Ian B. Hoffman, MD, FCCPPulmonary & Critical Care Medicine

Any disruption of function of respiratory system – CNS, nerves, muscles, pleura, lungs

Any process resulting in low pO2 or high pCO2 – arbitrarily 50/50

Acute respiratory failure can be exacerbation of chronic disease or acute process in previously healthy lungs

1940’s – polio, barbiturate OD 1960’s – blood gas analysis readily available,

aware of hypoxemia 1970’s – decreased hypoxic mortality,

increased multiorgan failure (living longer) 1973 – relationship between resp muscle

fatigue and resp failure

Type 1 (nonventilatory) – hypoxemia with or without hypercapnia – disease involves lung itself (i.e, ARDS)

Type 2 – failure of alveolar ventilation – decrease in minute ventilation or increase in dead space (i.e. COPD, drug OD)

Correct hypoxemia or hypercapnia without causing additional complications

Nonivasive ventilation vs. intubation and mechanical ventilation

Goal of mechanical ventilation is NOT necessarily to normalize ABGs

Failure of respiratory pump to adequately eliminate CO2

pCO2 : CO2 production alveolar ventilation

Healthy humans have V/Q matching

High V/Q areas – well ventilated but poorly perfused – wasted ventilation – increased dead space

Low V/Q areas – can cause hypercapnia if large amount of venous blood flows through

Decision to mechanically ventilate is clinical Some criteria

Decreased level of consciousness Vital capacity <15 ml/kg Severe hypoxemia Hypercarbia Vd/Vt >0.60 NIF < -25 cm H20

(formerly Adult Respiratory Distress Syndrome)

Severe end of the spectrum of acute lung injury Acute and persistent lung inflammation with

increased vascular permeability Diffuse infiltrates Hypoxemia – paO2/FiO2 <200

(i.e. pO2 70 / FiO2 0.5 = 140) No clinical evidence of elevated left atrial

pressure (PCWP <18 if measured)

1967 – Ashbaugh described 12 pts with acute respiratory distress, refractory cyanosis, decreased lung compliance, diffuse infiltrates

1988 – 4 point lung injury score (level of PEEP, pO2/FiO2, lung compliance, degree of infiltrates)

1994 – acute onset, bilat infiltrates, no direct or clinical evidence of LV failure, pO2/FiO2)

Annual incidence 75 per 100,000 9% of American critical care beds occupied by

patients with ARDS

Clinically and radiographically resembles cardiogenic pulmonary edema

PCWP can be misleading – high or low 20% of pts with ARDS may have LV dysfunction

Direct injury to the lung Indirect injury to the lung in setting of a systemic

process Multiple predisposing disorders substantially

increase risk Increased risk with alcohol abuse, chronic lung

disease, acidemia

Direct Lung Injury Pneumonia Gastric aspiration

Lung contusion Fat emboli Near drowning Inhalation injury Reperfusion injury

Indirect Lung Injury Sepsis Multiple trauma

Cardiopulmonary bypass Drug overdose Acute pancreatitis Blood transfusion

Inflammatory injury to alveoli producing diffuse alveolar damage

Proinflammatory cytokines (TNF, IL-1, IL-8) Neutrophils recruited – release toxic mediators Normal barriers to alveolar edema are lost, protein

and fluid flow into air spaces, surfactant lost, alveoli collapse Impaired gas exchange Impaired compliance Pulmonary hypertension

Severe initial hypoxemia Prolonged need for mechanical ventilation Initial exudative stage Proliferative stage

resolution of edema, proliferation of type II pneumocytes, squamous metaplasia, collagen deposition

Fibrotic stage

Early Inciting event, pulmonary dysfunction (worsening

tachypnea, dyspnea, hypoxemia) Nonspecific labs CXR – diffuse alveolar infiltrates

Subsequent Improvement in oxygenation Continued ventilator dependence Complications Large dead space, high minute ventilation requirement Organization and fibrosis in proliferative phase

Ventilator induced lung injury Sedation and neuromuscular blockade Nosocomial infection Pulmonary emboli Multiple organ dysfunction

Improved survival in recent years – mortality was 50-60% for many years, now 25-40%

Improvements in supportive care, newer ventilatory strategies

Early deaths (3 days) usually from underlying cause of ARDS

Later deaths from nosocomial infections, sepsis, MOSF Severity of gas exchange at admission does not correlate

with mortality Respiratory failure only responsible for ~16% of fatalities Long-term survivors usually show mild abnormalities in

pulmonary function (DLCO), impaired neurocognitive function

Failure to improve over 1st few days Initially increased dead space Advanced age Sepsis Multiple organ dysfunction (higher APACHE) Steroids given prior to onset of ARDS Blood transfusion Not managed by Intensivist

Provide adequate oxygenation without causing damage related to: Oxygen toxicity Hemodynamic compromise Barotrauma Alveolar overdistension

Reliable oxygen supplementation Decrease work of breathing

Increased due to high ventilatory requirements, increased dead space, and decreased compliance

Recruit atelectatic lung units Decreased venous return can help decrease

fluid movement into alveolar spaces

Low tidal volume, plateau pressure <30 (less alveolar overdistension)

PEEP – enough, not too much Pressure controlled vs. volume cycled Open lung strategy

PC-IRV ventilation Vt < 6ml/kg, PEEP 16, RR <30, Peak pressure <40

Prolong inspiratory time (increase mean airway pressure and improve oxygenation)

Permissive hypercapnia Secondary effect of low tidal volumes Maintain adequate oxygenation with less risk of

barotrauma Sedation/paralysis usually necessary

Decreases peak airway pressure Improves alveolar recruitment Increases ventilation of dependent lung zones Improves oxygenation BUT – no evidence yet of improved outcome

Increases FRC – recruits “recruitable” alveoli Decreases shunt, improves V/Q matching No consensus on optimal level of PEEP

Initial tidal volume of 6 ml/kg IBW and plateau pressure <30

vs.

Initial tidal volume of 12 ml/kg IBW and

plateau pressure <50

Reduction in mortality of 22% (31% vs 40%)

APRV High-frequency ventilation ECMO Beta agonists Nitric Oxide Surfactant Steroids (possible benefit if given early -or- in

late fibroproliferative phase) ?benefit from tube feeds containing

combination of eicosapentaenoic acid and gamma-linolenic acid (?antiinflammatory effects)

Selectively dilates vessels that perfuse better ventilated lung zones, resulting in improved V/Q matching, improved oxygenation, reduction of pulmonary hypertension

Less benefit in septic patients

No clear improvement in mortality

Known for decades that high levels of positive pressure ventilation can rupture alveolar units

In 1950’s became apparent that high FiO2 can produce lung injury

Macrobarotrauma Pneumothorax, interstitial emphysema,

pneumomediastinum, SQ emphysema, pneumoperitoneum, air embolism

? resulting from high airway pressures, or just a marker of severe lung injury

Higher PEEP predicts barotrauma

Microbarotrauma Alveolar overinflation exacerbating and

perpetuating lung injury – edema, surfactant abnormalities, inflammation, hemorrhage

Less affected lung accommodates most of tidal volume – regional overinflation

Cyclical atelectasis (shear) – adds to injury

Low tidal volume strategy (initial tidal volume 6 ml/kg IBW, plateau pressure <30) – lower mortality

Prophylaxis for DVT Prophylaxis for GI bleeding Measures to avoid nosocomial pneumonia Treat nosocomial pneumonia Nutritional support Sedation and paralysis Treating hypoxemia

Diuresis Prone positioning Decrease oxygen consumption