18 - Respiratory Failure & ARDS Flashcards
What is the onset of acute vs. chronic respiratory failure? Which one is more serious?
Acute - rapid onset, life-threatening
Chronic - weeks-years
What are the physiologic responses to hypoxemia and hypercarbia from acute respiratory failure?
Hypoxemia
- increased catecholamines –> tachycardia
- increased carotid body stimulation –> tachypnea and hyperventilation
Hypercarbia
- decreased pH and increased intracranial pressure –> CO2 narcosis
- increased PaCO2 –> cerebral vasodilation
What is the equation for O2 delivery?
DO2 = CO * CaO2
What are the physiologic responses to hypoxemia and hypercarbia from chronic respiratory failure?
Hypoxemia
- increased erythropoietin –> increased hemoglobin
Hypercarbia
- increased bicarbonate –> less severe acidosis
How does pulse oximetry work?
2 wavelengths of light due to different absorption by reduced and oxygenated hemoglobin –> allows us to calculate the percentage of oxyhemoglobin
What are the complications of oxygen therapy?
- reactive O2 species are cytotoxic
- blindness or bronchopulmonary dysplasia in children
- decreased mucuciliary clearance
- tracheitis
- acute lung injury
- absorptive atelectasis (removing N2 from air will create a much stronger gradient, causing instantaneous alveolar collapse as gas quickly diffuses out of alveoli)
What are the nonspecific and specific therapies for respiratory failure?
Nonspecific
- hypoxemia –> supplemental oxygen (ineffective if hypoxemia is due to shunt)
- hypercapnia –> avoid/correct
Disease specific
- pneumonia: antibiotics, secretion clearance
- atelectasis: remove secretions
- COPD/asthma: bronchodilators, steroids
- drug overdose: antidote
What are the indications for mechanical ventilation? What are the complications?
Hypoxemic failure
- shunt
- inadequate lung expansion due to atelectasis
Hypercapnic failure
- elevated work of breathing
- respiratory muscle weakness
- insufficient respiratory drive
What are the advantages, disadvantages, and indications for non-invasive ventilation?
Advantages
- avoid endotracheal tube
- less sedation
- care can be given outside of ICU
Disadvantages
- may not tolerate mask or pressure
- no access to airway to remove secretions
Indications
- respiratory failure that can get better in a day or two
- chronic respiratory failure (neuromuscular disease, OHS)
What is the pathogenesis of acute respiratory distress syndrome?
Inflammatory injury to alveoli –> increased alveolar-capillary permeability –> non-cardiogenic pulmonary edema –> reduced compliance and increased shunt –> hypoxemia
What are the common pulmonary and extra-pulmonary causes of acute respiratory distress syndrome?
Pulmonary
- pneumonia
- gastric aspiration
- inhalation
- near drowning
- toxic gas inhalation
- thoracic trauma (pulmonary contusion)
Extra-pulmonary
- sepsis
- pancreatitis
- non-thoracic trauma
- fat embolism
- massive transfusion
- drugs (heroin)
Heterogeneity injury to the lung with areas of poor ventilation and areas of better ventilation is suggestive of ___.
acute respiratory distress syndrome
What is the pathogenesis of acute respiratory distress syndrome?
- Injured alveolar and capillary endothelium –> increased permeability –> fluid leaks into interstitium then alveolar space –> fluid filled alveoli have decreased compliance and cause a shunt
- injury causes significant inflammation and leaking of protein into alveolar space
- type II cells are injured –> reduction in surfactant
- existing surfactant is inhibited by inflammatory cells, oxidation, and proteolytic enzymes –> decreased compliance, alveolar collapse, and alveolar flooding
How is pulmonary circulation affected in acute respiratory distress syndrome? What causes it?
- abnormal
- increased pulmonary arterial pressure
- increased pulmonary vascular resistance
- increased dead space fraction
Results from:
- vasoconstriction
- microthrombi
- compression of vessels by edema
What are the complications of placing someone with ARDS on a ventilator with normal settings? How should ventilator settings be modified?
Normal settings –> all or much of volume will go to better-ventilated areas of lung, leading to:
- barotrauma (disruption of lung with air leaking into pleural space, causing pneumothorax)
- volutrauma (injury to alveolar/capillary interface –> inflammatory process)
- atelectrauma - alveolar injury from opening and closing of alveoli
- biotrauma (increase in cytokines, causing systemic dysfunction)
Modified settings:
- low tidal volumes (to avoid overdistension)
- PEEP (to keep alveoli from completely collapsing at end of expiration)
What treatment will improve ARDS survival? What is an acceptable side effect of this treatment?
low tidal volume ventilation (increase respiratory rate to make up for lowered TV)
results in mild-moderate hypercapnia, which is okay
What is the prognosis for ARDS?
- 30-40% mortality
- those who survive –> generally no or minimal lung dysfunction
- long term side effects: fatigue, weakness, cognitive deficits, PTSD
What is neonatal respiratory distress syndome? How can it be prevented?
Hypoxemic respiratory failure in neonates born at 26-28 weeks due to insufficient quantities of surfactant
Administer corticosteroids prior to birth, administer surfactant after birth
Surfactant administration is beneficial in [neonatal respiratory distress syndrome/acute respiratory syndrome/both]. Why?
Neonatal respiratory distress syndrome only - primarily due to a lack of surfactant
ARDS involves the breakdown of surfactant in addition to a lack of production –> added surfactant will be broken down
What are the two types of respiratory failure? How do you differentiate between them?
Type I - due to hypoxemia (PaO2 < 60 mmHg)
Type II - due to hypercapnia (PaCO2 > 45 mmHg)
Have to get an arterial blood gas
What are the most common mechanisms for hypoxic respiratory failure?
- shunt
- V/Q mismatch
What two types of ILD can cause acute hypoxemic respiratory failure if severe enough?
- cryptogenic organizing pneumonia
- acute interstitial pneumonia
What are the common pulmonary and extra-pulmonary causes of chronic hypoxemic respiratory failure?
- COPD
- pulmonary fibrosis
- pulmonary hypertension
- intracardiac shunt
- pulmonary arteriovenous malformation
- hepatopulmonary syndrome
What are the common pulmonary and extra-pulmonary causes of acute hypoxemic respiratory failure?
- pneumonia
- acute respiratory distress syndrome (noncardiogenic pulmonary edema)
- cardiac pulmonary edema
- lobar collapse
- pulmonary embolism
- pneumothorax
- severe acute ILD (cryptogenic organizing pneumonia or acute interstitial pneumonia)
What are the common pulmonary and extra-pulmonary causes of acute hypercapnic respiratory failure?
- drug overdose
- acute spinal cord injury
- acute neuromuscular disease
- COPD exacerbation
- status asthmaticus
What are the common pulmonary and extra-pulmonary causes of chronic hypercapnic respiratory failure?
- chronic neuromuscular disease
- thoracic cage problem
- abnormal control of breathing (OHS)
- COPD
What is the definition of acute respiratory distress syndrome?
All must be present:
- acute onset (within one week of known clinical insult)
- abnormal CXR or CT (bilateral opacities with pulmonary edema) not fully explained by other processes
- respiratory failure (hypoxemic or hypercapnic) not fully explained by fluid overload or CHF
- hypoxemia: PaO2/FiO2 < 300
What is the approach to treat ARDS?
- mechanical ventilation
- supportive care (avoid excessive fluids, provide adequate nutrition, etc.)
- drug therapy if indicated
What does PEEP stand for? What does it do?
PEEP = positive end-expiratory pressure (setting used with ventilation)
- keeps alveolar pressure above atmospheric pressure at end-expiration to prevent alveolar collapse
- recruits atelectic lung and keeps alveoli open
- improves oxygenation, FRC, and lung compliance
