RADS Flashcards
RADS type I
hypoxemic; PaO2<60
RADS type II
hypercapnic and hypoxemic; PaCO2 > 45
Acute decrease in PaO2
increase in a catecholamine surge leading to increase heart rate - carotid body senses it and it leads to increase in resp. rate and ventilation
Acute increase in PaCO2
- decrease in pH and increase in intracranial pressure leading to CO2 narcosis, headache
most common mechanism for hypoxemic RADS
- shunt - V/Q
causes of chronic hypoxemic RADS
- V/Q mismatch: COPD, ILD, Pulm htn - shunt: pulm arteriovenous malformation, hepatopulm. syndrome
hypercapnic RADS
- increase in dead space - increase work of breathing - decrease in resp. drive and pump
causes of acute hypercapnic- hypoxemic RADS
- hypoventilation: drug overdose, acute spinal cord injury, acute neuromuscular dx. - v/q. increase in dead space, load and muscle fatigue: COPD, status asthmaticus
causes of chronic hypercapnic RADS
chronic Neuromuscular dx., thoracic cage, OHS
what is an issue with the nasal cannula?
variable FiO2
tell me about the standard face mask?
high flow O2 but FiO2 is still variable
HFNC
there is improved oxygenation, clearing of anatomic dead space and improved secretion clearance
complications of O2 therapy how should we try to prevent them?
- reactive O2 species are cytotoxic - peds: blindness and bronchopulmonary dysplasia - absorptive atelectasis use lowest FiO2 to maintain desired PaO2, SaO2
what is mechanical ventilation?
supportive therapy where there can be a reverse but recovery depends upon reversal of underlying disease process - can be either full or partial support
PEEP
positive end-expiratory pressure - increase lung volume, decrease in atelectasis
complication of mechanical ventilation
- can lead to over-distension of lung - intubation may be required - ventilator associated pneumonia
advantage of non-invasive ventilation? disadvantage?
advantages: less sedation, decreases chances of pneumonia disadvantages: hard to tolerate mask
inflammatory injury to alveoli leading to increase permeability of alveolar-capillary barrier
ARDS
all what must be present in ARDS
- acute onset - abnormal CT - respiratory failure - hypoxemia
what are some commone causes of ARDS
- direct: pneumonia, inhalation, pulm. contusion - extrapulmonary: sepsis, pancreatitis, drugs
acute lung injury leads to
increased permeability
abnormal surfactant
decreased compliance with alveolar collapse anda flodding
main cause of neonataal resp. distress syndrome
surfactant deficiency
ARDS network trial showed
lower tidal volumes protect the lung
ventilator-induced lung injury
- volutrauma - barotrauma - biotrauma - atelectrauma
repetitive opening and closing of alveoli can injury alveoli
atelectrauma
injury to lung releases harmful cytokines –> further lung injury and injury to other organs
biotrauma
injury to lung indistinguishable from ARDS
volutrauma
rupture of alveoli with gas escaping into pleural space (pneumothorax)
barotrauma
ARDS showing dense lower lobe atelectasis- alveoli in these areas are gasless
minute ventilation is
respiratory rate X volume
concentration of O2 equation
HbxSaO2 + .003xPaO2
is nasal cannula associated with CO2 rebreathing
nope
whne do you need to humidify air whne delivered through a device
at high flows
absorption atelectasis
happens when an obstructed alveoli is given Pure O2 washing out nitrogen and the partial pressure decreases. Alveoli collapses
non-ivasive mechanical ventilation works very well for
COPD exarcebation
ARDS cut off of symptoms
a week
alveolar ventilation mechanism
increase perfusion and thus imrpving oxygention but not mortality
lack of effectiveness of surfactant in adult ARDS
there are inhibtors that blcok surfactant
