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IPPV: Minimizing Ventilator Induced Injury

Steve Haskins United States

Positive pressure ventilation (PPV) procedures may be associated with a number of problems. Inappropriate ventilator settings and ventilator malfunction; breathing circuit and tracheal tube problems; patient-ventilator asynchrony; airway, mouth, eye, bladder/urine, and colon/fecal problems; and anesthetic agent-related complications have been recognized.

Thoracic blood flow impairment

Positive pressure ventilation impairs intrathoracic blood flow by increasing pleural pressure, which impedes venous return to both the right and the left side of the heart. To the extent that venous return is diminished, diastolic ventricular filling, stroke volume, cardiac output, and arterial blood pressure are also diminished. The degree of impairment of intrathoracic blood flow is directly proportional to the magnitude of the increase in pleural pressure, the length of time that the pressure is applied per breath (the inspiratory time) and per minute (the cycle rate), and indirectly proportional to the baseline central venous pressure (the blood volume). The magnitude of the circulatory impairment can be assessed by observing the effect of each inspiration on pulse quality or arterial blood pressure. If it is determined that excessive circulatory impairment is present, the inspiratory pressure and the inspiratory time or the breathing rate could be decreased, or the blood volume could be increased. Diseased lungs are poorly compliant, and while it may require higher airway pressures to ventilate these lungs, less of the pressure is transmitted to the pleural space and there is less tendency to impair circulation.

Alveolar septal rupture

The use of high airway pressures/volumes in normal and abnormal lungs may be associated with alveolar septal rupture, pneumomediastinum, pneumothorax, pulmonary hemorrhage, and air embolism. Alveolar septal rupture is reported to occur at a rate of between 3 and 40% (Streiter; Amato; Weg; Stewart; King). There is marked individual variation in susceptibility to this problem. Weg, et al., reported: “there was no airway pressure above which patients always developed alveolar septal rupture and no airway pressure below which it never occurred.” Pre-existing parenchymal bullae or recent parenchymal rupture, lower the threshold to ventilator-induced alveolar septal rupture. Airway pressure and tidal volume settings should only be as high as is minimally necessary to achieve acceptable ventilation and oxygenation. In diffuse pulmonary parenchymal disease, the total number of functional lung units is reduced. The introduction of normal tidal volumes causes over-distention of the remaining functional lung units. Lung protective strategies utilize smaller than normal tidal volumes to help prevent this volutrauma.

Monitoring for the development of a pneumothorax during positive pressure ventilation must be an ongoing endeavor. It should be one of the first rule-outs for patient-ventilator asynchrony. If a pneumothorax develops, a chest drain must be inserted and continuous chest drainage provided.


While inhalation is an active process orchestrated by the ventilator, exhalation is a passive process depending upon lung and chest wall elastance. If exhalation is not complete prior to initiation of the next breath, the next tidal volume will be increased by the amount of air remaining in the lung from the preceding breath. This “air trapping” or “breath stacking” or “auto-PEEP” can result in over-expansion of lung units (volutrauma). Air trapping is more likely to occur if exhalation is delayed by narrowed lower airways (chronic airway disease, bronchospasm) and with higher ventilator cycle rates. If the measured end-expiratory pressure exceeds that set on the ventilator, auto-PEEP is occurring.

Auto-PEEP is not necessarily bad unless it is excessive. PEEP (whether it comes intentionally from the ventilator or unintentionally from the patient-ventilator interaction) improves lung-oxygenating efficiency. It is important to know when auto-PEEP is present and then a decision can be made whether to keep it or to make it go away.

Capillary endothelial damage

Airways and alveoli are tethered together by strands of collagenous and elastic fibers. When the airways are expanded, tangential and longitudinal traction is placed upon on the adjacent endothelium cell layer. This widens intercellular junctions and increases capillary permeability and the flux of fluids into the pulmonary interstitium.

Airway and alveolar epithelial damage

In pulmonary disease, an increase in airway fluids increases surface tension and increases the tendency for small airway and alveoli collapse (when the transpulmonary pressure and functional residual capacity are below the critical closing point). Re-opening of these units during the next breath requires breaking the surface tension seal between two adjacent epithelial cells. These tangential forces eventually damage the cell membranes.

Adjacent lung units, for a variety of reasons, have different time constants and do not expand at the same time or rate. This causes a shear injury to the alveolar epithelium on each side of the thin septal membranes that form the common wall between the two adjacent alveoli.

Release of inflammatory mediators

Positive pressure ventilation and, particularly, over-distention of lung units, is thought to cause leuco-activation resulting in the release of inflammatory mediators (Ranieri). These at least enhance capillary permeability and at most, cause endothelial and epithelial cell damage and death.

These processes of endothelial and epithelial damage worsen the magnitude of the diffuse parenchymal disease in a manner that is indistinguishable from the underlying diffuse infiltrative disease for which the animal is receiving ventilator therapy. PEEP, sufficient to prevent airway/alveolar closure will minimize surface tension-induced and asynchronous lung unit expansion-induced epithelial damage. PEEP should be set above closing pressure.


Pneumonia is a common consequence of long-term positive pressure ventilation procedures: 1) positional stasis predisposes to atelectasis and decreased secretion clearance from the lower lung regions; 2) the bacterial population of the mouth and pharynx proliferate and become colonized by gram negative organisms; 3) these micro-organism invariably migrate down the trachea (past the inflated cuff) and into the lower airways; 4) invasive procedures such as tracheal intubation and tracheal suctioning predispose to the introduction of bacteria into the lower airways; 5) if antibiotics are utilized, the patient is predisposed to colonization by resistance micro-organisms; and 6) if histamine-2 blockers are utilized, the patient is predisposed to bacterial colonization in the stomach (such fluids invariably find there way up the esophagus and into the airways). The procedure of positive pressure ventilation, per se, is not considered an indication for prophylactic antibiotic therapy. In an unpublished experimental series (Haskins), all dogs were placed on antibiotics by the end of one week. Regular repositioning, aseptic airway procedures, and regular mouth and pharynx care help minimize the development of pneumonia. Ventilated patients should be monitored for indications of infection and placed on appropriate antibiotics if/when the need arises.

Open lung techniques/lung protective ventilator strategies

An open lung technique is a concept rather than a specific technique. The idea is to recruit as many alveolar units as possible (open them up) and then prevent them from collapsing again (keep them open). This will optimize blood oxygenation and minimize ventilator-induced injury. Positive pressure ventilation can induce lung injury ranging from alveolar septal rupture and pneumothorax to a diffuse infiltrative respiratory distress syndrome that is indistinguishable from the disease for which PPV was implemented. This injury derives from various deleterious aspects of over-inflation of individual lung units (volutrauma). Lung protective ventilation strategies seek the same objectives as the open lung ventilation techniques: 1) to recruit as many alveolar units as possible; 2) to prevent their re-collapse; and 3) to minimize alveolar over-distention. These strategies involve high initial peak pressures (40 to 60 cm H2O) for alveolar recruitment, for variable periods of time (the duration of one breath, up to a minute) and moderate to high PEEP (10–20 cm H2O) to keep alveoli open, and then moderate (usually less than 40 cm H2O) peak pressures (Amato; Stewart; Brochard; Brower; ARDS Network; Kloot; Medoff). The inevitable consequence of high PEEP pressures and moderate peak pressures is a small (compared to normal) tidal volume. A normal lung can easily handle a normal tidal volume, however, a lung with reduced vital capacity cannot (without volutrauma); the tidal volume needs to be appropriate for the patient. Unfortunately, the magnitude of the disease-induced reduction in vital capacity cannot be predicted in advance. It needs to be assessed in each patient and then must be re-assessed frequently since compliance and vital capacity can change over the course of a few hours. Tidal volume is a dependent variable that is determined by airway pressures and thoracic compliance. Protective lung strategies may also diminish the release of inflammatory mediators that promote capillary endothelial and airway epithelial damage (Ranieri).

We propose here a method that we think would be applicable to veterinary patients. This procedure should only be applied to animals with diffuse pulmonary parenchymal disease; it has no purpose in animals with relatively normal lungs being ventilated for neurologic reasons. You will need to be able to measure airway pressures and tidal volumes, and have the capability to set PEEP. Start with about +5 cm H2O of PEEP, set the peak pressure to 10 cm H2O with a long inspiratory time of about one second, and record the tidal volume. Increase the peak pressure to 15 cm H2O and record the new tidal volume. Calculate the change in tidal volume generated by the change in peak pressure (i.e., new-previous tidal volume). Repeat the process, increasing the peak pressure by 5 cm H2O each time either until the incremental increase in tidal volume starts to decrease, or until a peak pressure of 60 cm H2O is attained. In either case, total lung capacity is considered to have been reached. The peak pressure setting associated with the greatest incremental increase in tidal volume is now selected. The peak pressure associated with the first large increase in tidal volume is now selected as the PEEP setting. Alternately, if your ventilator has the ability to display a pressure-volume curve, PEEP is selected at the airway pressure that represents a 50% reduction in peak volume using the deflation portion of the curve. If these ventilator settings result in a tidal volume exceeding 10 ml/kg, the peak pressure should be further decreased until the tidal volume is 10 ml/kg. The ventilator cycle rate should then be adjusted to keep the PaCO2 below 60 mm Hg. The ventilator cycle rate is now selected. Start at 25 breaths per minute and adjust as necessary to obtain an acceptable PaCO2.

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