S&H 37, 39, 40; Cornell Mechanical Ventilation Video

How can nursing care affect complications in long term ventilation?

• Suggested that humans requiring short-term ventilation have better outcomes than patients requiring long-term ventilation

  • Multiple complications have been associated with long-term ventilation, many of which pertain to nursing care such as oral and corneal ulceration, tracheal tube occlusion or dislodgement, and gastric distension requiring decompression

  • In human medicine, the risk of late-onset, but not early-onset ventilator-associated pneumonia (VAP) is affected by a lower nurse staffing level

General Monitoring for the Ventilator Patient

• Ideal monitoring includes continuous electrocardiography, placement of a rectal thermistor for continuous temperature assessment, pulse oximetry, capnography, and serial blood pressure measurements

• Auscultation of the chest and a cardiovascular physical examination should be performed at least every 4 hours to detect abnormalities as early as possible

• Placement of an arterial catheter allows continuous blood pressure monitoring and arterial blood gas analysis, which should be performed every 4-8 hours or more frequently if indicated

• Patient that develop asynchrony with the ventilator are prone to having elevations in body temperature because of increased heat production from muscular effort

  • May be treated by improving ventilator-patient synchrony, using surface cooling methods (e.g. placement of a fan or use of a cold-water spray bottle), or turning off or removing the humidification system

• Removal of airway humidification should only be performed for short periods because humidification is key to airway management

• Hypothermia may occur as a side effect of anesthetic agents and should be treated with circulating warm-water blankets and forced-air warming devices or by covering the patient with a blanket to reduce heat loss

Hand Hygiene for Artificial Airways

• Whenever a patient with an artificial airway is being handled, hand hygiene should be performed first and examination gloves used to reduce risk of nosocomial infection

• The intubation process should be performed with sterile gloves, ideally with a sterile ET tube

What endotracheal cuffs and pressure are recommended for mechanically ventilated patients?

• Endotracheal tube cuffs can be either high or low volume and high or low pressure, but in veterinary medicine, size will likely restrict these options to low-volume, high-pressure or high-volume, low-pressure cuffs

  • The use of low-pressure cuffs is recommended because cuff pressure greater than 25 cm H2O has been shown to reduce tracheal blood flow which can lead to necrosis and cuff pressures greater than 30 cm H2O should be avoided

Recommendations to Prevent Tracheal Injury in Ventilated Patients

• Use of a cuff pressure monitoring device is recommended to help prevent tracheal damage

• As a precautionary measure to reduce the risk of tracheal injury, it has been suggested to deflate the cuff and reposition it every 4 hours in veterinary medicine

What should endotracheal tube cuff pressure be maintained at to help prevent VAP according to the American Thoracic Society?

At more than 20 cm H2O

ET Cuff Recommendations to Weight the Risk of Tracheal Necrosis vs VAP in Ventilated Patients

• Authors recommend: If a high-volume low-pressure ET tube is used and the cuff pressure can be monitored, the cuff should not be deflated and repositioned, but cuff pressure should be checked every 4 hours. If a low-volume high-pressure ET tube is used or if cuff pressure cannot be monitored, then the cuff should be deflated and repositioned every 4 hours

  • Before deflation and repositioning, oral care and suctioning should be performed to reduce the risk of aspiration

Maintenance of ET Tube Ties in Ventilated Patients

• Secure the ET tube with nonporous material such as plastic IV tubing

• The tie used to secure the ET tube should be retied every 4 hours to prevent damage to the lips and should be replaced every 24 hours to prevent biofilm accumulation

Recommendations for ET Tube Changes in Ventilated Patients

• Reintubation has been shown to increase the risk of VAP in humans

• ET tube occlusion has been reported to occur in up to 14% of animals

  • Patients with exudative pulmonary secretions and smaller diameter ET tubes put them at risk for occlusion and may benefit from an ET tube change every 24-48 hours

  • Patients being ventilated without significant pulmonary secretions or with relatively large diameter ET tubes may only need ET tube changes on an as needed basis

What can lack of humidification of the airways lead to?

Increased mucus viscosity and inspissation, which can cause ET tube occlusion, tracheal inflammation, and depressed ciliary function

What are the two major methods of humidification of the airways?

Heat and moisture exchangers (HMEs)

Heated water humidifiers

Heat and Moisture Exchangers (HMEs)

• Passive HMEs act as an artificial nose by trapping the heat and moisture of exhaled air in the device and then returning them on the following inspiration

• HMEs increase dead space and resistance to airflow

• Have the potential to become obstructed by airway secretions and are often avoided in patients that have copious or tenacious pulmonary secretions

• Should not be changed more frequently than every 48 hours unless they become soiled, obstructed, or mechanically fail

• Ventilator waveforms can be evaluated for increased resistance, indicating a partially occluded HME

Heated Water Humidifiers

• Traditionally considered the gold standard

• Placed in the inspiratory limb of the breathing circuit and allow air to be humidified by passing a heated water reservoir

• Potential complications include overheating and condensation of water in the inspiratory limb, which contributes to bacterial colonization of the breathing circuit

• Condensation in the circuit can be largely prevented by the use of heated wire circuits

What factors contribute to deciding which humidifier to use?

• Decision on which type of humidifier to use should be made based on availability, expected level of secretions, and concerns of increased dead space and resistance to breathing circuit

What are characteristics of the ideal catheter for suctioning the airway?

• Ideal catheter should be soft and flexible, have more than one distal opening, be sterile, and occlude no more than 50% of the internal diameter of the ET tube

What should occur prior to airway suctioning?

The patient should be preoxygenated with 100% oxygen for at least 5 minutes to help prevent hypoxemia during the process

How to Perform Open Suctioning

• With open suctioning, sterile gloves should always be worn by the person manipulating the suction catheter

  • A second person wearing nonsterile gloves should disconnect the breathing circuit from the ET tube to facilitate sterile insertion of the catheter, which should be inserted to the distal end of the ET tube

    • Insertion of the catheter farther than the distal opening of the ET tube risks tracheal inflammation, induction of coughing, or vagal-mediated bradycardia

  • Process should be quick, with the catheter partially occluding the lumen of the ET tube for no more than 10-15 seconds per suction pass

  • Repeat multiple times until secretions are no longer aspirated, with the patient being reconnected to the ventilator in between each suction pass

  • The suction catheter should be cleansed with sterile saline in between suction passes, using a new cup of sterile saline each time to prevent bacterial contamination of the saline container

Closed System Suction Catheters

• Closed system suction catheters are kept in place between the breathing circuit and the patient when not in active use

  • Advantage that the circuit doesn't have to be opened for suctioning, reducing the risk of contamination

  • Do increase dead space of the circuit

How often should the suction cannister and tubing be replaced?

Every 24 hours to minimize the change of bacterial colonization

Addition of Sterile Saline to the Airway to Facilitate Mucus Recovery During Suctioning

• Addition of sterile saline to the airway to facilitate mucus recovery during suctioning is controversial

  • Before suctioning, instillation of 0.1-0.2 mL of 0.9% NaCl into the airway can be considered to help mobilize dry secretions

  • Concerns of saline instillation center around dislodging bacteria from the ET tube and promoting VAP as well as inducing hypoxemia\

  • Benefit may be more effective removal of secretions, which may reduce the likelihood of VAP

Risks of Suctioning an ET tube or Tracheostomy Tube

• Iatrogenic hypoxemia

• Collapse of alveoli as a result of temporary lack of positive end-expiratory pressure

• Tracheal irritation

• Bradycardia

• Hypotension

Complications of Mechanical Ventilation Involving the Oral Cavity

Oral ulceration

Ranula formation

Reflux of gastric contents into the oral cavity

Moistening the Tongue During Mechanical Ventilation

• Tongue is usually moistened with an alternating dilute glycerin-soaked or saline-soaked gauze

  • Avoid wrapping the tongue circumferentially with gauze because this can lead to ranula formation

Oral Care for Mechanically Ventilated Patients

• Lack of swallowing allows for bacteria to proliferate and pool in secretions around the endotracheal tube, increasing the risk for VAP

  • Subglottic suctioning and selective oral decontamination has been shown to decrease the incidence of VAP and oral lesions

• Oral care should be performed every 4 hours

  • The tongue should be inspected for development of a ranula

    • If a ranula is forming, elevating the ET tube to avoid causing pressure on the base of the tongue may be helpful

  • Avoiding placement of the tongue over the teeth as well as the use of a mouth gag may help prevent ulceration

  • Inspect the mouth for mucosal ulcerations and record the depth and size of any identified

• Remove the pulse oximeter probe and any mouth gag and clean them with a dilute 0.12-2% chlorhexidine solution

• Cleanse the entire oral cavity with a specifically formulated 0.12-2% chlorhexidine solution

• Suction the oral cavity and caudal oropharynx to remove remaining chlorhexidine and oral secretions

• Brushing of the teeth twice daily can reduce bacterial oral load and may be considered

• Replace the mouth gag and pulse oximeter in a different position to help prevent ulceration

What eye pathology are ventilator patients at risk for?

• Ventilator patients are at increased risk of exposure keratopathy and microbial keratitis

  • They don't blink so the tear film can't be spread over the eye

• Many patients have lagophthalmos, predisposing them to exposure keratopathy

• Despite eye care, up to 25% of children and 37.5% of adults on mechanical ventilation may develop ocular surface disorders

When does the majority of corneal ulceration develop in ventilated patients?

• The majority of ulceration develops within the first week, however a significant proportion can develop within 48 hours of initiation of mechanical ventilation

What are the two major methods of providing lubrication to the eye in ventilated patients?

Lubricating ointments

Moisture chambers

Lubricating Ointments for Eye Lubrication in Ventilated Patients

• Involves regular cleaning of the eye with sterile saline and replacement with a hyaluronic acid-containing, petroleum-based lubricating ointment

• Considered the standard of care due to the difficulty in obtaining a good seal from a moisture chamber with the various skull structures of dogs and cats

Moisture Chambers for Eye Lubrication in Ventilated Patients

• Doggles or swimmer's goggles to completely seal off the eye from the environment

• Advantage - the cornea is protected even if the eye is open

Eye Care in Ventilated Patients

• Eye care should be performed every 2 hours

  • Lavage the eye and inspect for chemosis, corneal disease, and conjunctivitis

  • If no ulceration is present, a petroleum-based lubricant should be reinstilled

  • If ulceration is present, a broad-spectrum antibiotic ointment should be used every 4 hours

• Fluorescein staining should be performed every 24 hours to evaluate for ulcer formation

• If lagophthalmos or exophthalmos a temporary tarsorrhaphy may be needed

Urinary Care for the Ventilated Patient

• Bladder should be palpated every 4-6 hours and expressed as needed

• If long term ventilation is indicated, the patient may benefit from a urinary catheter

  • Avoids the repeated pressure and trauma of expressing the bladder and allow for more accurate documentation of urine volume

• Urinary catheter care should be performed every 8 hours as long as an indwelling urinary catheter is in place

Risks of Urinary Catheterization

• Development of bacteriuria from true urinary tract infection or colonization of the catheter

• In dogs, the incidence of urinary tract infections associated with indwelling catheterization in nonmyelopathic conditions ranges from 10-20%, with length of catheterization being a risk factor

GI Complications of Mechanical Ventilation

• Esophagitis

• Gastrointestinal bleeding

• Diarrhea

• Ileus

• Constipation

• Gastric distension

• Regurgitation

• Splanchnic hypoperfusion plays an important role in development of many of these complications because of diminished venous return from high levels of positive end-expiratory pressure and increased levels of circulating catecholamines or proinflammatory cytokines

• The incidence of gastrointestinal bleeding in human patients can be as high as 47% with clinically significant bleeding in 3.3% of patients ventilated for more than 24 hours

  • This is less likely in dogs and cats as they are less likely to have stress induced gastric ulceration

What is a modifiable risk factor for GI bleeding in ventilated patients?

Peak inspiratory pressure 30 cmH2O or greater

Benefits of Enteric Nutrition

• Shown to decrease the incidence of GI bleeding and prevent villous atrophy of the intestinal mucosa, potentially reducing the risk of bacterial translocation

Risks of Enteric Nutrition

• May increase the incidence of gastroesophageal reflux and aspiration pneumonia if ileus is present

How can enteral feeding be delivered to ventilated patients?

• Enteral feeding may be delivered via nasogastric, gastrotomy, or jejunostomy tube

  • Esophagostomy tube is not recommended for patients on mechanical ventilation as postesophageal feeding may be associated with a decreased risk of aspiration pneumonia

How should ventilated patients be evaluated for constipation?

The colon should be palpated daily

• If constipation is noted, enemas may be needed

Recumbent Patient Care

• Prolonged recumbency can induce decubital ulcers, tissue necrosis, atelectasis, muscle and ligament contracture, and regional dependent edema

• Passive range of motion should be performed every 4 hours, including the flexion and extension of every joint in the limbs as distal as the phalanges

• ICU-acquired weakness and critical illness neuromyopathy are possible sequelae in long-term ventilation in humans but have not been documented in clinical veterinary medicine

• The position of recumbency should be changed every 4 hours, alternating between sternal and each lateral position, if the patient's oxygenation status will tolerate it

  • If lateral recumbency is not possible, then the patient can be kept in sternal recumbency and the hips of the patient moved from right side down to left side down every 2-4 hours

  • Special attention for ulcer formation at the elbows or for development of dermal lesions in the antebrachium is needed if the cranial half of the patient is always in sternal recumbency

Current Recommendations for Degree of Elevation in Ventilated Patients

• Current recommendation if the patient is ventilated on a table that tilts is to elevate the torso 30-45 degrees

  • Ventilation with the trachea elevated above horizontal is thought to decrease gastroesophageal reflux, whereas ventilation with the trachea below horizontal may prevent aspiration of oropharyngeal secretions into the trachea

  • At this time ventilation with the trachea elevated 45 degrees cannot be recommended in veterinary medicine, at this point patients should be kept in neutral horizontal position

Apparatus Care in the Ventilated Patient

• The ventilator circuit should be sterilized before use and put together wearing sterile gloves to minimize the change of nosocomial infections

• Based on findings, it seems safe to change the circuit if gross contamination is noted rather than as a routine precaution

  • If frequent condensation occurs in the circuit due to use of a heated water humidifier, more frequent circuit changes may be indicated

Ventilator-Induced Lung Injury (VILI)

Injury to the lung caused by mechanical ventilation in experimental models

Ventilator-Associated Lung Injury

Worsening of pulmonary function, or presence of lesions similar to ARDS in a clinical patient that is thought to be associated with the use of mechanical ventilation, with or without underlying lung disease

Barotrauma Description

Extraalveolar air

• Pneumothorax

• Pneumomediastinum

• Subcutaneous emphysema

Barotrauma Preventative Strategies

Minimize plateau airway pressure

• Target <30 cm H2O

Volutrauma Description

Overdistension causing stretch injury

Volutrauma Preventative Strategies

Minimize TV

• Target TV <10 ml/kg

Atelectrauma Description

Cyclic recruitment - derecruitment injury

Atelectrauma Preventative Strategies

Application of PEEP

Mechanical Power Description

Total energy transferred to the lung - includes TV, driving pressure, respiratory rate, flow rate, and PEEP

Mechanical Power Preventative Strategies

Minimize all ventilator settings - all energy transferred to the lung has the potential to cause injury

Spontaneous Breathing while Receiving Mechanical Ventilation Description

Alveolar distension, shear stress, atelectrauma, etc., during spontaneous breathing is equally as injurious as mechanical ventilator breaths.

May promote edema formation more than positive pressure ventilation

Spontaneous Breathing while Receiving Mechanical Ventilation Preventative Strategies

Minimize spontaneous breathing including patient-ventilator asynchrony with appropriate sedation, optimization of ventilator settings ± neuromuscular blockade

Biotrauma Description

Release of inflammatory mediators from the injured lung leading to systemic inflammation, which may promote multiple organ dysfunction

Biotrauma Preventative Strategies

Lung-protective ventilation strategies to limit lung injury and implement strategies to reduce microaspiration of oropharyngeal fluid

Oxygen Toxicity Description

High oxygen concentrations may directly cause lung injury as well as contribute to absorption atelectasis

Oxygen Toxicity Preventative Strategies

Minimizing FiO2 within 24 hours

• Target FiO2 <0.60

Barotrauma

• Barotrauma implies pressure-related injury to the lung

• In terms of VILI, barotrauma is defined as extraalveolar air and is manifested clinically by pneumothorax, pneumomediatstinum, or subcutaneous emphysema

  • Disruption of the alveolar capillary membrane allows air to dissect along facial planes, accumulating within the pleural space or other compartments, or the development of subcutaneous emphysema

What was associated with a higher incidence of pneumothorax in human ARDS patients?

• In a study of human ARDS patients, the use of high airway pressures (peak inspiratory pressure >40 cm H2O) was associated with a higher incidence of pneumothorax than when lower airway pressures were used

• In another study, when plateau pressure was maintained at less than 35 cm H2O, no relationship was found between ventilator setting and the occurrence of pneumothorax

When does barotrauma occur?

In lungs ventilated with high alveolar pressures and large tidal volumes (VT)

Evaluation of what pressure is best to assess risk of VILI?

• Airway pressure may not accurately reflect the stress imposed on the lung parenchyma as it includes the pressure needed to expand the chest wall

  • The distending pressure of the lung is best reflected by the transpulmonary pressure and this would be a better measure to use when assessing the risk of VILI

Volutrauma

• Results in an increase in the permeability of the alveolar capillary membrane, the development of pulmonary edema, the accumulation of neutrophils and proteins, the disruption of surfactant production, the development of hyaline membranes, and a decrease in compliance of the respiratory system

• Stretch injury as a result of high volume is more injurious to the lung than high pressure, without a large increase in volume

• In a study, rats were ventilated with either high volume/high pressure, high volume/low pressure (negative pressure ventilation), or low volume/high pressure (chest wall was restricted)

  • Both high-volume strategies caused substantial lung injury while the low volume/high pressure strategy had far less evident injury

• Concerns for volutrauma are supported by human clinical studies showing improved outcomes with use of low tidal volume ventilation

Chest Wall Effects on Volutrauma

• Alveolar distension is determined by the difference between alveolar and pleural pressure so the chest wall has a role in determining the extent of overdistension

  • When the chest wall is stiff (low compliance) or heavy, a high Pplat may be associated with less risk of overdistension

  • A stiff or heavy chest (e.g. obesity, abdominal distension, massive fluid resuscitation, chest wall deformity, chest wall burns) protects the lungs from VILI

Effect of Active Breathing Efforts on Volutrauma

• The alveolar distending pressure can change markedly on a breath-by-breath basis in a spontaneous breathing patient

• When the airway pressure is constant and the patient forcefully inhales, the alveolar distending pressure may exceed what is expected by the airway pressure setting

  • During pressure-targeted ventilation, the contribution of patient's effort to alveolar distending pressure must be appreciated

• Dependent pleural pressure changes can exceed the average measured pleural pressure due to in pendelluft, movement of gas from one part of the lungs into another during inspiration but without increasing overall tidal volume

  • Causes local distension and an increased risk of VILI

  • Avoid excessive patient effort regardless of mode of ventilation

Effect of Preexisting Injury of Development of VILI

• Increases the likelihood of VILI

• Two-hit process of lung injury

  • Previous injury predisposes the lungs to a greater likelihood of ventilator induced injury

Atelectrauma

• Atelectrauma or cycle recruitment-derecruitment injury - trauma to epithelial cells and injury to adjacent alveoli via shear stress from repetitive opening and closing of collapsed alveoli

• In healthy lungs, there are relatively few collapsed alveoli, but in injured lungs, alveoli become progressively unstable, changing shape during inflation and completely collapsing at the end of expiration

  • The junction between an open and a closed alveolus serves as a stress raiser

• When rats are ventilated with high pressures and no PEEP, the rapidly develop severe, diffuse pulmonary edema

  • If they are ventilated at the same pressure with the addition of PEEP, it is far less injurious

• PEEP can reduce the cyclic collapse and reexpansion of alveoli and minimize atelectrauma

Mechanical Power

• The total mechanical power or energy transferred to the lung during ventilation may correlate with the likelihood for VILI

• It is recommended that the mechanical power is normalized to the area of ventilated lung available

  • This normalized value for mechanical power has been described as intensity

• In lungs with smaller areas participating in ventilation, the value for intensity for a given degree of mechanical power would be higher

• A novel aspect of this approach is the inclusion of respiratory rate and PEEP as potential contributors to VILI

  • PEEP can be protective of lung injury, but does increase the energy load transmitted to the lung and may contribute to VILI in some circumstances

What does mechanical power include?

• Mechanical power includes all components of a ventilator breath that can contribute to VILI

  • Tidal volume

  • Driving pressure

  • Respiratory rate

  • Flow rate

  • PEEP

What are the primary determinants of lung injury?

Stress and strain

Stress

The internal counterforce per unit area that balances an external load on a structure, or the pressure gradient across a structure (e.g. alveolar capillary membrane)

Strain

Deformation of the system as a result of the external load or the change in size or shape of the structure (alveolar distension)

What are stress and strain from a pulmonary perspective?

Stress is the alveolar distending pressure (alveolar pressure minus pleural pressure) and strain is the ratio of volume change (V_T plus volume increase caused by PEEP) to functional residual capacity (FRC) during the application of the stress

What lung strain is considered injurious to the lungs?

Lung strain of more than 2 (i.e. double the resting lung volume)

How are lung stress and strain related?

• Stress and strain are related by the specific lung elastance of 12 cm H2O

  • Lung stress is 12 cm H2O times lung strain

  • Surrogates for stress and strain are plateau pressure (Pplat) and V_T

Spontaneous Breathing and VILI

• Mechanisms of VILI are a product of the dynamic stress applied to the lung during breathing efforts and this stress can be equally injurious if breaths are generated by mechanical ventilation or spontaneous respiratory efforts

• The decrease in pleural pressure as a result of spontaneous breathing efforts increases transvascular pressure (the transmural pressure of pulmonary vessels)

  • Then there is distension of the vessels which can promote the formation of edema

• These concerns are relevant to spontaneous breathing modes, in addition to animals with patient-ventilator asynchrony

Biotrauma

• VILI causes cell damage and results in an inflammatory response

• The release of proinflammatory cytokines caused by VILI may promote multiple organ dysfunction and increased inflammatory cytokines can worsen VILI in a circular fashion

  • Pro-inflammatory and anti-inflammatory mediators increase edema formation, neutrophil migration, and relaxation of vascular smooth muscle

• The morbidity and mortality associated with VILI, from any mechanism, are largely the result of the subsequent systemic inflammation known as biotrauma

• Lung-protective ventilation strategies limit lung injury and have been shown to reduce multiple organ dysfunction and improve outcomes

Oxygen Toxicity

• Patients receiving PPV are invariably on supra-atmospheric levels of oxygen supplementation

  • This may have an additive effect to the injury caused by VILI, especially if a high oxygen concentration is delivered for an extended period

• Inspired oxygen concentration of 100% in the short term can cause absorption atelectasis and decreased oxygen diffusion capacity

• Beyond 24 hours, an FiO2 between 50-100% promotes the production of reactive oxygen and nitrogen species and causes pathologic changes similar to ARDS and VILI, including interstitial edema, hyaline membrane formation, damage to the alveolar membrane, altered mucociliary function, and fibroproliferation

  • The damage appears to be positively associated with the level of FiO2 and the length of time that oxygen was administered

• Laboratory data suggest that former exposure to bacterial endotoxin, inflammatory mediators, and sublethal levels of oxygen (less than or equal to 85%) protect the lungs from further injury when inspiring a high FiO2

• Combination of bleomycin and oxygen results in marked injury to the lungs

  • In this setting the lowest FiO2 should be used, tolerating a PaO2 as low as 50 mm Hg (SpO2 85-88%)

What FiO2 should be administered whenever there is uncertainty about the PaO2?

1

What should the target PaO2 when adjusting FiO2 be?

• FiO2 should be lowered to the level resulting in a PaO2 of 50-80 mmHg (SpO2 88-95%) as soon as possible

What is the target FiO2 in the mechanically ventilated patient?

Less than or equal to 0.50

Translocation of Cells and VILI

• Leakage of inflammatory mediators into the bloodstream increases systemic inflammation

• Bacteria instilled into the lungs of otherwise healthy animals produce bacteremia when inappropriate respiratory patterns are employed

Other Mechanisms of VILI

• Higher vascular infusion volumes, rapid respiratory rates and inspiratory flows, and high body temperature potentially cause greater injury

Histopathology Associated with VILI

• Histopathologic changes associated with VILI are hard to distinguish from changes associated with ARDS

• Include decreased integrity of small airway epithelial cells, destruction of type 1 alveolar epithelial cells, alveolar and airway flooding, hyaline membrane formation, interstitial edema, and infiltration of inflammatory cells

• Lesions usually have an uneven distribution but tend to be worse in the dependent lung, likely because of worsened airway flooding and shear injury

VILI and MODS

• Disruption of the alveolar-capillary membrane allows leakage of pulmonary inflammatory mediators into the bloodstream, allowing downstream organ failures

Low Tidal Volume Ventilation

• Growing evidence that high-volume/low-PEEP ventilation can cause harm and worsen preexisting lung injury

• Volume limitation in patients with ALI and ARDS has shown the most dramatic results in outcome, with the landmark ARDSnet study showing a decrease in mortality when 6 ml/kg tidal volume was used vs 12 ml/kg

  • The group receiving lower tidal volumes also, incidentally, received slightly higher PEEP and inspired oxygen concentration

• Evidence that low tidal volume ventilation may be of benefit in people without ARDS or ALI

  • Meta-analysis of intraoperative ventilation concluded that low tidal volume (<10 ml/kg) ventilation decreased the frequency of pneumonia and the need for postoperative ventilatory support

Lung Protective Ventilation Strategy

• Limits tidal volume to 4-8 mL/kg

• Maintains plateau pressure less than 28 cm H2O

• Maintains driving pressure less than 15 cmH2O

• Sets PEEP based on the patient's pathophysiology and respiratory mechanics

• Provides a FiO2 that maintains the PaO2 between 55 and 80 mmHg and SpO2 between 88 and 95%

Low Tidal Volume Ventilation to Prevent VILI

• There is strong evidence for limiting tidal volume to less than normal in human studies, where values of 4-6 ml/kg have been recommended in ARDS patients

• Optimal target for tidal volume in dogs and cats is unknown and likely varies between breeds due to anatomical differences

  • Most clinical veterinary studies on mechanical ventilation have reported the use of tidal volumes of greater than 10 ml/kg

  • Recommended to target the lowest possible tidal volume needed to maintain adequate blood gases, likely to be in the range of 6-12 ml/kg in dogs and cats

• Healthy dogs have a higher normal tidal volume than other species, but the volume of functional units available for gas exchange in injured lungs may be much reduced

• Inflammation in the lung causes heterogenous changes throughout, with regions of poorer compliance and atelectasis, which causes more compliant regions to become overdistended

  • Limit tidal volume to prevent portions of the lung from being overdistended

• Low tidal volume increases the risk of perpetuating atelectasis and creating further shear injury so application of PEEP is vital

What is a common consequence of low tidal volume ventilation?

Hypercapnia

• Permissive hypercapnia - tolerating higher than normal PaCO2 levels rather than increasing ventilator settings

• This approach may reduce the likelihood of VILI, but there are physiological consequences of hypercapnia that may impact patient outcome

Positive End-Expiratory Pressure to Prevent VILI

• Well established that some PEEP is better than no PEEP or zero end-expiratory pressure

• Minimum amount of PEEP needed to reduce VILI has not been established

• Common levels of PEEP considered adequate in human medicine are in the range of 5-10 cm H2O

Limitation of Plateau Pressure to Prevent VILI

• Plateau pressure best represents the pressure applied to the lung as it is not impacted by resistance of the system

  • Measured during an inspiratory hold maneuver and the animal should not be making active respiratory efforts during measurement

• The combination of high PEEP, auto PEEP (PEEP created by increased outflow resistance during expiration, asynchrony, or incomplete expiration), and tidal volume can lead to high end-inspiratory volume, which may be indicated by high plateau pressure

• Protective lung ventilation strategies in human medicine recommend targeting a plateau pressure of less than 30 cm H2O

  • Peak inspiratory pressure may be used as a surrogate for plateau pressure unless there is increased resistance in the system

Respiratory Rate and Inspiratory Flow to Prevent VILI

• Some evidence that high respiratory rates and inspiratory flow rates can promote VILI

Subjective Analysis of the Pressure Volume Loop to Prevent VILI

• An optimal ventilator breath avoids both alveolar collapse on exhalation and overdistension on inhalation

  • The upper and lower inflection points of the pressure-volume loop theoretically show where these events occur and maintaining PEEP and peak inspiratory pressure between these points could be beneficial

• Subjective analysis of the pressure-volume loop may be of some benefit, in particular recognition of overdistension from the presence of "beaking"

Recommendations for Spontaneous Breathing to Prevent VILI

• In severe ARDS, spontaneous breathing effort has been associated with poorer outcomes, while in less severe pulmonary disease, spontaneous breathing may actually provide benefits such as better lung recruitment and improved diaphragmatic tone

• A recent human clinical practice guideline recommended against the routine use of NMBA in patients with moderate or severe ARDS that tolerate light sedation

  • In patients that require deep sedation or prone ventilation, the use of NMBA is reasonable

Advanced Pulmonary Support Techniques to Prevent VILI

• Advanced strategies such as partial liquid ventilation, high-frequency oscillatory ventilation, extracorporeal membrane oxygenation, and carbon dioxide removal are being researched to look for strategies with lower risk of VILI than conventional mechanical ventilation

Ventilator-Associated Pneumonia (VAP)

Pneumonia that arises more than 48 hours after endotracheal intubation and mechanical ventilation that was not present at the time of intubation

What % of mechanically ventilated human patients does VAP occur in?

3-10%

Risk of Developing VAP and the Duration of Ventilation

• Risk of developing VAP varies with duration of ventilation

• Most animals receive mechanical ventilation for less than a week so the majority of cases of VAP would be expected to occur in the first few days of ventilation but the cumulative incidence will increase as the number of days of intubation increases

• Development of VAP increases the length of time mechanical ventilation is necessary

What are the potential outcomes once a pathogen gets past the cuff of the endotracheal tube?

• Pathogen may be cleared by normal respiratory defenses

• The lower airways may be colonized

• The tracheobronchial tree may become infected (ventilator-associated tracheobronchitis [VAT]), or if the pulmonary parenchyma becomes infected, VAP occurs

Normal Respiratory Defenses to Colonization or Infection of the Lower Airways

• Cough

• Mucus clearance

• Humoral and cellular immune responses

How are normal respiratory defenses compromised in an anesthetized critically ill animal?

• Reduced ability to cough due to sedation and presence of endotracheal tube

• Inflation of a cuffed endotracheal tube depresses mucociliary clearance rate

• Critical illness is associated with decreased immune system function and increased susceptibility to nosocomial infection

• Evidence for neutrophil dysfunction in VAP with a reduced phagocytic capability and elevation in neutrophil proteases in the alveolar space