Ventilator Management(Archived)

The need for mechanical ventilation is one of the most common causes of admission to the intensive care unit. It is imperative to understand some basic terms to understand mechanical ventilation. Ventilation: Exchange of air between the lungs and the air (ambient or delivered by a ventilator); in other words, it is the process of moving air in and out of the lungs. Its most important effect is the removal of carbon dioxide (CO2) from the body, not on increasing blood oxygen content. Ventilation is measured as minute ventilation in the clinical setting, and it is calculated as respiratory rate (RR) times tidal volume (Vt). In a mechanically ventilated patient, the CO2 content of the blood can be modified by changing the tidal volume or the respiratory rate. Oxygenation: Interventions that provide greater oxygen supply to the lungs, thus the circulation. In a mechanically ventilated patient, this can be achieved by increasing the fraction of inspired oxygen (FiO 2%) or the positive end-expiratory pressure (PEEP). PEEP: The positive pressure that will remain in the airways at the end of the respiratory cycle (end of exhalation) is greater than the atmospheric pressure in mechanically ventilated patients. For a full description of the use of PEEP, please review the article titled “Positive End-Expiratory Pressure (PEEP).”. Tidal volume: Volume of air moved in and outside the lungs in each respiratory cycle. FiO2: Percentage of oxygen in the air mixture that is delivered to the patient. Flow: Speed in liters per minute at which the ventilator delivers breaths. Compliance: Change in volume divided by change in pressure. In respiratory physiology, total compliance is a mix of lung and chest wall compliance, as these two factors cannot be separated in a patient.  Since having a patient on mechanical ventilation allows a practitioner to modify the patient’s ventilation and oxygenation, it has an important role in acute hypoxic and hypercapnic respiratory failure as well as in severe metabolic acidosis or alkalosis. Mechanical ventilation has several effects on lung mechanics. Normal respiratory physiology works as a negative pressure system. When the diaphragm pushes down during inspiration, negative pressure in the pleural cavity is generated; this, in turn, creates negative pressure in the airways that suck air into the lungs. This same negative intrathoracic pressure decreases the right atrial (RA) pressure and generates a sucking effect on the inferior vena cava (IVC), increasing venous return. The application of positive pressure ventilation changes this physiology. The positive pressure generated by the ventilator transmits to the upper airways and finally to the alveoli; this, in turn, is transmitted to the alveolar space and thoracic cavity, creating positive pressure (or at least less negative pressure) in the pleural space. The increased RA pressure and decreased venous return generate a decrease in preload. This has a double effect in decreasing cardiac output: Less blood in the right ventricle means less blood reaching the left ventricle and less blood that can be pumped out, decreasing cardiac output. Less preload means that the heart works at a less efficient point in the frank-startling curve, generating less effective work and further decreasing cardiac output, which will result in a drop in mean arterial pressure (MAP) if there is not a compensatory response by increasing systemic vascular resistance (SVR). This is a very important consideration in patients who may not be able to increase their SVR, like in patients with distributive shock (septic, neurogenic, or anaphylactic shock). On the other hand, mechanical ventilation with positive pressure can significantly decrease the work of breathing. This, in turn, decreases blood flow to respiratory muscles and redistributes it to more critical organs. Reducing the work from respiratory muscles also reduces the generation of CO2 and lactate from these muscles, helping improve acidosis. The effects of mechanical ventilation with positive pressure on the venous return may be beneficial when used in patients with cardiogenic pulmonary edema. In these patients with volume overload, decreasing venous return will directly decrease the amount of pulmonary edema generated by decreasing right cardiac output. At the same time, the decreased return may improve overdistension in the left ventricle, placing it at a more advantageous point in the Frank-Starling curve and possibly improving cardiac output. Proper management of mechanical ventilation also requires an understanding of lung pressures and lung compliance. Normal lung compliance is around 100 ml/cmH20. This means that in a normal lung, the administration of 500 ml of air via positive pressure ventilation will increase the alveolar pressure by 5 cm H2O. Conversely, the administration of positive pressure of 5 cm H2O will generate an increase in lung volume of 500 mL. When working with abnormal lungs, compliance may be much higher or much lower. Any disease that destroys lung parenchyma, like emphysema, will increase compliance; any disease that generates stiffer lungs (ARDS, pneumonia, pulmonary edema, pulmonary fibrosis) will decrease lung compliance. The problem with stiff lungs is that small increases in volume can generate large increases in pressure and cause barotrauma. This generates a problem in patients with hypercapnia or acidosis, as there may be a need to increase minute ventilation to correct these problems. Increasing respiratory rate may manage this increase in minute ventilation, but if this is not feasible, increasing the tidal volume can increase plateau pressures and create barotrauma. There are two important pressures in the system to be aware of when mechanically ventilating a patient: 1. Peak pressure is the pressure achieved during inspiration when the air is being pushed into the lungs and is a measure of airway resistance. 2. Plateau pressure is the static pressure achieved at the end of a full inspiration. To measure plateau pressure, we need to perform an inspiratory hold on the ventilator to permit the pressure to equalize through the system. Plateau pressure is a measure of alveolar pressure and lung compliance. Normal plateau pressure is below 30 cm H20, and higher pressure can generate barotrauma.