ARDS Flashcards
1
Q
what is VQ mismatch
A
- ventilation-perfusion mismatch
- normally, the volume of blood perfusing the lungs and the amount of gas reaching the avleoli are almost identical
- d/t secretions or mucus plug: this will either block blood flow or block air flow.
- low V/Q mismatch: d/t shunt and alveoli is perfused but not ventilated
- high V/Q mismatch: d/t deadspace and alveoli are ventilated, but not perfused
2
Q
what is ARDS
A
- sudden and progressive form of ARF in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid.
- non-cardiogenic pulmonary edema (pulmonary edema is caused by either indirect or direct injury
- Widespread inflammation (usually inflammation causes little inflammatory cells to travel the blood stream and when that blood reaches the lungs to get rid of CO2 and gain O2, those inflammatory cells damage the capillary cells of the alveoli in the lungs, which causes them to be more permeable and essentially leak)
- ARDs has a HIGH mortality rate (greater than 50%) (mortality is 70-90% in pts w/ septic shock and ARDs).
3
Q
etiology of ARDS
A
There are many predisposing conditions of ARDs.
- widespread inflammation after physiologic insults:
> systemic inflammatory response, SEPSIS, trauma, gut ischemia, lung injury, or as a consequence of multiple organ dysfunction syndrome (MODS).
4
Q
What is the most common cause of ARDS
A
sepsis
5
Q
what is the berlin cirteria for ARDS
A
- Timing: 1 week of clinical insult or worsening resp symptoms
- Chest X-ray: bilateral “opacities”-whiteout
- Oxygenation: P/F ratio-mild less than 300; moderate less than 200; severe less than 100;
All w/ PEEP or CPAP=greater than 5cmH2O
6
Q
risk factor for ARDS: indirect injury
A
- develops d/t a problem somewhere else in the body NOT in the lungs
- SEPSIS (esp. gram negative infection)
- Severe massive trauma
- severe TBI
- shock states (hypovolemic, cardiogenic, septic)
- burns
- DIC
- cardiopulmonary bypass
Other:
- acute pancreatitis
- cardiopulmonary bypass
- disseminated intravascular coagulation
- opioid drug overdose (heroin)
- transfusion-related acute lung injury (multiple blood transfusions)
- urosepsis
7
Q
risk factor for ARDS: Direct injury to lungs
A
The pathogen comes into contact w/ the tissue of the lung!
- aspiration of gastric contents or other substances
- bacterial or viral PNA
- sepsis (infection in the lung)
Other:
- Chest trauma (blunt or penetrating-pulmonary contusions)
- Embolism: fat, air, amniotic fluid, thrombus
- inhalation of toxic substances
- near-drowning
- O2 toxicity
- radiation pneumonitis
8
Q
Injury to alveolar-capillary membrane d/t damaged alveolar cell-
A
- damaged type II alveolar cell
- decreases surfactant production
- decreased alveolar compliance and recoil (harder to keep from collapsing!)
- atelectasis (alveoli collapse after gas exchange)
- Hyaline membrane formation
- decreased lung compliance and impaired gas exchange
= ARDs
9
Q
injury to alveolar-capillary membrane d/t release of inflammatory mediators-
A
- release of inflammatory mediators (bronchoconstriction and then impaired gas exchanged OR vascular narrowing and obstruction and then impaired gas exchange)
- increased alveolar capillary membrane permeability
- outward migration of blood cells and fluids from capillaries
- pulmonary edema
- impaired gas exchange
=ARDs
10
Q
What are the three phases of ARDs?
A
- injury phase or exudative phase
- proliferation phase
- fibrotic phase
11
Q
Exudative or injury phase:
A
- occurs 24-72 hrs after the insult
- generally lasts up to 7 days
- increase interstitial pulmonary edema (more of the blood is pass through the capillary membrane into the alveoli)
- intrapulmonary shunt: fluid moves into the alveolar space-type 1 and 2 alveolar cells are damaged, which leads to decreased surfactant (alveolar collapse after exhalation-atelectasis) and protein accumulation (pulmonary edema-interstitial and alveolar edema)
= severe atelectasis and decreased lung compliance
12
Q
What are the primary pathophysiologic changes that occur during the exudative phase?
A
- interstitial and alveolar edema (increased capillary permeability) and atelectasis (decreased surfactant)
- significant V/Q mismatch: increasing shunt bc the alveoli fill with fluid
- Refractory hypoxemia: hypoxemia unresponsive to increasing concentrations of oxygen delivered by our supplemental devices (blood in the capillary network cannot be oxygenated)
13
Q
Initial findings that occur during exudative phase:
A
- increase RR
- decrease tidal volume
- hyperventilation increases CO2 excretion
- leading to respiratory alkalosis
- CO increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow; however, as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails and hypoventilation, decreased O2, and decreased tissue O2 perfusion occur.
14
Q
Hyaline membrane during exudative phase:
A
- a hyaline membrane occurs during exudative phase
- necrotic cells, protein, and fibrin form a hyaline membrane that line the inside of each aveolus.
- these thick hyaline membranes contribute to the development of fibrosis and atelectasis, leading to a further decrease in gas exchange capability and reduced lung compliance.
15
Q
Refractory hypoxemia during exudative phase:
A
- severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of oxygen=refractory hypoxemia
- despite receiving higher concentrations of oxygen, the pts condition does not improve but continues to get worse
- this causes a diffusion limitation, caused by hyaline membrane formation, contributes to and worsens hypoxemia
- as the lungs become less compliant bc of decreased surfactant, pulmonary edema, and atelectasis, the pt must generate higher airway pressures to inflate “stiff” lungs.
- reduced lung compliance increases the pts WOB
16
Q
Reparative or proliferative phase:
A
- begins 1-2 weeks after the initial lung injury
- there continues to be an influx of neutrophils, monocytes, lymphocytes, and fibroblasts as part of the inflammatory response
- increased pulmonary vascular resistance and pulmonary hypertension may occur bc the fibroblasts and inflammatory cells destroy the pulmonary vasculature
- lung compliance continues to decrease d/t interstitial fibrosis
- hypoxemia worsens bc of the thickened alveolar membrane-> V/Q mismatch, diffusion limitation and shunting
- airway resistance is severely increases from fluid in the lungs and secretions in the airways
- this phase is complete when the diseased lung is replaced by dense, fibrous tissue
- persistence: widespread fibrosis results
- stops: lesions will resolve
17
Q
Short form of proliferation phase:
A
- occurs 1-2 weeks post injury
- inflammatory process continues!
- result: increase vascular resistance and pulmonary hypertension
- decreased lung compliance: r/t interstitial fibrosis
- completed phase: characterized by dense fibrotic tissue
- if we can stop the process: lesions will resolve
- Hypoxemia: worsens!!
- thick dense membranes=causing diffusion limitations and shunting
18
Q
Fibrotic phase:
A
- occurs 2-3 weeks after the initial lung injury
- not all pts who have ARDs will enter this phase
- the lung tissue completely remodels by collagenous and fibrous tissues
- diffuse scarring of the lungs, interstitial fibrosis and alveolar duct fibrosis result in decreased lung compliance (hypoxemia and hypercapnia)
- this reduces the surface area for gas exchange bc the interstitial is fibrotic, and hypoxemia continues
- varying degrees of pulmonary hypertension may result from pulmonary vascular destruction and fibrosis
- systemic dysfunction: result of decreased ventilation/oxygenation
- mechanical ventilation
- poor survival at this point
19
Q
Initial clinical manifestations of ARDs:
A
- SOB
- dyspnea
- tachypnea
- cough
- restlessness
- clear or mild crackles
- chest xray: mild infiltrates; these findings usually lag behind clinical presentation by about a day (24hrs)
- respiratory alkalosis caused by hyperventilation (increased RR)
- mild hypoxemia (normal or decreased CO2 despite complicated presentation)
20
Q
Progressive or worsening clinical manifestations of ARDs:
A
- Resp: increased WOB, chest retractions (skin is basically pulling over the ribs, making them more visible indicating the pt wants more air)
- Lungs: diffuse coarse crackles on expiration, rhonchi, productive cough
- non-cardiogenic pulmonary edema
- CXR: consolidation diffuse infiltrates (whiteout)
- systemic s/s of worsening hypoxemia
- ABGs: first resp alkalosis, but then turns to respiratory acidosis=muscle fatigue and hypoventilation
- finally metabolic acidosis
- hallmark sign: hypoxemia despite increased FiO2
- hypercapnia signifies that respiratory muscle fatigue and hypoventilation have severely affected gas exchange, and respiratory failure is imminent
other: - tachycardia, diaphoresis, changes in mental status, cyanosis, pallor
21
Q
Diagnostic findings of ARDs:
A
- timing: within 1 week of clinical insult or worsening condition
- Chest X-ray: bilateral infiltrates (whiteout or snow screen)
22
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): mild ARDS:
A
p/f is greater than 200-300 w/ PEEP or CPAP greater than 5cmH2O
23
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): MODERATE ARDS
A
p/f is less than or equal to 100-200 w/ PEEP or CPAP greater than 5cmH2O
24
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): severe ards
A
p/f is less than 100 w/ PEEP or CPAP greater than 5cm H2O
25
Q
What labs do we use to diagnose ARDs?
A
- ABG
- serum lactate: increased, increased lactate=anaerobic metabolism
- CBC: lesss than 4 or 10-12
- sputum, blood, urine cultures
- coags
- electrolytes
- liver/renal function tests
- progression from ARDs to MODs
