ARDS (Various PDFs, Harrisons) Flashcards
When was ARDS first recognized?
World War I, when it was recognized that some patients with non-thoracic injuries developed respiratory distress, diffuse lung infiltrates, & respiratory failure.
Jeopardy style!
The most severe form of acute lung injury, a form of diffuse alveolar injury.
What is acute respiratory distress syndrome, or ARDS?
In ARDS, the PaO2/FIO2 ratio is less than…
200
In ALI (acute lung injury), the PaO2/FIO2 ratio is less than…
300
For ARDS to be diagnosed, what other condition must be excluded? How do you exclude it?
Cardiogenic pulmonary edema; by clinical criteria or by pulmonary capillary wedge pressure < 18
Which phase of ARDS is exudative?
Early
Which phase of ARDS is fibroproliferative?
Late
The site of injury in ARDS may be either…
1) the vascular endothelium (as in sepsis)
2) the alveolar epithelium (as in aspiration of gastric contents)
2 types of alveolar epithelial cells
Type I & Type II
Oooh that was hard
Describe Type I alveolar epithelial cells
1) Make up 90% of the alveolar epithelium
2) Easily injured
3) Damage allows increased entry & decreased clearance of fluid into alveoli
Describe Type II alveolar epithelial cells
1) Fewer of them
2) More resistant to injury
3) Functions include: production of surfactant, ion transport, proliferation & differentiation into Type I cells after cellular injury (repair processes)
Why is it so much worse if Type II alveolar cells are damaged?
BECAUSE THEY’RE IMPORTANT!
Decreased surfactant results in decreased compliance & alveolar collapse, then interference with the normal repair process leads to fibrosis.
Neutrophils in ARDS
Thought to play a key role, but may be reactive rather than causative
Cytokines in ARDS
Imbalance of proinflammatory & anti-inflammatory cytokines thought to occur after inciting event.
Can happen because of positive pressure ventilation: ventilator-associated lung injury (VALI)
ARDS causes a marked increase in __________ (2 words), leading to severe hypoxemia.
intrapulmonary shunting
What’s the association between pulmonary hypertension & ARDS
You will see pulmonary hypertension in ARDS patient. It normalizes as the syndrome resolves.
Pulmonary artery vasoconstriction likely contributes to ventilation-perfusion mismatch, leading to hypoxemia.
ARDS resolution?
The acute phase usually resolves completely.
If the acute phase of ARDS doesn’t resolve completely, what do we end up with?
Residual pulmonary fibrosis.
How can we check for progression to fibrosis?
1) Increased levels of procollagen peptide III early in the course (in the fluid found by bronchioalveolar lavage)
2) Fibrosis findings upon biopsy
The indicators or findings of fibrosis correlate with…
…an increased mortality rate.
What percentage of ARDS patients have no identified risk factors?
20%
What is the most common risk factor for ARDS?
Sepsis
Risk factors for ARDS generally fall into these 3 categories:
1) Direct lung injury (as in aspiration)
2) Systemic illnesses
3) Injuries
Major risk factors associated with ARDS
#Bacteremia & sepsis #Trauma (with or without pulmonary contusion) #Fractures (particularly multiple or long bone) #Burns #Massive transfusion #Pneumonia #Aspiration #Drug overdose #Near drowning #Postperfusion injury after bypass #Pancreatitis #Fat embolism #Metabolic acidosis
Factors that increase the risk of ARDS after inciting event:
#Advanced age #Female sex (only in trauma) #Smoking #Alcohol use
As severity of illness increases (as gauged by a severity scoring system such as APACHE), what happens to risk for ARDS?
It increases!
The sicker you are, the sicker you’re likely to get! SURPRISE!
True or false: Most deaths in ARDS patients are attributable to primary pulmonary cause.
False. Most are attributable to sepsis or multi-organ failure.
Which is a better indicator of prognosis: PaO2/FIO2 ratio at the time of diagnosis, or lack of pulmonary improvement in the first week?
The PaO2/FIO2 ratio does not correlate with outcome, but the lack of improvement within the first week is a poor prognostic factor.
So how long does it take to get over ARDS entirely?
A freaking long time. ARDS patients have #prolonged hospital courses #frequent nosocomial infections (like VAP) #Functional impairment for months & years post-recovery #Decreased health-related quality of life (HRQL) compared to general population. #In short: ARDS SUCKS BAD.
Harrison’s defines ARDS as…
“a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.”
Important ratio in the diagnosis of ARDS & ALI:
FiO2 (percentage of inspired O2)
What percentage of ICU admissions have acute respiratory failure? What percentage of those patients meet criteria for ALI or ARDS?
10% of all ICU admits
20% of those meet ALI/ARDS criteria
When a patient is suffering from more than 1 of the ARDS- predisposing conditions, what happens to risk?
Goes up, of course!
So if I have trauma, I might get ARDS, but if I have trauma AND sepsis, I’m way more likely. HOW NICE FOR ME.
ARDS pathophysiology happens in 3 phases:
1) Exudative
2) Proliferative
3) Fibrotic
Exudative phase characteristics
Type I pneumocytes (alveolar epithelial cells) are injured»_space;
Loss of alveolar barrier»_space;
Edema fluid accumulates in interstitial/alveolar spaces»_space;
Cytokines & lipid mediators are present»_space;
Neutrophils go into interstitium & alveoli»_space;
Vascular obliteration by microthrombi & fibrocellular proliferation
On an AP CXR, the exudative phase of ARDS can be easily confused with what other condition?
The pulmonary congestion of left heart failure!
The alveolar edema of the exudative phase usually involves what part of the lung?
Dependent portions, leading to diminished aeration & atelectasis
When large parts of dependent lungs collapse, this decreases lung compliance. What happens next?
Intrapulmonary shunting & hypoxemia, leading to increased work of breathing and dyspnea.
Microvascular occlusions lead to…
…reduction in pulmonary arterial blood flow to the portions of lung that ARE ventilated, further increasing dead space and causing pulmonary hypertension and thus, hypercapnia.
ARDS (exudative phase) in a nutshell
1) Injury of Type I pneumocytes, then
2) Edema fluid enters alveoli, then
3) Alveoli collapse, especially in dependent portions of lung, then
4) Lung compliance is decreased, then
5) Intrapulmonary shunting & hypoxemia increase the work of breathing (so, dyspnea), while
6) Occlusions in microvasculature reduce pulmonary arterial flow, leading to pulmonary hypertension, which causes
7) Hypercapnia
TADA, YOU’RE A PRO!
When does the exudative phase happen?
The first 7 days after exposure to risk factor.
Usually 12-36 hours, but can be up to 5-7 days.
What does it look like clinically?
#Dyspnea with rapid, shallow breathing & air hunger #Tachypnea leading to fatigue & respiratory failure #CXR show interstitial opacities #CXR looks like cardiogenic pulmonary edema (to differentiate, ARDS rarely shows cardiomegaly, pleural effusions, or pulmonary vascular redistribution) #CT: heterogeneity of lung involvement (remember: look for dependent atelectasis)
What are some differentials for the exudative phase of ARDS?
COMMON: #Cardiogenic pulmonary edema #Diffuse pneumonia #Alveolar hemmorhage
LESS COMMON: #Acute interstitial lung diseases #Acute immunologic injury #Toxins #Neurogenic pulmonary edema
When does the proliferative phase of ARDS happen?
About days 7 to 21
ARDS (proliferative phase) in a nutshell:
1) Shift from neutrophil to lymphocyte pulmonary infiltrate and
2) Proliferation of Type II pneumocytes, which synthesize new surfactant & differentiate into Type II pneumocytes, which is basically
3) Initiation of lung repair
Most peeps recover rapidly & get to come off the vent during this phase. SCORE! We fixed it!
But if a patient in the proliferative phase has procollagen peptide, they may enter what phase? Why’s that bad?
Fibrotic phase dramatic music, which is associated with a longer clinical course & increased mortality. BOOOOO.
ARDS (fibrotic phase) in a nutshell:
1) Edema & exudates convert to alveolar & interstitial fibrosis, which
2) Disrupts acinar architecture, leading to
3) Emphysema-like changes with large bullae while
4) Fibroproliferation in microcirculation leads to progressive occlusion & pulmonary hypertension
Consequences: increased risk of pneumothorax, reduced lung compliance, increased dead space, and potentially long-term ventilator support. NOOOOO. We didn’t fix it. :(
We’ve recently reduced ARDS, but mostly because we got better at treating critically ill people in general. So, we should pay close attention to:
1) Treatment of the underlying conditions & disorders
2) Minimizing procedures/complications
3) Prophylaxis for VTE, GI bleeding, aspiration, sedation, & central line infections
4) Recognition of nosocomial infections
5) Adequate nutrition
For your ARDS patient: high or low tidal volume?
LOOOOOOOW!
Attempts to full inflate the collapsed dependent part of the lung may overdistend the normal, less involved portions, leading to injury.
Ventilator-induced lung injury requires 2 processes. What are they?
1) Repeated alveolar overdistention
2) Repeated alveolar collapse
Basically your alveoli were not meant to do jumping jacks, & they don’t handle it very well.
Our biggest advance to date in ARDS mortality:
Figuring out that lower tidal volumes in mechanical ventilation meant lower mortality rates.
In the study cited: low (6 mL/kg) vs high (12 mL/kg) ventilation. Mortality in low volume patients was 31%, but 40% in high volume patients.
What does PEEP stand for in the context of mechanical ventilation?
Positive end-expiratory pressure
Okay, so what does PEEP mean?
It’s the pressure required to keep alveoli from collapsing at the end of expiration
At what pressure should we set the PEEP?
Empirically to minimize FiO2 and maximize PaO2.
What’s “proning?” Why would we do it?
Proning: mechanical ventilation in the prone position
It has improved arterial oxygenation in randomized trials
If it’s so great, why would we NOT want to “prone” our ARDS patients?
Effect on outcomes is still uncertain, and unless your ICU team is trained & experienced in this positioning, you could screw up any number of things: lose the ET tube, pull out the CVLs, break the patient…y’know. That sort of thing.
It’s still a last-ditch effort until we know more about whether it works.
Some adjunctive ventilator therapies to be aware of:
#high PEEP #Inverse ratio ventilation (I:E > 1:1) #Recruitment maneuvers #Prone positioning #High frequency ventilation (extremely high resp rates of 5-20 cycles per second) with low tidal volumes #Partial liquid ventilation (promising preliminary data) #ECMO (extracorporeal membrane oxygenation) which has clear survival benefit in neonates; maybe some utility in certain adults
There is no evidence that these benefit survival as of yet.
How should we manage fluid in ARDS patients? Why?
Aggressively manage fluid with restrictions & diuretics to keep left atrial filling pressures low, minimizing pulmonary edema.
Benefits: prevents further decreases in lung compliance, improves pulmonary mechanics, shortens ICU stay, decreases mortality! Good times all around.
JUST DON’T HYPOPERFUSE THE KIDNEYS. They’re drama queens.
Glucocorticoids in ARDS: yes or no
Nope. We tried it in some studies, but it didn’t seem to help. Evidence does NOT support.
Nitric oxide in ARDS: yes or no
It does seem to transiently improve oxygenation, but doesn’t increase survival or decrease ventilation time, so there’s kinda no point.
