure

A

Diaphragm and thoracic muscles

Extra-thoracic muscles

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5
Q

What are the pulmonary causes of resp failure

A

Airway disease
Alveolar-capillary
Circulation

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6
Q

Where are respiratory problems more of a problem and in who

A

We see more chronic respiratory problems in northern America and Northern Europe - northern American males are worse off than females, and Russian women are worse off then males

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7
Q

What is the biggest rf for men

A

Smoking

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8
Q

What is the biggest rf for women

A

Household air pollution from solid fuels

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9
Q

What is ARDS

A

Acute respiratory distress syndrome

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10
Q

How do we define ARDS

A

Berlin definition

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11
Q

How can we class respiratory failure

A

Acute
Chronic
Acute on chronic

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12
Q

What are the causes of acute respiratory failure

A

Pulmonary causes e.g. infection, aspiration, primary graft dysfunction.

Extra-pulmonary causes e.g. trauma, pancreatitis, sepsis

Neuro-muscular e.g. myasthenia gravis, Guillain Barre syndrome

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13
Q

What are causes of chronic respiratory failure

A

COPD, lung fibrosis, CF, post lobectomy

MSK causes eg. muscular dystrophy

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14
Q

What are causes of acute on chronic resp failure

A

Infective exacerbation of chronic condition e.g. COPD/CF
Myasthenia crisis
Post op if you already have an underlying respiratory disease

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15
Q

What is type 1 resp failure

A 
Hypoxemic: 
PaO2 <60 at sea level 
Failure of oxygen exchange 
Increased shunt fraction 
Due to alveolar flooding e.g. heart failure 
Refractory to supplemental oxygen
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16
Q

What can cause type 1 resp failure

A 
Collapse of lobe
Aspiration
Pulmonary oedema
Fibrosis 
Pulmonary embolism 
Pulmonary hypertension
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17
Q

What is type 2 resp failure

A 
Hypercapnic 
PaCO2 > 45
Failure to remove CO2
Decreased alveolar minute ventilation
Dead space ventilation
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18
Q

What can cause type 2 resp failure

A 
Nervous system disease
Neuromuscular disease 
Muscle failure
Airway obstruction e.g. COPD
Chest wall deformity e.g. trauma/ ageing
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19
Q

What is type 3 resp failure

A

Perioperative:

Atelectasis (lung collapse) of airway due to low FRC
Often ude to abdominal wall mechanisms
Can get hypoxemia and hypercapnia

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20
Q

How do we prevent type 3 resp failure

A

Anaesthetic or operative technique, posture, incentive spirometry, analgesia

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21
Q

What is type 4 resp failure

A

Shock causing poor perfusion of the lung - seen in septic, cariogenic and neurogenic shock - get vsasoplegia so pooling f the blood in the periphery

22
Q

How do we manage type 4 resp failure

A

Intubation as consciousness falls due to shock - positive pressure ventilation

23
Q

What are chronic rfs for resp failure

A 
COPD
Pollution
Recurrent pneumonia
CF
Pulmonary fibrosis 
Neuromuscular diseases
24
Q

What are acute rfs for resp failure

A 
Infection
Aspiration 
Trauma 
Pancreatitis 
Transfusion
25
Q

What are the 2 main causes of ARDS

A

Pulmonary and extra-pulmonary

26
Q

What are the pulmonary causes of ARDS

A 
Largely infection 
Aspiration
Trauma 
Burns
Surgery
Drug toxicity
27
Q

What are the extra-pulmonary causes of ARDS

A 
Infection
trauma 
Pancreatitis 
Burns 
Transfusions 
Surgery 
BM transplant 
Drug toxicity
28
Q

How does the lung response to injury leads to ARDS

A

Injury leads to damage of the lung interstitium.
This causes macrophage activation and the release of cytokines e.g. TNF-a and IL-8
We get alveolar fluid build up therefore protein rich oedema in the lungs
Therefore we get degradation and inactivation of surfactant meaning that the alveolus is less efficient at expanding
Inflammation of the alveolus leads to migration of leucocytes e.g. neutrophils which cause further damage
This widens the distance between the alveolus and the capillaries therefore less efficient gas exchange and respiratory failure

29
Q

What in vivo evidence do we have for ARDS

A 
TNF signalling
Leucocyte activation and migration
DAMP release
Cytokine release e.g. IL-6/8
Cell death - necrotic tissue in ARDS
30
Q

What tried pharmacological therapies can be used for ARDS

A 
Steroids e.g. dexamethasone
Salbutamol
Surfactant
N-ACh - reduces viscosity of secretions
Neutrophil elastase inhibitors 
GM-CSF
Statins
31
Q

Why is evidence in ARDS for treatment very limited

A

ARDS is extremely severe and very heterogenous therefore hard to find overarching patterns for treatment

32
Q

What are the 3 aspects of therapeutic intervention for ARDS

A

Treat underlying disease
Respiratory support
Multi-organ support

33
Q

How do we treat underlying disease

A 
Inhaled therapies e.g. bronchodilators 
Steroids
ABx
Antivirals 
Drugs e.g. rituximab
34
Q

What can we give for respiratory support

A 
Physiotherapy
Oxygen (not in type 2)
Nebuliser
NIV
Extra corporeal support
35
Q

What can we give for multiorgsan support

A

CV support e.g. fluids. vasopressors
Renal support e.g. hemodialysis
Immune therapies e.g. plasma exchange

36
Q

What are the sequelae of ARDS

A

Poor gas exchange leads to multi-organ dysfunction
Infection leads to sepsis
Inflammation leads to oedema

37
Q

What do we base ventilation on

A

Pressure not volume - this is because pressure is more likely to cause damage to the lung

38
Q

What is the peak pressure

A

Pressure that drives into the lung

39
Q

What is the PEEP and why do we need it

A

Baseline pressure that keeps the airways open - this means less force is required at the start for recruitment therefore less likely to damage the airways - atelectasis is more likely if pressure falls below the PEEP

40
Q

What is assisted breathing

A

We use a sensor and then when the patient is trying to inhale then we can give them some driving pressure

41
Q

What is the difference between a normal PVL and a PVL in ARDS

A

There is marked reduction in compliance during ARDS therefore the PVL is much flatter - we are using a lot more pressure in order to generate a lower volume

42
Q

When may air trapping occur

A

In people with type 2 hypercapnic failure - their airways are often constricted therefore cannot normally exhale fully. This means that they get air trapping and breath stacking

43
Q

How do we mitigate air trapping

A

We give them longer periods to exhale in order to get as much air out as possible - make sure expiratory pressure is low enough fro them to be able to expire, but high enough to keep airways open

44
Q

What is a lung recruitment CT

A

We use a driving pressure to distend the lung and see if its recruitable - we need to make sure pressure isn’t too high otherwise we may over distend the lung and trap gas in the chest to damage the lung and impart perfusion.

45
Q

What are alternatives to CT lung recruitment

A

US at the bedside to examine the lung expansion and any fluid

46
Q

What do we use to guide escalation of therapy

A

Murray scoring

47
Q

What are the Murray score thresholds for escalating treatments

A

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

48
Q

How can we try and improve Murray score

A

Proning

49
Q

When is ECMo indicated

A

Severe resp failure - Murray score is 3+
Positive pressure ventilation is not appropriate e.g. tracheal injury
Reversible disease process that is unlikely to lead to prolonged disability

50
Q

When is ECMO contraindicated

A

Significant life-limiting co-morbidity - likely to remain on ECMO or life support

51
Q

What happens in ECMO

A

Large cannula is passed through the femoral vein to the IVC, we then run blood through an external pump across an artificial membrane. Here, we flow gas to allow removal of CO2 and blood oxygenation. This can also be done in the jugular

BRS YEAR 2 (37 decks)

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