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Flashcards in ARDS Deck (16):

Diagnostic criteria for ARDS

-Lung injury of acute onset <1 week w/ progressing symptoms
-bilateral (ground glass) opacities on chest imaging not explained by other pathologies (effusions, pneumothorax, nodules)
-respiratory failure (hypoxic and/or hypercapnic) not explained by cardiogenic cause or fluid overload
-PaO2/FiO2 ratio: worsening shunt
-mild ARDS 201-300 mmHg
-Moderate ARDS 101-200 mmHg
-Severe ARDS =<100 mmHg
-Increased PADP, while PCWP remains unaffected, worsening vascular resistance from microemboli and trauma to vasculature. Therefore PVR, high versus SVR low
-Worsening PIP/Plat - worsening compliance


Causes of ARDS

-Damage to alveoli caused by direct insult to lung tissue, like: aspiration, toxins, pneumonia, pulm contusions, oxygen toxicity

-Alveolar damage caused as a result of disfunction in other systems: #1 being sepsis, sirs, shock, others like trauma, DIC


Effect of SIRS/Sepsis in precipitating ARDS

ARDS is basically just sepsis in the lungs:
-Pulm vasodilation - Arachadonic Acid, Bradykinins
-Increased capillary permeability - archadonic acid
-Maldistribution of blood flow - platelets, inappropriately isolating vasculature


Basic pathophys of ARDS

-Lung either directly or indirectly insulted.

Exudative Phase
-Inflammatory response begins in ernest, resulting in mediator release (arachadonic acid, bradykinins, clotting factors, and MAC
-Alveolar wall permeability allows fluids filled with protein, RBC, fibrin to flood alveoli. Causes damage to alveolar wall, surfactant production is compromised and alveoli collapse
-Same time, microemboli form decreasing pulm blood flow, PA pressures rise
Proliferation Phase
-disordered healing occurs, alveoli heal fill of scar tissue, pulm capillaries scar, fibrotic tissue. overall decreasing lung compliance
Resolution Phase
-More organized healing and remodelling occurs with some restoration of AC membranes, type 2 cells multiple and restore surfactant and alveolar opening, fluid drains away as disorganized inflammatory response diminishes


Broad treatment foci in ARDS

1. Treat cause - ie ABX, trauma etc
2. Support oxygen supply and demand while healing
-Mechanical ventilation - foundational, PCV optimizing PEEP and PIP for vent and oxy. 4 strategies in forthcoming cards
-Hemodynamics support - maintain adequate PL to support CO, more in beginning, less later avoid fluid overload in lungs - Biphasic fluid management
-Positioning - kinetic beds and proning
-Pharma - sedation, analgesia, temp control, ?NMBA - reduce demand
-NO - improve VQ mismatch
-pulm focused meds - bronchodilators, mucolytics - improve airway resistance


Goals of mechanical ventilation as treatment modality in ARDS

*Protective lung strategies

*Optimizing ventilation with PCV

*Optimizing gas exchange

*Airway management


Difference between PIP and Plat

PIP reflected compliance and airway resistance since it is measured dynamically

Plateau pressure is measured at the end of expiration with the breath held in by the vent. This provides a static pressure measurement not involving airway diameter or resistance, therefore it reflects lung compliance only


What are protective lung strategies

-keep TV <6cc/kg, plat<30 cm, low tidal volumes and permissive hypercapnea (don't allow pH <7.2 though)
-cant really increase RR much either. Non-compliant lungs don't have enough time to distend adequately, therefore we get increase pressures and inc airway resistance with increased RR


How do we optimize ventilation

- on set AC vol mode where set volume is delivered irrespective of pressures, ventilation will be delivered too much to open alveoli, therefore causing overdistention and volutrauma. This damages functional alveoli, exacerbating inflammatory response and therefore ARDS. So PCV is ideal since it will not over inflate vulnerable tissue
• Allows Maximum pressure with each breath controlled
• decreases risk of barotrauma and volutrauma.
• will improve ventilation due to use of laminar flow for air delivery laminar flow (compared to volume cycled) contributes to lowering airway pressure and assists in opening up smaller collapsed airways
• will decrease V/Q mismatch and hopefully improve oxygenation


How do we optimize gas exchange?

We employ strategies to:
• Recruit alveoli that have collapsed
• Prevent others from collapsing
• Thinning membrane to support diffusion
This is done with high PEEP sometimes as high as 15-18
-Keeping FiO2 low also prevents damage from oxygen toxicity

Severe shunting and refractory hypoxemia (hypoxemia regardless of increased inspired FiO2) are hallmarks of ARDS, therefore higher peep recruits more alveoli, prevents collapse and thins AC membranes


Optimize airway?

-supporting ventilation and gas exchange functions in the lungs is dependent on an adequate airway
-suctioning, bronchodilators, and mucolytics lower airway resistance is essentially a first step in allowing all other strategies to work


What is biphasic fluid management

-During early phases of ARDS with shocky hemodynamics instability, we target preload optimization with crytaloid boluses, targeting PCWP between 12-18
-Later, after initial instability has passed, we restrict fluid intake to avoid fluid shifts into the lungs. Aim for PCWP as low as possible to maintain adequate CO


How to we evaluate fluid status in ARDS using PA pressures

Difference of >4mmHg between PAD and PCWP indicates lung pathology with increased vascular resistance, from microemboli

Therefore we judge preload from PCWP and treat hemodynamics status from that


Normal PA values

PAS 20-30
PAD 10-15
PAP 10-20
PCWP 8-12
SVR 800-1500
PVR 155- 255
CO 4-8


Pharmacological interventions

- sedation, analgesia, temp control, ?NMBA
- reduce demand
-NO - improve VQ mismatch
-pulm focused meds - bronchodilators, mucolytics
- improve airway resistance


Best lab indicators of EOP

Lactate, pH, O2ER, SVO2