JJM Medical College ,Davangere

Department of Anaesthesiology and Critical Care

Chair Person:

Dr. PRABHU M.D

Presented By:

Dr. TANMOY ROY

INTRODUCTION

HISTORY

EPIDEMIOLOGY

CAUSES

PATHOGENESIS AND PATHOLOGY

CLINICAL FEATURES

INVESTIGATIONS

MANAGEMENT

PROGNOSIS

INTRODUCTION

• ARDS is an expression of myriad other diseases that produce diffuse inflammation in the lungs, often accompanied by inflammatory injury in other organs.

• Known by many other names: Shock lung, Non-Cardiogenic pulmonary oedema, Adult respiratory distress syndrome, Acute lung injury etc.

• It is actually defined as a disease complex presenting as:

severe arterial hypoxemia being resistant to treatment with supplemental O2 therapy

acute lung injury characterized by diffuse alveolar damage

Non-Cardiogenic pulmonary oedema.

HISTORY• Since World War I, it has been recognized that some patients

with non thoracic injuries, severe pancreatitis, massive transfusion, sepsis, and other conditions may develop respiratory distress, diffuse lung infiltrates, and respiratory failure sometimes after a delay of hours to days

• Ashbaugh et al described 12 such patients in 1967, using the term adult respiratory distress syndrome to describe this condition.

• Clear definition of the syndrome was needed to allow research into its pathogenesis and treatment. Such a definition was developed in 1992 by the American-European Consensus Conference (AECC) on acute respiratory distress syndrome (ARDS).

EPIDEMIOLOGY

• Incidence of acute lung injury (ALI): 17.9-78.9 cases per 100,000 person-years

• Incidence of acute respiratory distress syndrome (ARDS): 13.5-58.7 cases per 100,000 person-years

• Approx 9% of ICU beds in US

N Engl J Med. 2005;353:1685-93. Am J Respir Crit Care Med. 1999;159:1849-61

CAUSESThis information shows the various causes of ARDS, and how common these diseases or conditions are in the general population.

1 disease that is "very common".

3 diseases those are "common".

1 disease that is "uncommon".

8 diseases those are "rare".

30 diseases without any prevalence information.

CAUSES OF ARDS THAT ARE VERY COMMON:The following causes of ARDS are diseases or medical conditions that affect more than 10 million people in the USA: •Asthma

CAUSES OF ARDS THAT ARE COMMON:The following causes of ARDS are diseases or conditions that affect more than 1 million people in the USA: •Bone fractures - if they cause shock. •Emphysema •Pneumonia

CAUSES OF ARDS THAT ARE UNCOMMON:The following causes of ARDS are diseases or conditions that affect more than 200,000 people, but less than 1 million people in the USA: •Burns

CAUSES OF ARDS THAT ARE RARE:The following causes of ARDS appear in the population at a rate of substantially less than 200,000 people per year in the USA: •Drowning •Guillaine-Barre syndrome •Hantavirus •Muscular dystrophy •Myasthenia gravis •Pancreatitis •Pancreatitis, acute •Poliomyelitis

CAUSES OF ARDS WITHOUT ANY PREVALENCE INFORMATION:The following causes of ARDS are ones for which we do not have any prevalence information:

Anaphylaxis

Bacterial lung infection

Blood transfusion adverse reaction

Bone fractures - if they cause shock.

Cardiac arrest

Circulatory collapse

Fat embolism

Fungal lung infection

Gastric content aspiration

Heart bypass surgery adverse reaction

Human monocytotropic ehrlichiosis

Lung trauma

Pneumonia

Sepsis

Severe blood loss

Severe infections

Shock

Smoke inhalation

Toxic fume inhalation

Uremia

Viral lung infection

Vomit inhalation

Water inhalation

Weil's syndrome - ARDS

Mitomycin C

Near-drowning

Pancreatitis

Pancreatitis, acute

Septic shock

Severe acute respiratory syndrome

PATHOGENESIS• Principal role of neutrophil has been questioned.

•ARDS can develop in neutropaenic patients also.

•Variety of inflammatory mediators are produced also by alveolar macrophages.

•Airway obstruction, which seems to be mediated by thromboxane.

PATHOPHYSIOLOGY

•Exudative/Acute phaseLasting for 1-6 days .

Alveolar oedema with a high protein content and large number of inflammatory cells indicating increased capillary permeability.

Collection of fluid, which is rich in protein along with cellular debris of destroyed alveolar cells, exudated RBCs and granular cells, lead to the formation of a coating over the denuded alveolar basement membrane called as the hyaline membrane.

At this stage, the amount of fluid is minimal to moderate and applying PEEP to the ventilation at this stage can improve oxygenation.

•Proliferative/Sub acute phaseLasting for 6-10 days.

Characterized by infiltration of the interstitium by fibroblasts and collagen.

There is proliferation of the type 2 epithelial cells.

PEEP may not be effective in this stage.

Since pulmonary capillary inflammation causes narrowing of vessels, pulmonary hypertension sets in which may be aggravated by Hypoxic Pulmonary Vasoconstriction (HPV). This leads to increase in dead space.

•Fibrotic/Chronic phaseFrom 10-14 days onwards.

There is large destruction resulting in emphysema and the dead space further increases.

Functionally the oxygenation improves, but there is pulmonary vascular obliteration due to fibrosis.

In survivors beyond 3-4 weeks, the lungs are completely remodeled by sparsely cellular collagenous tissue.

PEEP is not at all effective here and an increase in PaO2 does not correlate to increase in FiO2. There is increased chance of barotraumas and volutrauma.

CLINICAL FEATURES• The earliest clinical signs of ARDS include Tachypnea and

progressive hypoxaemia, that is refractory to supplemental oxygen.

• Tachycardia and respiratory alkalosis usually develop within the first 24 hrs after the initiating event and may precede to the development of infiltrates in the chest x-ray.

• There will be rapid worsening of dyspnoea and restlessness.

• Auscultation reveals scattered crackles and occasional wheeze.

• The inflammatory process and alveolar flooding lead to severe V-Q mismatch and intrapulmonary shunting, which is manifested clinically as severe hypoxia with decrease in PaO2/FiO2 ratio.

• The clinical picture can be divided into 4 stages:Stage1- Hyperventilation is the only clinical abnormality, No cyanosis. Chest X-ray is normal.

Stage2- Hyperventilation persists. Cyanosis ensures.

Stage3- Increasing respiratory distress with hyperventilation and cyanosis +chest x-ray showing diffuse consolidation.

Stage4- Hypercarbia, Metabolic acidosis and multiple organ failure manifest in this stage.

• The multiple organ failure may be:CVS- 10-23% cases, may be due to sepsis and depression of myocardium by TNF.

Renal- 40-55% cases, may be due to hypotension, nephrotoxic drugs and sepsis.

Liver- Fulminant hepatitis in 10% cases, while reversible enzyme changes in 95% cases.

Blood- DIC in 26% cases.

GIT- 7-30% cases, as hemorrhage, ilius, malabsorption etc.

ARDS Lung compliance:

•The pressure-volume (PV) curve demonstrates changes in compliance as intrapulmonary volume changes.

•The PV curve consists of 2 sigmoid curves with the lower one representing inspiration and the upper one representing expiration.

•Composed of 3 segments, the initial segment is flat representing low lung compliance due to collapse of peripheral airways and lung units. The next segment has a steeper slope representing improved lung compliance.

•The lower inflection point marks the transition point between these first 2 segments. The steepness of the slope then decreases as compliance decreases with increasing lung volumes and pressures.

•The upper inflection point represents the transition point at which compliance decreases. ARDS decreases pulmonary compliance altering the PV curve from normal lung.

Effect on cardiopulmonary mechanics:

Lungs-

Reduced FRC

Reduced Residual Volume

Reduced compliance (2/3rd of lung; rest 1/3rd having normal compliance)

Reduced TLC

Increased dead space

Increased airway resistance

Micro atelectesis

Pulmonary circulation-

Pulmonary HTN

Increased Rt to Lt shunting- resistance to increase in FiO2

Right Ventricle-

Stroke volume is decreased to pulmonary HTN.

PEEP may aggravate this by decreasing the preload and increasing the afterload.

Myocardium-

Endotoxins can depress the myocardial functioning.

• Diagnostic criterias:

In 1992, the American-European Consensus Conference (AECC) defined ARDS and this criterion is still used today. Limitations of the AECC criteria include variability in radiography interpretation and lack of lung compliance measurement and PEEP level when degree of hypoxemia is measured:

1.Acute onset and reasonable etiology

2.Bilateral infiltrates on frontal chest X-ray

3.PaO2/FiO2 <200 mmHg for ARDS and <300 mmHg for ALI

4.Pulmonary artery occlusion pressure (PAOP) ≤18 mmHg or CVP

<4mmHg or no clinical evidence of left atrial hypertension

Similarity between ARDS and other causes of respiratory failure

INVESTIGATIONS• ABG studies:

This helps in finding the extent of derangement and is useful to judge the effect of alteration in respiratory therapy. Each adjustment of PEEP must be followed by an ABG to assess its effects, efficiency and complications. Depending on the different stages of the pathological process, the ABG findings can be as follows:

• Radiological studies:

The chest x-ray typically shows bilaterally fluffy involvement that initially led clinicians to think that the pathology was homogenous.

But now with the advent of pulmonary imaging techniques, there has been convincing evidence that the involvement is segmental.

From the provided chest x-ray of a patient with ARDS, it appears that the infiltration is homogenous and equally distributed to both the lower lung fields.

The following CT images of the lung slices in the region of the hilum shows that the consolidation is not homogenous but is confined to the posterior or dependent lung regions. The uninvolved lung in the anterior 1/3rd of the thorax represents the functional portion of the lung in ARDS. In severe cases, the involvement may be up to 80% of lung fields.

Based on these findings, the lungs in patients with ARDS may be divided into 3 parts- one third represents a complete consolidated non ventilated region; one third is healthy with normal ventilation/perfusion matching; and one third is a region that is hyperdistended with bullae formation.

Anaesthetic implication-

Contrary to the previous belief, the compliance of the lung in a patient with ARDS is normal for 1/3rd of the lung parenchyma and “stiff” for the rest. The healthy portion is frequently referred to as “baby lung” and is subject to injury because of injudicious assignment of tidal volume.

By selecting tidal volume on the basis of body weight (≥10 ml/kg), clinicians have overlooked the important fact that only a small fraction of the total lung in patients with ARDS participates in gas exchange. Therefore, a disproportionate share of tidal volume will travel to the better compliant baby lung, subjecting it to over distention and injury.

Proponents of using lower tidal volume (6-8 ml/kg) in ARDS stress that utilizing a larger tidal volume in such settings is as inappropriate as ventilating an infant’s lung with a tidal volume equivalent to that of an adult.

• Hemodynamic measurements:The insertion of a Swan Ganz catheter is not essential for the diagnosis of ARDS; however at times it may be the only way to exclude ARDS from cardiogenic pulmonary oedema. Pulmonary oedema with pulmonary wedge pressure < 15-18 mmHg in the presence of a normal colloid oncotic pressure is diagnostic of ARDS.

• Routine tests:For the evidence of other organ dysfunction like renal, hepatic, hematological parameters should be done.

• Bronchoalveolar lavage:It is most reliable method for confirming or excluding the diagnosis of ARDS.

Lavage fluid is then analyzed for neutrophil density and protein concentration.

Neutrophils-

In normal subjects, the neutrophils make up less than 5% of the cells recovered in the lavage fluid, whereas in cases of ARDS, as many as 80% of the recovered cells are neutrophils.

A low neutrophil count in lavage fluid can be used to exclude diagnosis of ARDS, while a high neutrophil count can be considered as evidence of ARDS.

Total protein-

Because inflammatory exudates are rich in proteinaceous material, lung lavage fluid that is similarly rich in protein can be used as an evidence of lung inflammation.

When the protein concentration in lung lavage fluid is expressed as a fraction of the total protein concentration, the following criteria can be applied:

• Protein (lavage/serum) <0.5= Hydrostatic oedema

• Protein (lavage/serum) >0.7= Lung inflammation

MANAGEMENT• MANAGEMENT OF UNDERLYING DISEASE:

The underlying disease condition has to be managed and taken care of to prevent the progression of ARDS.

• SUPPORTIVE MEASURES:

Nutritional support-

Fluid management-Mainly aimed at reducing extra vascular lung water.Urine output of 0.5-1 ml/kg/hr is consistent with an adequate cardiac output and intravascular fluid volume. Normally a daily weight loss 0.2-0.4 kg is anticipated in adult patients receiving conventional intravenous fluid therapy. Frusemide is particularly effective

Pitfalls of Diuretic therapy in ARDS-

The lung inflammation in ARDS is an inflammatory process and diuretics don’t reduce inflammation.

Risk of hemodynamic compromise.

Antibiotics-Based on culture report, proper instillation of appropriate antibiotic regimen can be helpful in treating sepsis as well as in counteracting nosocomial infection.

Promoting Oxygen transport-The determinants of systemic oxygen delivery (DO2) is represented as:

DO2 = Q X 1.36 X Hb% X SaO2

Q is the cardiac output; Hb is the Hemoglobin saturation; SaO2 is the arterial oxygen saturation.

It should be maintained at a normal rate of 900-1100ml/min.

Removal of secretions- Done by:

Adequate systemic hydration

Humidification of inspired gases

Chest physiotherapy

Tracheal suctioning

Bronchodilators-

This is to decrease airway resistance and airway reactivity.

Aerolised β-agonists are particularly helpful.

Sedation and Analgesia-

Sedation by Lorazepam 0.5-2 mg

Analgesia by Morphine 0.08-0.1 mg/kg.

Neuromuscular Blockers-

In very high PEEP or inverse ratio ventilation, neuromuscular blockers may be required.

Corticosteroids-

No effect on ARDS when given within 24hrs of onset.

During the fibro proliferative phase that begins 7-14 days after the onset of illness, there is definite survival benefit.

Methylprednisolone in the dose of 2-3 mg/kg/day can be used.

The strategy is low dose steroid; started early, and continued for a longer duration.

The benefits of steroid in late ARDS may be explained by the ability of steroids to promote collagen breakdown and inhibit fibrosis.

• VENTILATORY MANAGEMENT:

Historical aspect- The pathway of the advent of ventilatory support for ARDS.

Problems associated with high TV (>10ml/kg):

Volutrauma, which means over distention and rupture of distal air spaces during mechanical ventilation due to a large tidal volume.

VILI, also known as ventilator induced lung injury, which is a complication of excessive inflation volumes leading to stress fractures in the alveolar capillary interface. These further progresses to infiltration of the distal airspaces with inflammatory cells and proteinaceous materials. This condition strikingly resembles the picture in ARDS.

Biotrauma- Bronchoalveolar lavage studies have shown that volutrauma is accompanied by the release of inflammatory cytokines from neutrophils that infiltrate the lungs. This effect is not explained by the mechanical forces and is called as biotaruma. These cytokines released into the circulation can enter distal organs to produce widespread inflammatory injury and multi organ failure.

Now the concept has again reverted back to the favor of pressure support ventilation with a lower TV to maintain adequate oxygenation. This lowered TV, especially in the presence of increased dead space of ARDS, can lead to hypercapnia. But the current concept of permissive hypercapnia overrules this objection.

Concept of permissive hypercapnia-

It is one of the consequences of low volume ventilation and is basically a decrease in CO2 elimination via lungs leading to hypercapnia and respiratory acidosis.

One of the most troublesome side effects of hypercapnia is brainstem respiratory stimulation with consequent hyperventilation, which often requires neuromuscular blockade to prevent ventilator asynchrony.

Data from clinical trials of permissive hypercapnia shows arterial pCO2 levels of 60-70 mmHg and arterial pH of 7.2-7.25 safe for most patients.

Lung protective ventilation: Low volume ventilation and PEEP-

To mitigate the complications associated with the conventional high TV.

Aka “Open Lung Approach” or better known as “Lung Protective Ventilation”

The basic principles are:

Maintenance of lower inspiratory drive pressure

Acceptance of permissive hypercapnia over higher airway pressure

Providing liberal sedation to improve patient ventilator synchronization

Open collapsed lung units with recruitment maneuvers

Prevention of alveolar over distention by:

Plateau Airway Pressure ( Pplat) <30-35 cm H2O

TV<8ml/kg

Pressure Controlled Ventilation

Minimum I: E=1:1-1.2:1

The Advantages gained ;the Problems faced ; the Solutions stated:

Ventilation with low TV was associated with a 9% reduction in mortality when the end expiratory plateau pressure was <30 cmH2O.

Low volume ventilation was associated with collapse of the terminal airways at the end of expiration and reopening of airways during lung inflation. This repetitive cycle itself can be a source of lung injury.

PEEP was introduced to mitigate this problem by acting as a stent to keep small airways open at the end of expiration. Addition of low level PEEP (5-7 cm H2O) has become a standard practice during low volume ventilation.

PEEP acts as an aid to arterial oxygenation in ARDS.

Addition of PEEP often allows a reduction in FiO2 to safer levels.

Use of PEEP to promote arterial oxygenation is a flawed practice as PEEP can decrease CO.

“CURRENT TREND OF VENTILATORY SETTINGS USED IN ards”

LUNG RECRUITMENT STRATEGIES:

• Patient to be put in prone position.

• Pillows are to be put beneath him; one beneath the upper chest and other beneath the pelvic area so that the abdomen hangs between them.

• Monitors are to be attached (pulse oximeter, EtCO2 monitor etc.) and a baseline ABG is to be taken.

• PEEP of 20 cm of H2O is to be kept for 90 sec.

• ABG is again repeated; if PaO2 is <300 mm Hg, PEEP to be increased to 30 cm H2O.

• To prevent derecruitment, maintain PEEP of 15 cm H2O with a tidal volume of 6 ml/kg.

• Inverse Ratio Ventilation (IRV):

Normal I: E ratio is 1:2.

When the TV of air gets into the respiratory tract with 1/3rd of the respiratory cycle, the peak airway pressure reaches high level. If the same TV is breathed over a more prolonged period, airway pressure rises gradually and the peak airway pressure reached is much less.

The incidence of barotrauma is much less.

During this prolonged inspiration, air gets into the atelectic alveoli and distends it and in the short expiration period, not whole of the air may be vented out; thus leaving a residual amount of air which acts as an auto PEEP and increases the FRC.

Responsible for improved oxygenation but at the same time has tendency to cause hypotension.

I: E ratios selected may vary from 1:1 to 1.2:1.

Patient has to be properly sedated or paralyzed as they may not tolerate this change in ratio.

•Partial Liquid Ventilation:

The lungs are partially filled with plerfluorocarbon (PFC) and ventilation is provided with a standard mechanical ventilator.

PFC is a clear inert liquid that improves gas exchange by:• recruiting dependent lung regions •clearing retained secretions •its anti-inflammatory properties•Least surface tension and high affinity for O2 and CO2. So it also causes a mass gas transfer.

PLV has been shown to decrease lung injury and improve gas exchange in acute lung injury compared to conventional mechanical ventilation (CMV).

• Nitric Oxide (NO):

NO cause vasodilatation of pulmonary vasculature, mostly the vessels perfusing the normal alveoli. The diseased alveoli are atelectic and do not get NO and so their corresponding vessels do not react to NO.

Thus blood supply is diverted to normally perfused alveoli thus reducing the shunt percentage. So oxygenation is increased without any increase in airway pressure.

The right ventricular performance is improved as the pulmonary artery pressure is decreased.

Disadvantage-

Combines with Hb and is immediately inactivated.

Formation of NO2 and methaemoglobin.

Formation of NO2 depends upon the % of O2 and the % of NO.

If kept within 5 ppm-40 ppm, the amount of NO2 produced is negligible.

Epithelial damage, pulmonary exudates, hemorrhage and death.

Amount of met Hb formed depends on the concentration of Hb

• Prone position ventilation:

It is seen in CT scans that lower lobes are most affected and even within the same lobe, the disease is not homogeneous.

Ventilation in different postures may be beneficial.

Prone position ventilation may be advantageous (mean 17hrs/day).

Even in this position, after some hours or days, if response is not good other modes of ventilation must be adopted.

• Extra Corporeal Membrane Oxygenation (ECMO):

The oxygenation and CO2 removal are taken care of by the membrane oxygenator.

This gives rest to the lung which is allowed to have time for recovery.

• Intra Venous Oxygenation (IVOX):

Extra Pulmonary Intracorporeal membrane oxygenation.

Introduced into the central veins and does the oxygenation and CO2

removal.

Gives rest to the lungs for recovery.

Still in experimental stages.

• Tracheal Gas Insufflation (TGI):

Aim of this technique is to deliver the inspired volume of gas, bypassing the dead space, direct to the alveoli and/or to wash out the expired gases by a passive flow of fresh gas.

Three types of TGI-

Inspiratory bypass

expiratory washout

continuous catheter flow

• Permissive Hypercapnia:

All efforts to decrease the PaCO2 are associated with problems of barotrauma or volutrauma or are associated with overshooting to hypocarbia.

Better to accept the Hypercarbia and to some extent respiratory acidosis.

Respiratory acidosis can be reduced by IV Carbicarb, which is an equimolar mixture of Na2CO3 and NaHCO3.

NaHCO3 alone infused in the presence of respiratory acidosis can lead to rise in the CO2 content, raised ICP, increased pulmonary hypertension, right ventricular failure and acute coronary syndromes.

• High Frequency Ventilation (HFV):

Ventilation at high rates (100-300breaths/min) with tidal volume less than dead space is found to maintain oxygenation without increasing the transtracheal pressure, thus avoiding barotrauma.

Types include:

High frequency PPV

High frequency jet ventilation

High frequency oscillation.

Complications include tracheitis and desiccation of tracheobronchial secretions, which can be treated by aerosolisation with water or frequent instillation of saline into trachea.

• MONITORING OF TREATMENT:

Oxygen exchange and arterial oxygenation-

Adequacy of oxygen exchange across alveolar capillary membranes is reflected by the PaO2.

This efficacy is paralleled by the differences between the calculated PaO2

and measured PaO2.

Calculation of A-a DO2 is useful for evaluating the gas exchange function of the lungs.

CO2 elimination-

The adequacy of alveolar ventilation relative to the metabolic production of carbon dioxide is reflected by the PaCO2.

The efficacy of carbon dioxide transfer across the alveolar capillary membrane is reflected by the VD/VT.

This ratio depicts areas in the lung that receive adequate ventilation but inadequate or no pulmonary blood flow.

Ventilation to these alveoli is described as “wasted ventilation”. Normally the ratio is less than 0.3 but may rise to 0.6 if wasted ventilation increases.

Mixed venous partial pressure of oxygen-

Mixed PvO2 and the arterial to venous differences for oxygen (CaO2-CvO2) reflect the overall adequacy of the oxygen transport system relative to the extraction of oxygen by the tissues.

PvO2 less than 30 mmHg or a CaO2-CvO2 value more than 6ml/dl indicates need to increase cardiac output to facilitate tissue oxygenation.

Arterial pH-

Necessary to detect acidaemia or alkalaemia.

Intrapulmonary Shunting-

Right to left intrapulmonary shunting of blood occurs when there is perfusion of alveoli that are not ventilated.

Physiologic shunt compromises normally about 2%-5%.

•WEANING FROM VENTILATOR:Assessment of weaning readiness-

Resolution of the cause of respiratory failure.

Central ventilatory drive must be adequate.

The patient must be able to maintain a patent airway, if extubation or

decannulation is contemplated.

The patient must be able to cough and adequately clear secretions.

Airway resistance must be adequately low; airway edema or obstruction can

preclude extubation.

The work of breathing must be adequately low; decreased lung compliance,

increased airway resistance, and hyperinflation impose an increased load upon

respiratory muscles.

Stable cardiovascular status.

Adequate arterial oxygenation (e.g., PaO2 > 60 mm Hg with FIO2 < 0.5 and PEEP<

5 cm H2O).

Failure to wean-

Failure to adequately clear tracheobronchial secretions by coughing, and

dynamic hyperinflation in patients with COPD or asthma are common

causes.

Acute congestive heart failure and myocardial ischemia are common and

significant causes of weaning difficulty, but can be difficult to detect.

Muscle weakness due to acute myopathy or polyneuropathy.

Occult muscle weakness can be due to inadequate rest following

exhausting breathing trials.

Malnutrition and severe electrolyte imbalance also can contribute to

weakness.

Auto-PEEP and hyperinflation.

Insufficiently treated pulmonary disease.

Inadequate rest following an exhausting spontaneous breathing trial.

Weaning parameters-

A parameter derived from measured respiratory rate and tidal volume, therapid shallow breathing index (RSBI), has been shown to be predictive of weaning success.

To calculate this parameter, the patient’s respiratory rate and minute ventilation are measured for one minute during spontaneous breathing. The measured respiratory rate is then divided by the tidal volume (expressed in liters).

A RSBI < 105 is reasonably predictive of weaning success.

Intubated with smaller diameter (<7 mm inner diameter) endotracheal tubes tend to have a higher RBSI.

If the patient meets criteria for weaning readiness and has a RSBI < 105, a spontaneous breathing trial can be performed.

The trial can be conducted with the patient breathing spontaneously while attached to the ventilator (CPAP mode), with a low level of pressure support ventilation (5 – 7 cm H2O), or disconnected from the ventilator and attached to a T-piece that provides humidity and supplemental oxygen. The spontaneous breathing trial should be terminated if the patient shows signs of respiratory distress (e.g., respiratory rate > 35/min; SpO2 < 90%; heart rate > 140/min or 20% change from baseline; systolic blood pressure >180 mm Hg or <90 mm Hg; anxiety; or diaphoresis).

Weaning techniques-

Weaning can be accomplished by gradually reducing the set rate of the ventilator during SIMV (SIMV weaning); gradually reducing the level of pressure with PSV (pressure support weaning); or by providing for periodic trials of spontaneous breathing (T-piece weaning).

The disadvantage of SIMV may be that little adaptation by the patient’s effort to volume-cycled machine assistance appears to occur on a breath-by-breath basis during IMV.

Noninvasive mechanical ventilation can be an important adjunct to facilitate weaning in selected patients.

Noninvasive PSV weaning led to reduced weaning time, fewer ICU days, a decreased nosocomial pneumonia rate, and improved 60-day survival.

Long-term ventilatory requirements-

Some patients require a prolonged time (weeks or months) to wean.

A comprehensive focus on generalized rehabilitation, strength and endurance training, and adequate attention to nutrition may be successful.

If desirable, mechanical ventilation may be continued in a long term care facility or at home.

PROGNOSIS

The mortality rate in ARDS;

though reduced now, still remains

between 40-50% in well developed

countries. Majority of the deaths

occur in the first few days, either due

to the original disease or due to the

respiratory failure. This improvement

in mortality is due to the better

supportive care, that is being given

and not due to any drugs. Those

persons, who recover after prolonged

ventilatory therapy, get back their

normal lung functions within six

months after the treatment.

REFERENCES• MILLER’S ANAESTHESIA 6TH EDN.

• CLINICAL ANAESTHESIA (PAUL G. BARASH) 4TH EDN.

• A PRACTICE OF ANAESTHESIA (WYLIE AND DAVIDSON) 7TH EDN.

• THE ICU BOOK (PAUL L. MARINO) 3RD EDITION.

• CLINICAL APPLICATION OF MECHANICAL VENTILATION (DAVID W. CHANG) 3RD EDN.

• INTERNATIONAL ANAESTHESIOLOGY CLINICS (VOL:47; NUMBER 1) WINTER 2009.

• INTERNET.