Respiratory Failure Flashcards
what is respiratory failure?
Inadequate gas exchange due to dysfunction of one or more components of resp system
main classifications?
Acute
Chronic
Acute on chronic
Acute subsets
Pulmonary and extra pulmonary
Chronic subsets
Pulmonary/airways
Muskoskeletal
Copd
Fibrotic lung disease
Cystic fibrosis
Lobecto t
Muscular dystrophy
Possible causes of acute on chronic
infective exacerbation, myasthenic crisis, post-op
What components of the resp system can fail for resp disease to occur
nervous system (CNS, peripheral, neuromuscular junction)
respiratory muscle (diaphragm, thoracic muscles and extra thoracic muscle )
pulmonary (airway disease, alveolar/capillary issues, circulation)
Chronic risk factors for respiratory failure
Males smoking is the biggest risk factor and in females household pollution from solid fuels
COPD pollution recuurent pneumonia cystic fibrosis pulmonary fibrosis and neuromuscular disease
acute respiratory failure risk factors
Infection,aspiration,trauma,pancreatitis,transfusions,primary
Where in the lung is perfusion greatest and why
Bottom due to higher Intravascular pressure due to effect of gravity
Causes more recruitment less resistance and higher flow rate
Where in the lung is ventilation greatest and why
Bottom as less transmural pressure difference,smaller and more compliant alveoli
O2 saturation of blood before and after gas exchange?
before → 75%
after → close to 100%
pressure pO2 change?
5.3 kPa to 13.1 kPa
Approx pulmonary transit time
0.75 seconds
Gas exchange time
0.25 seconds
Where in the lung is alveolar pressure highest
Top
hierarchies of alveolar, arterial, venous pressures in top/middle/bottom?
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
Normal V/Q is 0.8-1
Structural properties of lung tissue
Compliance:v/p which is the tendency to distort under pressure
Elastance:p/v the tendency to recoil to its original volume
difference between lung volumes and lung capacities?
Volume-discrete
Capacities-sum if volumes
Tidal volume
Difference between min and max volume during relaxed breathing
Inspiratory reserve volume
Difference between max in tidal and max possible
Expiratory reserve volume
Difference between min tidal and min forced
Residual volume
difference between min forced and 0 (residual air that can’t be exhaled)
Type 1 resp failure
Hypoxemic
pO2 < 60 mmHg = 8 kPa
failure of oxygen exchange due to alveolar flooding ,increased shunting fraction (QS/QT which is the ratio of shunted blood to cardiac output ,normally is less than 5 if above the 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
Type 2 resp failure
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
Type 3 resp failure
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
Type 4 resp failure
Shock
On ventilation/intubation during shock (septic/cardiogenic/neurologic)
optimise ventilation by improving gas exchange, lower oxygen consumption to unload resp muscles
Ventilators effects on right and left heart
Reduced afterload (good for LV) and increased preload (bad for RV)
What is ARDS
acute respiratory distress syndrome → alveoli fill with fluid and make breathing less effective
heterogenous disease presentation
Components driving ARDS Pathophysiology
leukocyte recruitment, inflammation
How does ARDS occur
leaky endothelium in alveolar capillaries, edema fluid in alveoli, necrosis and fibrosis in alveolar cells
Examples of causes of ARDS
pulmonary → aspiration, trauma, drug toxicity,surgery,burns:inhalation
extrapulmonary → pancreatitis, transfusion, bone marrow transplant,trauma,burns,drug toxicity,pancreatitis
both: infection !!
Effect on gas exchange for ARDS
distance for gas to exchange across increases due to inflammation and capillary damage
gas exchange becomes less efficient
especially relevant pathways, processes and leukocytes?
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)
- what does management involve?
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
what does respiratory support involve?
low volume ventilation, conservative fluid management
moderate to severe → prone positioning, increased PEEP, neuromuscular blockade, inhaled vasodilators, extracorporeal membrane oxygen
consideration for ventilation in ARDS?
compliance is less in injured lung than normal lung→ same pressure yields less volume
what are upper and lower inflection points?
upper → above this pressure, more alveolar recruitment requires disproportionate pressure increase
lower → minimum baseline pressure for optimal alveolar recruitment. Can be thought of as a minimum baseline measure (PEEP)
potential points for consideration in ventilation?
pCO2 control → good minute ventilation
alveolar recruitment → monitor PEEP (positive end expiratory pressure) reopening collapsed alveoli
V/Q mismatch ventilation without gas exchange
ventilation induced lung injury
who to treat?
severe resp failure, non cardiac cause (murray score 3+)
positive pressure ventilation not appropriate (eg significant tracheal injury)
what are the ventilatory affects on the right and left heart for type 4 shock
reduced afterload which is good for LV
increased preload which is bad for RV
Pharmacological intervention
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
Murray score
0=normal
1-2.5=mild
2.5=severe
3=ECMO
Exclusion criteria
Contraindications to continue active treatment
Significant co morbidity dependent to ECMO support
Significant life limiting co morbidity
Evidence for ECMO
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
ARDS sequele
Poor gas exchange
Inadequate oxygenation
Poor perfusion
Hypercapneoa
Infection-sepsis
Inflammation
Systemic affects
Minute and alveolar ventilation
Minute ventilation measures gas entering and leaving the lungs
Tidal volume times breathing frequency
Alveolar ventilation measures volume of gas entering and leaving alveoli
Tidal volume-dead space times breathing frequency Alveolar
How can we define ARDS
Berlin classification
Timing-within 1 weeks of a known clinical insult or new or worsening resp symptoms
Chest imaging-bilateral opa opacities which aren’t fully explained by effusions lobar or lung collapse or nodules
Origin of odemia not fully explained by cardiac failure of fluid overload
Oxygenation
Mild-200mmHG<o2>5cmh2o
100mmhg<o2 with peep greater than 5
Severe 100< with peep greater than 5</o2>
What do we see in CT/mRi in ards
Poor perfusion
Inflammatory endo types of ARDS
Hyper and hypo inflammatory endotypes
In ARDS harp-2 levels are associated with alveolar injury
TNFR1 mediates inflammation causing alveolar damage
Both causes necroptosis
What is the overall mechanism of acute lung injury?
Alveolar macrophages are activated due to inflammation and cause release of IL6!8,TNF-A
Fuses protein rich Oedema
Inactivation of surfactants means alveolus becomes less efficient at expanding
Neutrophils migrate jn GI jnterstitium causing secretion of proteases
More Odema increasing diffusion distance between capillary and alveoli
