Acute Respiratory Failure Flashcards
DEFINE: acute respiratory failure
respiratory system no longer able to meet the metabolic demands of the body, resulting in dropping levels of O2 and rising levels of CO2 for either or both of impaired gas exchange (diffusion/perfusion) or impaired ventilation
What are the two major functions of the lung?
oxygenation of blood and elimination of carbon dioxide
What are the two types of respiratory failure and how are they defined?
HYPOXEMIC: when arterial partial pressure of O2 (PaO2) = <60mmHg at room air
HYPERCAPNIC: PaCO2 >50mmHg
(acute vs chronic - depending on duration of respiratory failure and nature of compensation)
What are the main mechanisms of acute respiratory failure?
- LOW INSPIRED PARTIAL PRESSURE OF O2
- HYPOVENTILATION
- VENTILATION PERFUSION MISMATCH
- DIFFUSION ABNORMALITY
- decreased diffusion of O2 across alveolar-capillary membrane → reduced PaO2 → hypoxia
How does LOW INSPIRED PARTIAL PRESSURE OF O2 cause acute respiratory failure + give causes
LOW INSPIRED PARTIAL PRESSURE OF O2
- reduces diffusion gradient of O2 across alveolar membrane
(PaO2 = product of inspired O2 FiO2 and barometric pressure)
eg: high altitude
How does HYPOVENTILATION cause acute respiratory failure + give causes
HYPOVENTILATION
- complicated by both hypoxia and hypercapnia
CNS: respiratory centre depression, drugs, anaesthetics, head injury, encephalopathy, fatigue etc
Disruption of resp signal during transmission of nerves to respiratory muscles: spinal cord injury, motor neuron disease, Guillain-Barre syndrome
Dysfunction of NMJ (neuromuscular junction): paralytic agents, myasthenia gravis
Dysfunction of muscles of respiration: myopathy, fatigue, malnutrition, muscular dystrophy etc
Chest wall abnormalities: kyphoscoliosis, ankylosing spondylitis, pleural fibrosis etc
Airway obstruction: upper or lower
Decreased Lung compliance:
How does VENTILATION PERFUSION MISMATCH cause acute respiratory failure + give causes
VENTILATION PERFUSION MISMATCH
- most common cause of hypoxemic respiratory failure
(1) reduced perfusion to alveolus:
- gas passes in and out of alveolus but doesnt come into contact with capillary bed, effectively increasing the deadspace - Co2 cant be eliminated and O2 cant diffuse across
eg: PE, hypovolaemia, poor cardiac output, high intrathoracic pressures (from positive pressure ventilation), COPD
(2) reduced ventilation to alveolus
eg: alveolus full of fluid or pus ∴ not ventilated → capillary bed is not oxygenated → this deoxygenated blood mixes with oxygenated blood → ↓O2 sats
- hypoxic pulmonary vasoconstriction reduces proportion of blood perfusing non-ventilated lung ∴ minimising shunting
- NOTE: increasing FiO2 in this setting has little effect as well ventilated units are already 100% saturated
eg: pneumonia, ARDS, pulmonary oedema, pulmonary haemorrhage, contusion, atelectasis, pneumothorax etc
(3) anatomical shunting (intracardiac)
eg: Fallot tetralogy, Eisenmenger syndrome
How does DIFFUSION ABNORMALITY cause acute respiratory failure + give causes
DIFFUSION ABNORMALITY
- decreased diffusion of O2 across alveolar-capillary membrane → reduced PaO2 → hypoxia
- less common
eg: severe destructive diseases of the lung - late fibrosing diseases, severe pulmonary oedema, ARDS
What is the A-a gradient?
gradient between partial pressure of O2 in alveolus and arterial blood (normal = <20mmHg - but this is altered by age and FiO2)
Normal Aa gradient implies that any hypoxaemia can be explained by the hypercapnia
Increased gradient implies a ventilation/perfusion mismatch (shunt) or diffusion abnormality is causing the hypoxaemia
What are common causes of breathlessness based on speed of onset?
MINUTES
- pneumothorax
- PE
- APO
HOURS
- asthma
- pneumonia
- APO
- metabolic acidosis
DAYS/WEEKS
- pleural effusion
- exacerbation of COPD
- pneumonia
What are the clinical signs of RESPIRATORY DISTRESS?
RESPIRATORY DISTRESS
1) Increased WOB
- ↑RR
- use of accessory muscles of respiration
- nasal flaring
- intercostal/suprasternal/supraclavicular retraction
- pardoxic/dyskinetic (see-saw) breathing
2) Sweating, ↑HR, ↑BP -> hypotension and bradycardia = late signs
3) Altered mental status eg: agitation to coma/seizures
4) Cyanosis - peripheral and central
Why do we use O2 cut off of SpO2 >90%?
S-shaped oxyhaemoglobin dissociation curve describes the relationship btw O2 saturation and PaO2 blood lvls
- a saturation of ~90% is the critical threshold because below this level -> a small fall in arterial O2 produces a sharp fall in O2 saturations
NB: it is O2 saturation not PaO2 that is the main determinant of O2 content of blood and O2 delivery to tissues
What are some sources of error is SpO2 interpretation?
poor peripheral perfusion false nails/varnish dark skin ( oximeter over-reads slightly) lipaemia bright ambient light poorly adheretn probe excessive motion carboxyhaemoglobin curve
How does capnography work?
CO2 only produced by lungs ∴ presence of CO2 in expired gas confirms that ETT is in correct position
- if pt has relatively normal lungs and cardiac output -> end tidal CO2 tension gives estimate o PaCO2
What are the different methods of delivering supplemental O2 and give examples of devices
1) FIXED PERFORMANCE DEVICES = supply a relatively constant O2 concentration to lungs
- air-entrainment masks (venturi masks)
-
2) VARIABLE PERFORMANCE DEVICES = provide variable concentrations of O2 depending on patient’s respiratory rate and inspiratory flow pattern
- - nasal cannula (prongs)/high flow nasal cannula