ARDS (Acute Respiratory Distress Syndrome)
ARDS is a form of respiratory failure caused by acute lung injury. Disruption of alveolar-capillary membrane, leading to increased vascular permeability and accumulation of inflammatory cells and protein-rich edema fluid within the alveolar space. It is not a single entity, but an expression of multiple diseases that produced diffuse inflammation in the lungs, often accompanied by inflammatory injury in other organs. It is also the leading cause of acute respiratory failure in the United States.
American-European Consensus Conference has defined ARDS as follows:
acute onset
presence of a predisposing condition
bilateral infiltrates on frontal chest x-rayy
Ratio of PaO2 to FiO2 <200
no evidence of heart failure or volume overload as the principal cause of the pulmonary infiltrates
pulmonary artery capillary hydrostatic pressure (measured by PCWP x 2) of 18 mm of mercury or less or no clinical evidence of left atrial hypertension
the criteria are for ARDS masses severe pneumonia and nearly matches acute pulmonary embolus.
Viable method for confirming or excluding the diagnosis of ARDS as bronchoalveolar lavage. The lavaged fluid is then analyzed for neutrophil density in protein concentration.
In normal subjects neutrophils make up less than 5% of cells recovered and lung lavaged fluid, where as in patient with ARDS as many as 80% of the recovered cells are neutrophils. This can also be seen in pneumonia.
Total protein. Infiltrate 3 exudates are rich and proteinaceous material, lung lavaged fluid is similarly rich in protein and can be used as evidence of lung inflammation. The protein concentration in the lung lavaged fluid is expressed as a fraction of the total protein concentration.
Protein in lavage fluid/Sr. Protein <0.5 = hydrostatic edema
Protein in lavage/Sr. Protein >0.7 = Lung inlammation.
a positive test result of is not specific for ARDS, it can be used as evidence of ARDS other causes of lung inflammation including pneumonia is excluded on clinical grounds.
FiO2 expressed as a decimal (e.g., room air is 0.21).
For example, if pO2 is 100/0.21, the ratio is 476.
ALI is acute lung injury is a less severe disorder but has the potential to evolve into ARDS.
PaO2/FiO2 between 200 - 300 mmHg.
Clinical disorders commonly associated with ARDS:
Direct Lung Injury
Pneumonia, aspiration of gastric contents, pulmonary contusion, near-drowning, toxic inhalation injury
Indirect Lung Injury
Sepsis (the most important single cause of ARDS), severe trauma (multiple bone fractures, flail chest, head trauma, burns), multiple transfusions, drug overdose, pancreatitis, post-cardiopulmonary bypass.
Clinical course and pathophysiology: 3 phases
Exudative: 1-7 days. Occurs within 12-36 h after initial insult. Can be delayed by 5-7 days.
Injury to alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells), by systemic activation of circulating neutrophils and that stick to the vascular endothelium in the pulmonary capillaries; release of proteolytic enzymes that damages the capillary wall > loss of tight junctions of the alveolar capillary barrier > edema fluid rich in protein accumulates in the interstitial and alveolar spaces. High conc of cytokines (IL1, IL8, TNF-alpha) and lipid mediators (LTB4) are present in the lung in the acute phase. Leukocytes (neutrophils) respond to these proinflammatory mediators and join the party. Condensed plasma protein aggregate in the air spaces with cellular debris and dysfunctional pulmonary surfactant to form hyaline membrane whorls. Pulmonary vascular injury also occurs early in ARDS, with vascular obliteration by microthrombi and fibrocellular proliferation.
Alveolar edema predominantly involves dependent portions of the lung, leading to diminished aeration and atelectasis. Large sections of dependent portion of lungs collapse > decreased lung compliance. Intrapulmonary shunting and hypoxemia develops and the work of breathing rises, leading to dyspnea. There is decreased pulmonary arterial blood flow to ventilated portions of the lung, increasing the dead space, and pulmonary HTN. Thus, in addition to severe hypoxemia, hypercapnia secondary to increase in pulmonary dead space is also prominent in early ARDS.
Clinical features: Dyspnea, tachypnea, respiratory fatigue > resp. failure. Lab values are nonspecific. CXR reveals alveolar and interstitial opacities involving at least 3/4 of lung fields. Again these radiographic findings are not specific, although characteristic of ARDS or ALI. It's also seen in CPE. Unlike CPE, however, there is rarely cardiomegaly, pleural effusions, or pulmonary vascular redistribution. CT of chest, shows extensive heterogeneity of lung involvement.
Early in the course of ARDS, patients may appear stable without respiratory symptoms. The PCWP would be normal or low in ARDS, but elevated left ventricular failure.
DDX of ARDS in exudative phase:
CPE, pneumonia, alveolar H'ge, acute ILD (AIP), radiation pneumonitis, neurogenic pulmonary edema
Proliferative: lasts from 7 - 21 days.
Most Pts recover rapidly and are liberated from mechanical ventilation during this phase.
Dyspnea, tachypnea, and hypoxemia occur.
Some patients develop progressive lung injury and early changes of pulmonary fibrosis during the proliferative phase.
Reparative processes occur
Fibrotic: 3 - 4 weeks
fibrin deposit in the lungs is another characteristic feature of ARDS, and this fibrin can undergo remodeling and produce pulmonary fibrosis.
Long term support and O2 dependency.
ARDS versus cardiogenic edema:
chest x-ray appearance is usually of little or no family. A homogenous infiltrate and the absence of pleural effusions is more characteristic of ARDS, while patchy infiltrates arising from the hilum and prominent pleural effusions is most characteristic of cardiogenic pulmonary edema. This pleural effusion however can't a PA and ARDS and so the consensus view is stat chest x-rays are not reliable for distinguishing IRDS from cardiogenic pulmonary edema.
The superior hypoxemia can sometimes help distinguish ARDS from cardiogenic pulmonary edema. In early stages of ARDS, hypoxemia is more pronounced than the chest x-ray abnormalities, whereas in the early stages of cardiogenic pulmonary edema, the chest x-ray abnormalities are often more pronounced than the hypoxemia.
Initial Management of ARDS:
Treat the underlying cause
Minimize procedure and their complications
VTE and GI prophylaxis
Prevent nosocomial infection
Provide adequate nutrition
Initiate volume/pressure-limited ventilation
Goals and limitis:
Vt 6 mL/kg PBW or less (PBW Her weight at which lung volumes are normal). Use of low tidal volume mechanical ventilation Is not really a specific therapy for ARDS, but is a lessening of the harmful effects of mechanical ventilation of the lungs. The benefit of low tidal volume she is grand and inspiratory plateau pressure ( which correlates with the risk of volutrauma) is above 30 cm water.
Plateau pressure <30 cm H2O or less
RR 35 bpm or less
Oxygenate: Oxygen delivery DO2 = Q x 1.36 x Hb x SaO2 (Q=CO). Systemic oxygen delivery must be maintained at a normal rate of 900-1100 mL/min or 520-600 mL/min/m2 when adjusted for body size.
FiO2 of 0.6 or less
PEEP of 10 cm H2O or less
SpO2 88 - 95%
and cardiac output at 5-6 L per minute or 3-4 L/min/m2 when adjusted for body size. If cardiac output is below the normal ranges, check CVP. if CVP is low, volume infusion as indicated. Despite this he hadn't infuse fluids will move into the lungs, a tendency for fluids to movement of the lungs should be the same for ARDS and pneumonia. If volume infusion as not indicated, dobutamine is preferred over her vasodilators for augmenting the cardiac output because vasodilators will increase intrapulmonary shunt and will add to the gas exchange abnormality in ARDS. Dopamine should be avoided in ARDS because it constricts the pulmonary veins, and this will cause an exaggerated rise in pulmonary capillary hydrostatic pressure.
Hemoglobin should be maintained above 10 g per deciliter. It is wise to avoid blood transfusion in patient with ARDS. If there is no evidence of tissue dysoxia or impending dysoxia (O2 extraction ration >50%), there is no need to correct anemia with blood transfusion. His
Minimize acidosis
pH of 7.3 or more
RR of 35 bpm or less
Diuresis: diuretics don't reduce inflammation of ARDS, although minimal the watery edema fluid that falls as a consequence of heart failure. It can also result in hemodynamic compromise. This can be monitored by checking cardiac filling pressures and cardiac output.
MAP of 65 mmHg or more
Avoid hypoperfusion
Fluid conversative
high-dose steroids have no effect on ARDS when given within 24 hours of the onset of illness. When steroids are given later in the course of illness, during the fibroproliferative phase that began 7-14 days after the onset of illness, there is a definite survival benefit. may be explained by the ability of steroids to promote collagen breakdown and inhibitor fibrosis. His
Methyprednisolone, 2-3 mL/kg/day.
most deaths from ARDS or not due to respiratory failure. Only 40% of deaths in the attribute it to ARDS, majority are due to multiorgan failure. Age is also an important factor, with mortality being as much as 5 times higher in patients over 60 years of age.
PBW chart:
http://www.ardsnet.org/system/files/pbwtables_2005-02-02_0.pdf
Card:
http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf
protocol for low volume ventilation ARDS.
Goals: Tidal volume = 6 mL/kg, Ppl <30 cm H20, pH = 7.30 - 7.45
First Stage:
calculate patient's predicted body weight
said initial tidal volume to 8 mL/kg PBW
add PEEP at 5-7 cm of H2O
reduce tidal volume by 1 mL/kg every 2 hours until tidal volume = 6 mL/kg PBW
Second Stage:
When TV is down to 6 mL/kg, measure Ppl
Target Ppl <30 cm H2O
If Ppl >30 cm H2O, decrease TV in 1 mL/kg steps until Ppl drops below 30 cm of H2O or TV down to 4 mL/kg.
Third Stage:
Monitor ABGs for respiratory acidosis.
Target pH = 7.30 - 7.45
if pH 7.15-7.30, increased respiratory rate until pH > 7.30 or RR = 35 bpm
if pH < 7.15, increase RR to 35 bpm. If pH still < 7.15, increase TV at 1 mL/kg increments until pH > 7.15
permissive hypercapnia
The consequences of low volume ventilation is a reduction in CO2 elimination via long sleeping to hypercapnia and respiratory acidosis. Allowing hypercapnia to devil up in favor for maintaining lung protective low volume ventilation is no mass permissive hypercapnia. The limits of tolerance to hypercapnia and respiratory acidosis is not clear but they are reports to show that PaCO2 levels as high as 375 mmHg and pH levels as low as 6.6 are remarkably free of serious side effects as long as tissue oxygenation is adequate. troublesome side effect of hypercapnia his brainstem respirate restimulation with subsequent hyperventilation, which often requires neuromuscular blockade to prevent ventilator asynchrony. Data from clinical trials or permissive hypercapnia showed an arterial pCO2 levels of 60-70 mmHg and arterial pH levels of 7.22-7.25 are safe for most patients.
positive and expiratory pressure (PEEP) pitted low-volume ventilation can be accompanied by collapse of the terminal airways at the end of expiration and reopening of the airways during lung inflation. PEEP can mitigate this problem by acting as a stent to keep small airway is open at the end of expiration. For this reason, the addition of low level PEEP (5-7 cm H2O) has become a standard practice in low-volume ventilation. PEEP is also used as an aid to arterial oxygenation and ARDS. PEEP and decreased cardiac output and this affect can be counterproductive to her PEEP induced increase in arterial oxygenation.