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Yr2 Lily BRS CardioResp > respiratory failure > Flashcards

respiratory failure Flashcards

1
Q

what is respiratory failure?

A

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

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2
Q

wha tare the signs and symptoms of respiratory failure?

A

basically shortness of breath

all other symptoms are the effects of inadequate gas exchange due to damage to any parts of the respiratory system:
nervous system - 
CNS/Brainstem
Peripheral nervous system
Neuro-muscular junction

respiratory muscle - Diaphragm & thoracic muscles
Extra-thoracic muscles

pulmonary - Airway disease (copd, asthma)
Alveolar-capillary disease
Circulation

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3
Q

what is the epidemiology of chronic respiratory disease?

A

Chronic respiratory disease 3rd leading cause of death* (2017) 39.8% rise from 1990

worse in the more developed world

worse in females than males

getting worse over time

Costs: EU 380m Euro’s annually (2019) care for chronic respiratory disorders
Accounts for: Inpatient care, lost productivity
Despite extensive costs: limited granular data

biggest risk factors:
Males: Smoking
Women: Household air pollution from solid fuels

treatments are getting more effective as morbidity is dropping faster than prevalence

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4
Q

what is the epidemiology of acute respiratory failure?

A

Limited data:
Heterogenous disease presentation (pneumonia, pulmonary hypertension, CF)
Acute respiratory distress syndrome

Prevalence: 6-7 per 100,000 = 6-700 people/yr in UK

30 to 40% Mortality (ALIEN/Esteban)
35, 40 and 46% (Severity dependent. Bellani)

Severity and advance age
 increase mortality

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5
Q

how do we define ARDS?

A

Acute respiratory distress syndrome

we use the berlin definition to classify it:

timing - Within 1 week of a known clinical insult or new/worsening respiratory symptoms.

chest imaging - Bilateral opacities not fully explained by effusions. Lobar/lung collapse or nodules.

origin of oedema -
Respiratory failure not fully explained by cardiac failure or fluid overload.
Needs objective assessment (e.g. echocardiography) to exclude hydrostatic oedema if no risk factor present.

oxygenation - 
mild
moderate 
severe
PF ratio
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6
Q

what are the three different classifications of respiratory failure?

A

acute:
Pulmonary: Infection, aspiration, Primary graft dysfunction (Lung Tx)
Extra-pulmonary: Trauma, pancreatitis, sepsis
Neuro-muscular: Myasthenia/GBS

chronic:
Pulmonary/Airways: COPD, Lung fibrosis, CF, lobectomy
Musculoskeletal: Muscular dystrophy

acute on chronic:
Infective exacerbation
	COPD, CF
Myasthenic crises 
Post operative
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7
Q

how do we classify respiratory failure based on physiological measures?

A

Type I or Hypoxemic (PaO2 <60 at sea level)

Type II or Hypercapnic (PaCO2 >45)

Type III Respiratory Failure: Perioperative respiratory
Failure

Type IV Respiratory Failure: Shock

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8
Q

what is type I respiratory failure?

A

Failure of oxygen exchange

Increased shunt fraction (Q S /QT )
Due to alveolar flooding
Hypoxemia refractory to supplemental oxygen

eg. aspiration, pulmonary oedema, fibrosis, pulmonary embolism, pulmonary hypertension

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9
Q

what is type II respiratory failure?

A

Failure to
exchange or remove carbon dioxide

Decreased alveolar minute ventilation (V A )
Dead space ventilation

eg. nervous system, neuromuscular, muscle failure, airway obstruction, COPD

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10
Q

what is type III respiratory failure?

A

Increased atelectasis (collapse of the airways) due to low functional residual capacity
(FRC) with abnormal abdominal wall mechanics
n Hypoxaemia or hypercapnoea
n Prevention: anesthetic or operative technique, posture,
incentive spirometry, analgesia, attempts to lower intra- abdominal pressure

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11
Q

what is type IV respiratory failure?

A

Type IV Respiratory Failure: Shock
n Type IV describes patients who are intubated and ventilated
During shock (Septic/cardiogenic/neurologic)
n Optimise ventilation improve gas exchange and to unload the
respiratory muscles, lowering their oxygen consumption
Ventilatory effects on right and left heart
Reduced afterload (good for LV) Increased pre-load (bad for RV)

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12
Q

what are the risk factors for chronic respiratory failure?

A 
COPD
Pollution
Recurrent pneumonia
Cystic fibrosis
Pulmonary fibrosis
Neuro-muscular diseases
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13
Q

what are the risk factors for chronic (I think I meant acute) respiratory failure?

A 
Infection
	Viral
	Bacterial
Aspiration
Trauma
Pancreatitis
Transfusion
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14
Q

what are the possible origins (causes) of shortness of breath in acute respiratory failure?

A

Lower respiratory tract infection:
viral
bacterial

aspiration (of gastric acid)

trauma:
transfusion

pulmonary vascular disease:
pulmonary embolus
haemoptysis

Extrapulmonary: pancreatitis, new medications

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15
Q

what are the causes of ARDS?

A 
Pulmonary:
Aspiration
Trauma
Burns: Inhalation
Surgery
Drug Toxicity
infection!
(effects airways down to the alveoli)
Extra-pulmonary:
Trauma
Pancreatitis
Burns
Transfusion
Surgery
BM transplant
Drug Toxicity
infection!
(more systemic)
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16
Q

what biology drives acute lung injury in respiratory failure?

A

leukocytes and inflammatory cells in the lungs

macrophages produce cytokines like IL-6, IL-8, TNF-a

this causes alveolar oedema
and makes them less efficient at expanding as the surfactant round the lungs is degraded

this causes migration of immune cells like neutrophils to migrate out of the blood vessels
this causes more oedema

this increases the distance between the alveoli and the capillaries

making gas exchange less efficient

also angiogenesis

(leukocyte response, inflammatory response, governed by infection

17
Q

what evidence has been discovered in in vivo experiments for respiratory failure biology?

A

TNF signalling implicated in vivo and in vitro:
Reduced injury in TNFR-1 animal KO

Leucocyte activation and migration:
Macrophage activation: alveolar
Neutrophil lung migration

DAMP release: HMGB-1 and RAGE

Cytokine release IL-6,8,IL-1B, IFN-y

Cell death:
Necrosis in lung biopsies
Apoptotic mediators: FAS, FAS-l, BCl-2

these molecules can be produced in the lungs and released into the systemic vasculature, to cause damage in other organs such as the kidneys, heart and liver

18
Q

what pharmacological therapies have been tried to treat respiratory failure?

A 
steroids
salbutamol
surfactant
N-acetylcysteine
neutrophil esterase inhibitor
GM-CSF
statins
trialling now:
mesenchymal stem cells:
ex vivo benefit
keratinocye growth factor
microvesicles
high dose vitamin C
ECCO2R

not much on either of these lists work in humans

19
Q

what is evidence in ARDS like?

A

very limited

because it is a severe disease
and wildly heterogenous

ie. lower concentrations of oxygen work better
proning redices mortality
and reducing fluid administration reduces time on a ventilator

but all these studies are quite old

20
Q

what are the three mechanisms of acute lung injury?

A

inflammation
infection
immune response

21
Q

what are the three main categories of therapeutic intervention for respiratory failure?

A

treat the underlying disease

respiratory support

multiple organ support

22
Q

how do you treat the underlying cause of respiratory failure?

A

Inhaled therapies
Bronchodilators
Pulmonary vasodilators

Steroids
Antibiotics
Anti-virals

Drugs
	Pyridostigmine
	Plasma exchange
	IViG
	Rituximab
23
Q

what respiratory support can be given for respiratory failure?

A 
Physiotherapy
Oxygen
Nebulisers
High flow oxygen
Non invasive ventilation
Mechanical ventilation
Extra-corporeal support
24
Q

what multiple organ support can be given for respiratory failure?

A 
Cardiovascular support
	Fluids
	Vasopressors
	Inotropes
	Pulmonary vasodilators

Renal support
Haemofiltration
Haemodialysis

Immune therapies
Plasma exchange
Convalescent plasma

25
Q

what are the sequelae of ARDS?

A

Poor gas exchange:
Inadequate oxygenation (so stress on highly metabolic organs)
Poor perfusion
Hypercapnoea

Infection:
Sepsis

Inflammation:
Inflammatory response

Systemic effects

26
Q

how is ARDS treated?

A

respiratory support (mechanical)

intubation and ventilation

ARDS necessitates mechanical intervention

types of ventilation:
Volume controlled
Pressure controlled (preferred)
Assisted breathing modes
Advanced ventilatory modes

procedures to support ventilation (eg. proning)

27
Q

what are some pitfalls of ventilation?

A

for patients with COPD/asthma , you van get trapping of air. so not all the inhaled air leaves the lungs, and over time, volume in the lungs increases (breath stacking) (build up of carbon dioxide)
so you have to allow enough time on expiration fir most of the air to be expelled

Minute ventilation:
PaCO2 control

Alveolar recruitment:
Positive end exspiratory pressure (PEEP)

V/Q mismatch:
Ventilation without gas exchange vice-versa

ventilatory induced lung injury

28
Q

what imaging can be used for ARDS?

A

Lung recruitment: CT
opens up recruitable areas of the lungs and shows this on images
(but is not easy and involves radiation)

Lung USS (ultrasound scan)
(can be used at the bedside)
(less information)

29
Q

what guidelines are used to escalate treatment of ARDS?

A

Murray score

uses:
P/F ratio
chest x ray
PEEP
compliance

average in all parameters

to worse each one is the higher your score (0-4)

above 3 = ECMO
only done at 5 places across the UK
also requires pH<7.2

30
Q

what are the inclusion criteria for ECMO?

A

Inclusion Criteria:
• severe respiratory failure:
non-cardiac cause (i.e. Murray Lung Injury score 3.0 or above)
• Positive pressure ventilation is not appropriate (e.g. significant tracheal injury).

Exclusion Criteria:
• Contraindication to continuation of active treatment;
• Significant co-morbidity -> dependency to ECMO support
• Significant life limiting co-morbidity

must have
REVERSIBLE DISEASE PROCESS
UNLIKELY TO LEAD TO PROLONGED DISABILLITY

also consider aaetiology

31
Q

what essentially is ECMO?

A

you take blood from the femoral vein

oxygenate it artificially

then out blood back into the body higher up the femoral vein

32
Q

what are the advantages and disadvantages of ECMO?

A

Advantage:

improve oxygen delivery, improve carbon dioxide removal, rest lung and prevent ventilator associated lung injury, resolve respiratory acidosis, reduce multiple organ dysfunction arising from hypoxaemia and hypercarbia

Disadvantage:

Case selection, not universally available/inequity of provision of care, bleeding: intra-cerebral, venepuncture sites, epistaxis, haemoptysis, Haemolysis, infections from central dwelling canulae, cost.

Yr2 Lily BRS CardioResp (10 decks)

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