ards old problem current strategies november 4, 2013

ARDS OLD PROBLEM

CURRENT STRATEGIES

NOVEMBER 4, 2013

David W. Chang, EdD, RRT University of South Alabama

Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications

Definition of ALI and ARDS (1994 AECC)

Acute onset Hypoxemia (PaO2/FIO2 = 200 or 300 mm

Hg) Bilateral infiltrates PCWP <18 mm Hg

Outline1. Definitions of ALI and ARDS

Definition of ARDS (2011 Berlin)

P/F index mild ARDS: 201 - 300 mmHg (≤ 39.9 kPa) moderate ARDS: 101 - 200 mmHg (≤ 26.6

kPa) severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)

Radiographic severity Respiratory compliance ≤ 40 mL/cm H2O PEEP ≥ 10 cm H2O Corrected minute ventilation ≥ 10 L/min

History

1950’s – Pulmonary edema (respirator lung, DaNang lung, shock lung, post-traumatic lung, wet lung)

1959 – Neonatal RDS (Avery and Mead) 1967 – ARDS (Ashbaugh et al)

History

Late 1960s – intensive care units became common in the U.S.

1930s to 1950s – Drinker respirator (negative pressure ventilation, iron lung, chest cuirass)

1950s to present – manual ventilation, positive pressure breathing, mechanical ventilator, microprocessor controlled ventilator

Mortality ranges from 90% (untreated) to 25% (treated aggressively)

Pathophysiology

Direct injury (e.g., pneumonia, aspiration, inhalation of toxins, near drowning, pulmonary contusion, fat embolism)

Indirect injury (e.g., sepsis, severe trauma, acute pancreatitis, cardiopulmonary bypass, transfusion of blood products, drug overdose)

Pathophysiology

Direct injury may lead to (A) activation of alveolar macrophages(B) development of inflammatory response

within the lungs(C) alveolar epithelial damage(D) alveolar walls are thickened due to

acute distention of capillaries and interstitial edema

Pathophysiology

Direct injury may lead to (E) pathological abnormality in the intra-

alveolar space(F) alveolar filling by edema, fibrin,

collagen, neutrophilic aggregates or blood

(G) V/Q mismatch and intrapulmonary shunting

Pathophysiology

Indirect injury may lead to(A) Inflammatory mediators released from

the extrapulmonary foci into the systemic circulation

(B) target of damage is the pulmonary vascular endothelial cell

(C) Endothelial dysfunction causes fluid extravasation from the capillaries and impaired drainage of fluid from the lungs

Pathophysiology

Indirect injury may lead to(D) Dysfunction of type II pulmonary

epithelial cells leads to reduction of surfactant

(E) Increase of vascular permeability (transudate – a pale esinophilic finely granular, replaces the air)

*Exudate is caused by inflammation Transudate is caused by disturbance of

hydrostatic pressure and colloid osmotic pressure

Pathophysiology

Indirect injury may lead to(F) Recruitment of monocytes,

polymorphonuclear leukocytes, platelets, and other abnormal cells

(G) Primary pathological alteration is microvascular congestion and interstitial edema

(H) V/Q mismatch and intrapulmonary shunting

Mechanical Stress

In ARDS, lung structure and function are not homogenous (i.e., healthy and sick lung units are mingled)

Collapsed lung units require higher positive pressure

Normal lung units become overdistended at high pressures (video)

Barotrauma or volutrauma is more likely to occur in normal lung units

Clinical presentations (ventilation & oxygenation)

Tachypnea Rapid shallow breathing (↑f/VT)

↑VD/VT↓VA (VA = VT – VD)↑V/Q mismatch

↑Intrapulmonary Shunting ↓PaO2/FIO2 (P/F) index ↑PaCO2 due to fatigue of respiratory muscles Impending ventilatory failure Acute ventilatory failure

Clinical presentations (radiographic)

Bilateral infiltrates No signs of large pleural effusion (normal

costophrenic angles) No signs of atrial enlargement No signs of heart failure (e.g., PCWP >18

mm Hg) or volume overload (high systemic blood pressure, peripheral edema)

Management Strategies(ineffective, controversial, transient positive

effects or not validated in large studies)

Drugs Inhaled synthetic surfactant, IV antibody to

endotoxin, ketoconazole (anti-fungal), ibuprofen (NSAID), simvastatin (cholesterol reduction), and inhaled nitric oxide (pulmonary vasodilator)

Nutritional support and supplement Devices

ECMO, HFOV

Management Strategies(reasonable and potentially useful)

Fluid management Infection control (early intervention) Prevention of VAP Noninvasive ventilation (early

intervention) Nutritional support (enteral feeding tube) Frequent position changes and range of

motion

Management Strategies(current practice)

Mechanical ventilation with PEEP Decramental recruitment maneuver for

optimal PEEP Low VT and permissive hypercapnia Airway pressure release ventilaiton Inverse ratio ventilation Prone positioning

Management Strategies

Mechanical ventilation (volume-controlled or pressure-controlled) to reduce work of breathing

Keep airway pressures below thresholdsPIP < 50 cm H2OPlateau pressure < 35 cm H2O (ARDSNet recommends < 30 cm H2O)Mean airway pressure < 30 cm H2OPEEP < 10 cm H2O


Oxygen and PEEP to provide oxygenation Note effects of PEEP and other factors on

airway pressures (Figure) mPaw = (f x I time / 60) x (PIP – PEEP) + PEEP mPaw may be used to monitor hemodynamic

effects plateau pressure may be used to monitor

overdistentionRecommended FIO2/PEEP combinations (Table)Recruitment maneuver to determine optimal PEEP (Video)


Low VT and Permissive Hypercapnia to minimize lung injury (Table)

6 mL/Kg as low as 4 mL/Kg to keep PPLAT < 30 cm H2O permit PaCO2 to rise acidosis is managed by bicarbonate or

tromethamine


Airway Pressure Release Ventilation (APRV) (Figure)↓decreased airway pressure requirement↓ minute ventilation↓ dead-space ventilationpromote spontaneous breathing

↓ use of sedation & neuromuscular blockade optimized ABG results↑ FRC↑ cardiac output


Inverse ratio ventilation (IRV)Pressure-Controlled + IRV

(pressure titrated to low VT 4 to 7 mL/kg)Long inspiratory time

(inspiratory flow titrated to desired inverse ratio)


Inverse ratio ventilation (IRV) Facilitate gas exchange (esp. O2) Reduce FIO2 and PEEP requirement Require sedation and neuromuscular

blockade Monitor for improvement & hemodynamic

effects


Prone positioning Lung zones Lung volume distribution

* Improvement in oxygenation is temporary

Complications

Ventilator-associated pneumonia Prevention and intervention

Hypoxic-ischemic encephalopathy Brain (2% body weight, 15% energy

consumption, cannot hold or store energy in the form of glycogen, cannot utilize fatty acids, depends on a constant supply of oxygen and glucose)

CPP = MAP – ICP (normal 70 to 80 mm Hg)

Summary Early intervention Team approach Tailor management strategies to patient’s need Prevent complications

Go Prone

ards old problem current strategies november 4, 2013

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