Low Compliant lung ventilator strategies

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Transcript Low Compliant lung ventilator strategies

LOW COMPLIANT LUNG VENTILATOR STRATEGIES

By: Maria Lopez & Rebecca Lentz

DEFINITIONS

 Compliance is defined as the relative ease with which a structure distends.

 Elastance is defined as the tendency of a structure to return to its original form after being stretched or acted on by an outside force.  In terms of the lungs the compliance is the ability of the lungs to expand and accept an increased volume of gases, where elastance is the ability to recoil to the original/smaller shape and results in a decreased volume. These changes in the lung shape allow for changes in volume that will result in the ability to move gasses in and out of the lungs – ventilation. A decrease in either of these critical lung mechanics will affect the patient’s ability to exchange gas and thus will reduce their ability to maintain a normal pH, acid base balance and/or oxygenation.

CONDITIONS RESULTING IN ↓ COMPLIANCE

 ARDS decreases compliance as the lung parenchyma is often times replaced with fibrotic tissue making the lung less able to accept volume or less compliant. The stiffness associated with ARDS is a result of this fibrotic scar tissue and not only reduces compliance and ventilation but also reduces the tissue participating in gas exchange.

 VILI or ALI are disease processes that are initiated by damage resulting from mechanical ventilation and are considered indistinguishable from ARDS.

 Pneumoconiosis like ARDS will result in replaced lung parenchyma with fibrotic scar tissue that is much less compliant than healthy lung tissue. Additionally the replacement with fibrotic tissue will also result in less tissue participating in gas exchange. Pneumoconiosis is different from ARDS as it is a result of exposure to dust particles that cause the encapsulation of the dusts and thus causes scar tissue.  Kyphoscoliosis decreases lung compliance but by way of reduced thoracic compliance as the thoracic cage is restricted by the spinal position resulting in smaller overall volume changes in the lungs. The lungs will likely have good characteristics – however their reduced function is completely related to the decreased complicate of the thoracic cage.

DECREASED COMPLIANCE

WHAT IS OVERDISTENTION

   Over distention is the overstretching of alveoli as a result of excessive pressure being delivered during mechanical ventilation which can be a result of therapist neglect or decreased lung compliance.

When a patients lung compliance decreases as a result of a disease process, such as ARDS, then the pressures are quickly increased inside the alveoli when a patient is on VC.

Overdistention can also cause a disease process within the lung parenchyma indistinguishable from ARDS and is known as ALI or VILI.

WHAT ARE THE PHYSIOLOGICAL EFFECTS OF OVERDISTENTION?

Mechanical ventilation over distention can cause biochemical injury which will release cytokines, complement, prostanoids, leukotrienes, reactive oxygen species, proteases due to the biophysical injury of over distention, cyclic stretch and increased intrathoracic pressures which cause the release of bacteria in the distal organs at the level of the tissue injury secondary to inflammatory mediators cells, which can impair O2 delivery and cause bacteremia resulting to MODS.

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WHAT ARE THE PHYSIOLOGICAL EFFECTS OF OVERDISTENTION?

Destruction of type 1 cells (alveolar) epithelial cells leads to detachment of the underlying basement membrane which results in impairment of the normal anatomic barrier Which leads to increased permeability Resultant influx of protein rich edema fluid in the interstitium and alv space.

In patients with persistent over distention causing lung injury (3-7 days) after initial lung injury, the disease processes to a stage at which the basement membrane is replaced with a more fibrotic material enhanced by proliferation of alveolar type II cells; The fibrosis contributes to the poor compliance of the lung, which can contribute to loss of alveolar capillary interface. In addition to the destruction of the vasculature in the alveoli is caused by fibrosis and thrombosis which can lead to pulmonary hypertension. In comparison of protein concentration in pulmonary edema fluid to the protein concentration in plasma soon after initiation mechanical ventilation for resp failure has shown a higher ratio in pts with permeability pulm edema (ALI AND ARDS) than in pts with hydrostatic pulm edema (left heart failure)

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WHAT ARE THE PHYSIOLOGICAL EFFECTS OF OVERDISTENTION?

Over distention causes ALI & ARDS and is characterized by: Acute alveolar inflammation Neutrophil activation Surfactant deficiencies Damage to alveolar capillary membrane (increase permeability neutrophil and bacterial migration) Development of proteinaceous pulmonary edema and alveolar collapse.

WHAT ARE THE PHYSIOLOGICAL EFFECTS OF OVERDISTENTION?

Over distention can lead to VILI and result to ARDS resulting to biotrauma which is the migration of bacteria, neutrophils and pro inflammatory mediators from the lungs through the porous alveolar capillary membrane. Addition to this neutrophils are adhering to the injured capillary endothelium and marginating through the interstitium into the airspace, which is protein rich edema fluid. In the airspace art alveolar macrophage is secreting cytokines, interleukin 1,6,8 and 10, tnf alpha (tumor necrosis factor alpha), which act to stimulate chemotaxis and activate neutrophils. Macrophages also secrete other cytokines Interleukin 1, 6, and 10. Interleukin 1 can also stimulate the production of extracellular matrix and fibroblasts. Neutrophils will release oxidants, proteases, leukotrienes, and other proinflammatory molecules such as PHF (platelet activating factor). There is also a number of anti inflammatory mediators also present in alveolar milieu, including interleukin 1receptor antagonist, soluble tumor necrosis factor receptor, auto antibodies against interleukin 8 and cytokines such as IL 10 and IL 11. In addition to this, the influx of protein rich edema fluid into the alveolus has led to the inactivation of surfactant.

ASSESSMENT TO DETERMINE THE DEGREE OF LUNG DAMAGE

Lung injury can be measured by the lung injury score developed by Murray, which:

 It incorporates the level of PEEP  the Pa02/Fi02 ratio  a chest radiographed score  lung compliance into a summary score that can be used to describe how severe of the lung injury is.

ASSESSMENTS TO DETERMINE OVERDISTENTION

  The best determination form overdistention is to look at the Pressure/Volume loop.

If there is a beaked shape present then this will indicate that the patient is experiencing overdistention as a result of decreased lung compliance or a Vt too high for their current lung mechanics.

ASSESSMENTS TO DETERMINE OVERDISTENTION

  Always thoroughly assess the patients Plateau Pressure and compare it with previous values - as an increase in this pressure can be indicative of overdistention. It is important to insure that this pressure remains under 30cmH2O to avoid all the potential risks associated with overdistention.

   ASSESSMENTS TO DETERMINE VENT SETTINGS TO AVOID OVERDISTENTION AND ATELECTRAUMA Esophageal pressure (Pes) can be measured to have an estimate of Transpulmonary Pressure (PL) and its effect on Pleural Pressure (Ppl) to be able to estimate the impedance on the lungs resulting from pressures exerted by the chest wall.

Although this technique is not commonly used, it has been shown in research studies to be beneficial in treating patients with decreased compliance and improving the final outcome for these mechanically ventilated patients. The use of a ballooned catheter placed inside the esophagus is able to obtain this information.

Having a good estimate of Ppl will allow for optimal ventilator settings to be used – such as:   Optimal Vt to avoid overdistention Optimal PEEP to avoid atelectrauma from repetitive opening and collapse of compromised alveoli.

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VENTILATOR STRATEGIES TO TREAT LOW LUNG COMPLIANCE

Mode Choices:   Assist Control (AC) is the most likely choice for a patient experiencing severe respiratory failure.

SIMV may also be used if there is persistent asynchrony with the patient and ventilator. However it is likely that the patient would be sedated in order to achieve desired ventilation with AC prior to moving to this mode. Breath type Choices:   Volume Control (VC) is the most commonly used breath type as it allows for more precise control of Minute Ventilation (Ve) and CO2 clearance. Pressure Control (PC) may also be used as a strategy to reduce risk of overdistention as it will not allow for excessive pressures to be reached and the Vt will be reduced to insure safe pressures.

  VENTILATOR STRATEGIES TO TREAT LOW LUNG COMPLIANCE VC   PC It is important to remember that low Vt be used with VC when treating a patient with low lung compliance. The Vt should be set at 5-8ml/kg (IBW) Increasing the RR to offset the difference in Vt will allow for an adequate Ve to be reached. Set at 12-20 bpm   When using PC it would be worth noting that the pressures will likely be at the higher end of the acceptable range (20 25cmH2O)to insure an sufficient Vt when treating a patient with low lung compliance.

Again – increasing the RR with PC will also help to meet an adequate Ve to support CO2 clearance. Set at 12-20 bpm

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VENTILATOR STRATEGIES TO TREAT LOW LUNG COMPLIANCE

Positive End Expiratory Pressure (PEEP) is used to recruit collapsed alveoli and reduces the need for high pressure to do such and will prevent overdistention in alveoli that are already open. PEEP is able to maintain patency of newly recruited alveoli by preventing their complete collapse PEEP is able to transfer pressure to collapsed alveoli by maintaining a small pressure over that of ambient pressure which will then have the ability to open collapsed alveoli by passing through the Pores of Kohn and Canals of Lambert.

PEEP is able to help reduce shear stress associated with the abrupt closing and opening of the alveoli that often occurs with high pressures.

PEEP is set at a beginning pressure of up to 5cmH20 and may be set as high as 25cmH20. PEEP Should be set just above the lower inflection point on the pressure/volume loop to insure that the alveoli remain patent.

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VENTILATOR STRATEGIES TO TREAT LOW LUNG COMPLIANCE

Oxygen / FiO2 should be maintained as low as possible to support a PaO2 of >55mmHg and a SpO2 of >88%. Using PEEP should reduce the overall need for increased FiO2 and possible complications associated with ROS as a result of long term exposure to increased FiO2.

Patients with ARDS will likely require higher FiO2 due to the lung parenchyma that has been replaced with fibrotic tissue and no longer participates in gas exchange.

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VENTILATOR STRATEGIES TO TREAT LOW LUNG COMPLIANCE

Surfactant replacement for patients with ARDS is being studied at this time. Preliminary studies may indicate that a formula different from that used with neonates may be required to treat adult patients that have reduced surfactant due to alveolar damage and dysfunction in the late stages of ARDS. Early stages of the disease processes related to decreased lung compliance have been found to have better responses to the current exogenous surfactant.

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FUTURE VENTILATOR STRATEGIES BEING RESEARCHED AT THIS TIME

Surfactant Replacement  To help prevent atelectrauma Partial Liquid Ventilation  Oxygen soluble fluro carbon liquid is used to recruit compromised alveoli Nitric Oxide  Pulmonary vasodilator that may help with excessive oxygen exposure Extracorporeal Membrane Oxygenation Systems (ECMO)  Reduces need for positive pressure ventilation High Frequency Ventilation  Helps with alveolar recruitment and avoid atelectrauma and decreases risk of overdistention

WORK CITED

 Cairo, J., & Pilbeam, S. (2012). Pilbeam's mechanical ventilation: Physiological and clinical applications (5th ed.). St. Louis, Mo.: Elsevier Mosby.

 Egan, D. (2003). Acute and Critical Care. In Egan's fundamentals of respiratory care (8th ed. / [edited by] Robert L. Wilkins, James K. Stoller, Craig L. Scanlan ; consulting ed.). St. Louis, Mo.: Mosby.

 Hess, D. (2012). Ventilatory Support Involves Trade-Offs. In Respiratory care: Principles and practice (2nd ed.). Sudbury, Mass.: Jones & Bartlett Learning.

 Kacmarek, R., & Dimas, S. (2005). ARDS, SARS and Sepsis. In The essentials of respiratory care (4th ed.). St. Louis, Mo.: Elsevier Mosby.

 Ludwig, M. (2007, September 1). Proteoglycand and Pathophysiology. Retrieved August 19, 2014.

 Mac Intyre, N. (1999, May 1). Mechanical Ventilation Strategies. Retrieved August 14, 2014.

 Piantadosi, C., & Schwartz, D. (2004, September 21). The Acute Respiratory Distress Syndrome. Retrieved August 18, 2014.

 Souza-Fernandes, A. (2006, November 10). Bench-to-bedside review: The role of glycosaminoglycans in respiratory disease. Retrieved August 18, 2014.

 Talmor, D. (2008, November 13). Mechanical Ventilation Guided by Esophageal Pressure in Acute Lung Injury — NEJM. Retrieved August 14, 2014.

 https://v.cdn.vine.co/r/videos/DA00277CC01101978909580591104_1f85d8dab91.3.2.mp4?versionId=SwmNvqVAn90ve4fB8qq5ls75.Jjx4cSV