Open Lung Ventilation - Condition and Management

Introduction

Lung protective ventilation is considered the standard management in acute respiratory distress syndrome. A significant risk factor in developing bronchopulmonary dysplasia is ventilator-induced lung injury. Therefore, lung protective ventilation strategies decrease tidal volumes and recruit and stabilize atelectatic lung units.

What Is Acute Respiratory Distress Syndrome?

The term ARDS (acute respiratory distress syndrome) is often limited to patients requiring ventilatory support in the intensive care unit (ICU); a less severe form, also known as acute lung injury, can occur in acute medical and surgical wards. It is an acute, diffuse inflammatory response to either direct or indirect insults that originate from extrapulmonary pathology.

It is typically characterized by the following:

• Neutrophil sequestration in lung capillaries.

• Increased capillary permeability.

• Protein-rich pulmonary edema along with hyaline membrane formation.

• Destruction of type 2 pneumocytes leads to decreased surfactant production.

• The collapse of the alveoli.

• Reduction in lung compliance.

If the initial phase does not resolve with the treatment of the underlying cause, a fibroproliferative phase may follow and lead to pulmonary fibrosis. It is usually associated with other organ dysfunction as a part of multiple organ failure. Typical signs and symptoms vary depending on the underlying causes and severity. They are nonspecific, with many features overlapping with other pulmonary conditions.

• Severe shortness of breath.

• Unusual rapid breathing.

• Hypotension or low blood pressure.

• Fatigue.

• Confusion.

What Are the Conditions That Predispose to ARDS?

Conditions that may lead to ARDS:

Direct or Inhalation:

• Aspiration of gastric contents.

• Toxic gasses or burn injury.

• Pneumonia.

• Blunt chest trauma.

• Near drowning situations.

Indirect or Blood Borne:

• Sepsis.

• Necrotic tissue.

• Multiple trauma.

• Pancreatitis.

• Cardiopulmonary bypass.

• Severe burns.

• Drugs such heroin, barbiturates, and thiazides.

• Major transfusion reactions.

• Anaphylaxis (wasp, bee stings, snake venom).

• Fat embolism.

• Carcinomatosis.

• Obstetric crises such as eclampsia and amniotic fluid embolism.

The Criteria Defining ARDS Are:

• Hypoxemia is defined by the partial pressure of oxygen to a fraction of inhaled oxygen less than 200 mmHg; in the case of acute lung injury, it should be less than 300 mmHg (millimeters of mercury).

• Chest X-ray showing diffuse bilateral infiltrates.

• Absence of a raised left atrial pressure where the pulmonary artery wedge pressure is less than 15mmHg.

• Impaired lung compliance.

How Is ARDS Managed?

Damage to the lungs can be exacerbated by mechanical ventilation, overdistension of alveoli, and repeated opening and closing of distal airways. Therefore, ARDS can be managed with the help of protective ventilator support, which aims at minimizing lung injury and the associated inflammatory response with limited tidal volumes and airway pressure. The other strategies which may be beneficial in severe ARDS are

• The prone position improves oxygenation by decreasing the thoracoabdominal compliance and the pleural pressure gradient, ensuring a uniform distribution of ventilation and better matched to perfusion.

• Nitric oxide inhalation is a short-acting vasodilator. Therefore, it improves the blood flow to the ventilated alveoli, thus improving ventilation-perfusion matching.

• Corticosteroids may be helpful if given in the fibroproliferative stage.

What Are the Principles of Mechanical Ventilation in ARDS?

The principles of mechanical ventilation are:

1.Optimum ventilator settings are:

• Pressure control or limited.

• Small tidal volumes less than 6ml/kg.

• Long inspiratory to expiratory volume.

• Positive end-expiratory pressure.

2. It allows partial pressure of carbon dioxide to rise and tolerate lower oxygen saturation levels than normal.

3. Large tidal volumes, airway pressure of more than 35 cm (centimeter) H2O (hydrogen peroxide), and a fraction of inhaled air of more than 0.8 should be avoided.

4. Maintain a balance between improving gas exchange, minimizing the risk of subsequent pulmonary fibrosis due to lung injury, and avoiding adverse circulatory effects.

What Is Ventilator-Induced Lung Injury (VILI)?

Ventilator-induced lung injury can be due to

• High tidal volume to inflate the alveoli can lead to volutrauma.

• Insufficient PEEP (positive-end expiratory pressure) can lead to atelectrauma.

• Distribution of tidal volume to only open alveoli can lead to regional overdistension.

• Half of the lung is not open so suddenly; it can cause a high fraction of inhaled oxygen (FiO2) which can further lead to free radical injury.

All these lead to barotrauma and ultimately lead to ventilator-induced lung injury.

What Are the Benefits of Open Lung Ventilation?

The benefits of open lung ventilation in ARDS are that it increases the recruitment of alveoli and thus prevents alveolar overdistension and leads to decreased volutrauma. Reduces cyclic atelectasis and atelectrauma.

It also reduces the biotrauma from alveolar collapse by releasing inflammatory mediators and it also reduces denitrogenation atelectasis and oxygen toxicity by lowering the fraction of inhaled oxygen.

How Does Open Lung Ventilation Prevent VILI?

Open lung ventilation can prevent VILI by giving optimal PEEP (positive-end expiratory pressure) to recruit the atelectatic lung. However, an optimal PEEP is different for every child. So, all areas which were not participating in ventilation are now opened up, as the efficiency and surface area for gaseous exchange has increased.

Conclusion

Lung collapse is not only due to a primary disease but is a prerequisite. Open lung ventilation is an early intervention in managing acute respiratory distress syndrome. It improves oxygenation and driving pressure. It increases the alveolar recruitment with the application of optimal PEEP (positive-end expiratory pressure) and efforts to reduce the derecruitment. A single figure cannot measure optimal PEEP (positive-end expiratory pressure).

The alveolar recruitment causes the reopening of the collapsed alveoli by an intentional increase in the transpulmonary pressure that may lead to a marked improvement in oxygenation. Sometimes, hypotension may occur due to decreased venous return. Also, along with alveolar recruitment, lung stretching above the tidal volume is the most powerful stimulus for the secretion of surfactant from type 2 pneumocytes. This leads to a reduced lung elastance with improved lung perfusion. Therefore, open lung ventilation can prevent VILI by giving optimal PEEP, and the recruitment maneuvers improve the gaseous exchange compared to conventional ventilation strategies.