MECHANICAL VENTILATION:
AN OVERVIEW
by Kevin T. Martin BVE, RRT, RCP V7117 HC 04RC Educational Consulting Services, Inc. P.O. Box 1930, Brockton, MA 02303-1930
(800) 441-LUNG / (877) 367-NURS www.RCECS.com
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ECHANICAL VENTILATION: AN OVERVIEW
BEHAVIORAL OBJECTIVES
UPON COMPLETION OF THE READING MATERIAL, THE PRACTITIONER WILL BE ABLE TO:
1. Compare and contrast spontaneous breathing to positive pressure ventilation. 2. List the effect positive pressure ventilation has on ventilatory, circulatory, central nervous, renal and digestive systems.
3. Explain acute hypoxemic respiratory failure (Type I). 4. Explain acute hypercapnic respiratory failure (Type II).
5. Compare and contrast the goals of mechanical intervention for Type I and Type II respiratory failure.
6. List the indications for mechanical ventilation.
7. Summarize the complications of positive pressure ventilation. 8. Define the common modes and new of mechanical ventilation.
9. List the initial parameters and setting guidelines for mechanical ventilation.
10. Discuss adjustment of ventilator parameters after reviewing ABG results and patient’s clinical status.
11. Identify the mode of ventilation used in the treatment of obstructive sleep apnea.
12. Select the amount of pressure support level needed to overcome patient circuit resistance. 13. Describe the modes of ventilation that are combination modes.
14. Describe the operational functions of selected modes of ventilation. 15. Define automode ventilation.
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ECHANICAL VENTILATION: AN OVERVIEW
COPYRIGHT © October, 1985 BY RC Educational Consulting Services, Inc.COPYRIGHT © April, 2000 By RC Educational Consulting Services, Inc. (# TX 1 762 726)
AUTHORED 1985 By Kevin T. Martin, BVE, RRT, RCP
REVISED 1988, 1990, 1993, 1996, By Kevin T. Martin BVE, RRT, RCP REVISED 2001 By Susan Jett Lawson, RCP, RRT-NPS
REVISED 2003 By Helen Schaar Corning, RRT and Michael R. Carr, BA, RRT, RCP REVISED 2006 By Helen Schaar Corning, RRT and Michael R. Carr, BA, RRT, RCP REVISED 2010 By Aimee D Staggenborg, MA, BA, RRT
ALL RIGHTS RESERVED
This course is for reference and education only. Every effort is made to ensure that the clinical principles, procedures and practices are based on current knowledge and state of the art
information from acknowledged authorities, texts and journals. This information is not intended as a substitution for a diagnosis or treatment given in consultation with a qualified health care professional.
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ECHANICAL VENTILATION: AN OVERVIEW
TABLE OF CONTENTS
INTRODUCTION ... 6
SPONTANEOUS VENTILATION... 6
POSITIVE PRESSURE VENTILATION ... 7
EFFECTS OF POSITIVE PRESSURE VENTILATION ...8
Pulmonary Effects...8
Circulatory Effects ...8
Cerebral Effects ...9
Central Nervous System (CNS) Effects...9
Renal System Effects ...9
Digestive System Effects ...10
INDICATIONS... 10
Type I: Hypoxemic Respiratory Failure (Oxygenation Failure)...10
Type II: Hypercapnic Respiratory Failure (Ventilatory Failure)...10
COMPLICATIONS ...11
MODES OF VENTILATION...13
Continuous Positive Airway Pressure (CPAP) ...13
Positive End-Expiratory Pressure (PEEP) ...14
Pressure Support Ventilation (PSV) ...15
Automatic Tube Compensation ...15
Bilevel Positive Pressure Ventilation (BIPAP)...16
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ECHANICAL VENTILATION: AN OVERVIEW
Synchronized Intermittent Mandatory Ventilation (SIMV) ...17
SIMV Pressure Control + Pressure Support (SIMV PC + PS) ...17
Potential Indications...18
Contraindications ...19
Assist-Control (A/C) or Volume Control (V/C) ...19
Pressure Regulated Volume Control (PRVC)...20
Potential Indications...21
Contraindications ...22
Pressure Control Ventilation (PC or PCV) ...22
Volume Support ventilation (VS)...22
Auto-mode ...23
Mandatory Minute Ventilation (MMV), or Augmented Minute Ventilation (AMV), or Extended Mandatory Minute Ventilation (EMMV) ...23
High Frequency Positive Pressure Ventilation (HFPPV or HFV), High Frequency Jet Ventilation (HFJV) and High Frequency Oscillation (HFO) ...23
Inverse Ratio Ventilation (IRV)...24
Airway Pressure Release Ventilation (APRV) ...24
Independent Lung Ventilation (ILV) ...25
Proportional Assist Ventilation (PAV)...25
INITIAL SET-UP GUIDELINES... 26
Mode ...26
Tidal Volume/Minute Volume...26
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ECHANICAL VENTILATION: AN OVERVIEW
FIO2...28 Sensitivity ...28 Flow Rate ...28 PEEP/CPAP ...29 Alarms...29ROUTINE VENTILATOR ADJUSTMENTS ... 30
SUMMARY OF NEW AND COMMON VENTILATOR MODES ... 31
Dual Control Modes Of Mechanical Ventilation...31
Pressure Ventilation: Advantages / Disadvantages...31
Volume Ventilation: Advantages / Disadvantages...31
Modes Summary...32
POINTS TO REMEMBER...38
OVERVIEW OF THE MECHANICAL VENTILATOR SYSTEM AND CLASSIFICATION...39
CRITERIA FOR DETERMINING THE PHASE VARIABLES DURING A VENTILATOR BREATH...40
CLINICAL PRACTICE EXERCISES………...41
PRACTICE EXERCISE DISCUSSION ... 41
CONCLUSION... 42
SUGGESTED READING AND REFERENCES ... 43
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ECHANICAL VENTILATION: AN OVERVIEW
INTRODUCTION
his course is an overview of the traditional modes of positive pressure ventilation. Nontraditional modes are briefly discussed when appropriate. Negative pressure ventilation is not discussed. The modes of: Synchronized Intermittent Mandatory Ventilation (SIMV), Assist-Control (A/C), Pressure Support Ventilation (PSV), and Pressure Control Ventilation (PCV) are discussed. Continuous Positive Airway Pressure (CPAP), Positive End-Expiratory Pressure (PEEP), and Bilevel Positive Airway Pressure (BIPAP) also are reviewed. High frequency ventilation, independent lung ventilation, inverse ratio ventilation, and other new modes are also discussed. Our discussion begins with a review of spontaneous ventilation versus positive pressure ventilation. The effects, indications, and complications of positive pressure follow this. We conclude with the modes, initial set-up, and routine
management guidelines. Unless otherwise stated, the discussion is limited to the adult patient population.
SPONTANEOUS VENTILATION 1
pontaneous ventilation is a result of a negative intrathoracic pressure being created by the inspiratory muscles. When these muscles contract they exert an outward pull on the pleura. This, in turn, lowers the pressure in the pleural space. The lowered pressure is transmitted to the lungs and air is pulled in from the atmosphere.
Spontaneous ventilation also results in a “thoracic pump” to aid venous blood flow. When a negative pressure is created in the thorax from a spontaneous breath, there is less resistance to blood returning to the heart. Less resistance means increased flow. Therefore, spontaneous ventilation increases venous return and right heart filling on inspiration.
T
S
SPONTANEOUS BREATHING Time P R E S S U R E POS 0 NEGSpontaneous inspiration results in a negative intrathoracic pressure
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POSITIVE PRESSURE VENTILATION 2
ositive pressure ventilation (PPV) is the exact opposite of spontaneous ventilation. Spontaneous ventilation creates a subatmospheric pressure at the mouth. This “pulls” air into the lungs. PPV creates a supra-atmospheric pressure at the mouth. This “pushes” air into the lungs. Therefore, PPV has the opposite effect on intrathoracic pressure, creating a positive intrathoracic pressure on inspiration. This impedes venous blood flow on each breath and abolishes the “thoracic pump” mechanism. If significant, peripheral edema becomes apparent, cardiac output and blood pressure drop, and intracranial pressure rises.
A person with normal cardiovascular status is able to compensate for the decrease in venous blood flow caused by properly applied PPV. Very few patients suffer any ill effects. Likewise, a person with normal intracranial regulatory mechanisms is able to compensate for venous
congestion and maintain a normal intracranial pressure. However, patients with cardiac disease or head trauma may not be able to compensate. As for the cardiac patient, a drop in cardiac output may be compensated for with volume replacement therapy.
P
SPONTANEOUS
pleura venous return
Spontaneous inspiration produces a negative intrapleural pressure enhancing venous return.
Positive pressure ventilation produces a positive intrapleural pressure impeding venous return.
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EFFECTS OF POSITIVE PRESSURE VENTILATION 3
PV has numerous effects on the body. The most obvious are those relating to the pulmonary and cardiovascular systems. In addition, PPV affects the central nervous system, renal system, and digestive system. Some of these effects are a direct result of PPV, while others are a result of procedures and activities related to PPV, such as intubation, suctioning, medications, the stress of illness, and sleep deprivation.
Pulmonary Effects - PPV obviously has effects on the pulmonary status of the patient. The vast majority of patients are placed on PPV due to inadequate effects of spontaneous ventilation. PPV can correct this and provide adequate alveolar ventilation. The expected outcomes of PPV include an increase in tidal volume, adequate minute volume, effective alveolar recruitment and ventilation, and a normalization of the patient’s ABG’s. By the time many patients are placed on PPV they have been combating an elevated work of breathing for some time. When the respiratory muscles begin to fatigue to the point of failure, mechanical ventilation is instituted. The ventilator then takes over much of the effort involved in the work of breathing. This is evidenced by a decrease in the work of breathing (WOB), evaluated by decreased accessory muscle use, and a decrease in the respiratory rate (RR).
Initiating PPV does not always immediately decrease the WOB. We like to think that as soon as a patient triggers a mechanical breath, they relax and let the ventilator fill their lungs. This is rarely the case. Most patients who have a spontaneous ventilatory drive continue to inhale during the mechanical breath. Depending on the strength of their ventilatory effort, they can continue to do a considerable amount of work on PPV.
There are many factors contributing to a patients’ WOB while receiving PPV. This includes the selected modes, settings, and ventilator manufacturer(s) utilized. Some modes are designed to provide maximum mechanical support and minimize the patient’s WOB. While other modes vary the amount of support and therefore vary the WOB. The ventilator settings being utilized can increase or decrease a patient’s WOB. The clinical situation dictates which modes and settings are appropriate. In the acute stage of respiratory failure, one wishes to decrease the patients’ WOB. In a muscle rebuilding (weaning) stage, one wishes to gradually increase the WOB. At all cost, one wishes to avoid inadvertently increasing patient WOB through improper settings. For example, inadequate flow results in air hunger; improper expiratory time causes air trapping (auto-PEEP); excessive PEEP causes overdistention. All of these increase patient WOB unnecessarily. The responsiveness of the ventilator to patient inspiration is another factor in WOB. Lastly, the set parameters for the ventilator to deliver, monitor, and regulate ventilation are also factors. Ideally, however, PPV will overall decrease the patient’s WOB.
Circulatory Effects - The effect on circulatory status (decreased venous return) has been mentioned. This results in decreased cardiac output. To prevent this, vascular reflexes are stimulated to increase vascular tone and overcome the increased resistance to venous return. For most patients, this is sufficient to avoid any serious decrease in cardiac output. (In some
patients, the opposite can occur. If the cardiac output has been compromised by hypoxia or acidosis, it can increase when PPV reverses these conditions). Pulmonary hypertension is
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another potential circulatory effect of PPV. If there is pressure transmission from the alveoli to the pulmonary capillaries, intra pulmonary pressures rise. The amount of positive pressure and the patient’s lung compliance are factors in determining the total circulatory effects.Auto-PEEP is another potential complication of PPV that profoundly influences cardiac status. (Auto-PEEP is also referred to as “inadvertent” PEEP). Auto-PEEP is a result of excessive air trapping from inadequate expiratory times, high frequencies, excessive VT’s, and other factors. Auto-PEEP can severely depress the cardiac output and blood pressure, despite a high pulmonary artery wedge or pulmonary artery pressure. These latter pressures remain high due to pressure transmission. However, disconnecting the patient from PPV, can result in a drop in wedge and pulmonary artery pressures and a rise in cardiac output and blood pressure. If patient
disconnection results in improved cardiac status, the lungs are probably overdistended from auto-PEEP.
The same phenomenon occurs during CPR situations. Manual hyperventilation with a
resuscitation bag can and may result in high levels of auto-PEEP. The resulting outcome is no detectable blood pressure with a cardiac rhythm. This is diagnosed, electro-mechanical dissociation, and CPR is terminated. As the auto-PEEP diminishes, the pulse returns. For patients with severe airtrapping, this can take as long as 20 seconds.
Cerebral Effects - Changes in CO2 levels directly influence cerebral blood flow. An increase in
CO2 increases cerebral flow and a decrease in CO2 does the opposite. Remember the
relationship between COPD and head trauma patients when ventilating. COPD patients who have chronic hypercapnia have adjusted to high cerebral blood flow. If PPV results in a low or “normal” PaCO2 (40 mm Hg) cerebral blood flow is compromised in this patient population.
Head trauma patients are often purposely hyperventilated to lower cerebral blood flow and maintain noncritical intracranial pressure. This helps decrease cerebral edema.
Central Nervous System (CNS) Effects - PPV can directly and indirectly affect the central nervous system. Positive pressure directly stimulates numerous pressure and stretch receptors (baroreceptors and proprioceptors) in the lung. These provide feedback to the CNS on lung mechanics. If these receptors are overstimulated from excessive distention, ventilatory drive is decreased. Changes in ABG’s as a result of PPV can obviously alter CNS function. Correction of acidosis and hypoxia increases CNS activity and relieves lethargy. Correction of alkalosis decreases hyperexcitability and decreases CNS activity.
Although not a direct effect of PPV, there is massive sympathetic nervous system discharge from intubation, suctioning, and the ICU environment. Obviously this affects CNS stimulation and activity. In addition, suctioning stimulates vagal nerve endings and irritant receptors in the trachea. All of the above affect CNS function.
Renal System Effects - Renal blood flow and perfusion pressure can be decreased with PPV. This decreases urine output and may lead to significant fluid retention and pulmonary edema. Positive pressure on the right atrium triggers an increase in anti-diuretic hormone (ADH) causing further fluid retention.
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ECHANICAL VENTILATION: AN OVERVIEW
Digestive System Effects - PPV affects the digestive system indirectly. Prolonged PPV often leads to malnutrition. Stress ulcers are possible and oral intake is usually not possible.
Nutritional assessment and monitoring are very important for patients on mechanical ventilation. Supplemental nutritional support must be initiated as soon as possible to meet the daily
requirements of vital nutrients. Proper balance of carbohydrates, protein, fat, liquids, vitamins, minerals, and electrolytes must be maintained. Malnutrition causes weakening of all muscles in the body including the respiratory muscles. Severe malnutrition also causes muscle wasting. As a result of this, malnourished patients are often difficult to maintain and wean from mechanical ventilation, and they experience increased morbidity and mortality. Although supplemental nutrition is necessary and very beneficial to the patient, it does have risks and adverse effects. With TPN, the normal digestive system is completely bypassed. Adverse effects include atrophy of the gastric cavity and infections. The addition of gastric tubes, possible aspiration and
infections are potential complications.
INDICATIONS 3
ndications for mechanical ventilation are divided into 2 broad categories:
• Type I: Acute hypoxemic respiratory failure, also called “oxygenation failure”.
• Type II: Acute hypercapnic respiratory failure, also called “ventilatory failure”, “Mechanical failure”, or “pump failure”.
Oxygenation failure(acute hypoxemic respiratory failure Type I), is characterized by a decreased PaO2 and % oxygen saturation. Oxygenation failure is the result of many disorders. PaCO2 and
pH can be low, normal, or high depending upon the severity of the problem and how well the patient is compensating. The low PaCO2 reflects the physiologic hyperventilation as an attempt
to increase the PaO2.
Initially, oxygenation failure is treated with O2 therapy rather than mechanical ventilation.
Noninvasive CPAP, noninvasive BIPAP, (or ET tube CPAP or BIPAP) may be sufficient to correct oxygenation failure. However, if noninvasive ventilation is unsuccessful or unwise, mechanical ventilation can be initiated in order to decrease the work of breathing sufficiently, and keep FIO2 out of a toxic range. Oxygenation failure has many causes including any
conditions that cause ventilation/perfusion mismatch, shunt, or diffusion problems. Examples are pulmonary emboli, pulmonary edema, airway obstructions, ARDS, pneumonia, alveolar fibrosis and alveolar destruction. These conditions initially affect oxygenation rather than ventilation. When the problem becomes severe and the patient tires themselves, ventilation is affected. The goal of mechanical ventilation for oxygenation failure is to prevent complete respiratory failure. If 60% O2 or greater is necessary for extended periods, CPAP, BiPAP, or
mechanical ventilation should be considered, before advancing FIO2 into toxic levels.
Hypercapnic respiratory failure is characterized by an inability to adequately ventilate. This is associated with an increase in PaCO2 and decrease in the pH, resulting in respiratory acidosis,
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and respiratory failure. Respiratory failure is a result of incurring neuromuscular, fatigue, CNS depression, or musculoskeletal disorders.Respiratory muscle fatigue occurs when there is an increase in the work of breathing for an extended period. Eventually the muscle fatigues to the point of failure. Mechanical ventilation is then necessary. An example is acute exacerbation of COPD. Often, in a COPD patient, pneumonia has lead to increased patient’s WOB. For this type of patient, the added work is too much and respiratory failure is the result.
Examples of neuromuscular disorders leading to respiratory failure are Guillain-Barre syndrome and myasthenia gravis. There is no conduction of the impulse to the muscles to breathe in the former. In the latter, there are inadequate amounts of neurotransmitter chemical to continue the task of stimulating muscles for breathing. Neuromuscular blocking drugs may also disrupt impulse transmission, such as pavulon and aminoglycosides.
CNS disorders requiring ventilation include trauma, drug overdose, sedation and perhaps intracranial pressure disorders. Musculoskeletal defects requiring ventilation include chest trauma and anatomical deformities, such as severe kyphoscoliosis. These decrease compliance and may lead to fatigue or failure. Any condition that increases airway or elastic resistance increases the work of breathing. Patients with borderline pulmonary reserve, such as, COPD and severe kyphoscoliosis, who suffer an acute increase in the work of breathing can easily fatigue, and suffer respiratory failure.
COMPLICATIONS 4
omplications of mechanical ventilation fall into 5 categories: those associated with the intubation and extubation procedure, artificial airways, ventilator operation, medical complications, and psychological effects.
Complications associated with intubation, extubation, and artificial airwaysare far too numerous to list here. They include: oral trauma, broken teeth, intubation of the main stem, tracheal stenosis, dilatation, necrosis, infection, edema, and swallowing dysfunction, among others. Complications associated with ventilator operation include: ventilator or alarm failure, alarms set improperly or turned off, improper humidifier setting, overheating of gas, bacterial
contamination, and ventilator asynchrony with the patient. These are avoided with proper knowledge and maintenance. Obviously, some improper ventilator settings lead to medical complications, such as, alveolar hypoventilation and hyperventilation. Other medical
complications are: infection, barotrauma/volutrauma, fluid retention, decreased cardiac output, and cardiogenic shock. Many of these are avoided with proper adjustment and monitoring of the ventilator parameters, and most importantly, monitoring of the patient. Several complications are discussed in more detail below.
Infection is a common complication of mechanical ventilation. An artificial airway provides a direct avenue for transmission of microorganisms to the patient. Repeated suctioning,
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attachment of tubing, warm air and moist gas also foster the growth and transmission of bacteria. Proper decontamination procedures, use of universal precautions and aseptic technique minimize this complication. Minimizing the times the ventilator circuit is opened decreases the risk of infection. The use ofclosed-systemsuction catheters and heated wire circuits helps achieve this. The less times the circuit is opened, the less possibility of bacteria transmission. Proper oral hygiene performed frequently also reduces the risk of infections.Barotrauma and volutrauma are a result of the peak inspiratory pressure (PIP) or inspiratory volume being too high for a particular patient or lung segment. High pressures and volumes cause overdistention of compliant lung units and lead to stretch injury. Patients with bullous emphysema or those receiving PEEP are at particular risk. Careful attention should be paid to setting pressure limits on each patient. Any sudden upward change in the PIP warrants
immediate evaluation. Always use the lowest PIP pressure possible to minimize stretch injury. There is a greater than 40% possibility of alveolar rupture when PIP is more than 70 cm H2O.
However, much lower pressures can result in alveolar stretch injury. Alveolar stretch injury results in increased lung water, interstitial edema, surfactant dysfunction and infiltrates. In normal lung units, plateau pressures of 30-40 cm H2O indicate overdistention and injury to
alveolar walls may occur. In the past, VT’s of 10-15 cc/kg were recommended. Today it’s felt that these may cause overdistention. VT’s of 8-12 cc/kg or even less may be more appropriate to avoid injury. The patient with nonhomogenous disease is at the greatest risk. Newer modes of ventilation are an attempt to avoid barotrauma/volutrauma. Pressure regulated volume control and volume assured pressurecontrol/support use feedback mechanisms to keep pressure and volume within limits set by the practitioner.
Fluid retention is the result of a decrease in renal perfusion pressure and an increase in circulating antidiuretic hormone (ADH). Cardiogenic shock results from venous stasis and decreased cardiac output. These can be avoided by limiting pressure and volume to prevent overdistention. Fluid replacement therapy can be used to bolster cardiac output if necessary. This fluid must be diuresed as PPV is decreased to prevent pulmonary edema or CHF.
Psychological disturbances are common among ventilator patients. In addition to the stress of being intubated, the ICU environment and sleep deprivation profoundly influence psychological status. Anxiety, fear, panic, and insecurity are common feelings experienced by the patient receiving mechanical ventilation. The inability to talk or communicate increases these feelings. The most common complaints of patients following intubation are pain and discomfort from the ET tube, a sense of choking or gagging, and an inability to breath adequately. (This is one of the reasons why so many patients extubate themselves. It is a simple protective response from the patient).
Psychological dependence on the ventilator is a particularly difficult complication to treat. The patient meets all physiological parameters for weaning, yet repeatedly fails weaning attempts. It is easy to understand how this dependence occurs. Many patients are placed on the ventilator in a state of severe distress and near death. This creates a strong association of the ventilator with
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survival. To break this association requires all the interpersonal skills of the practitioner. The patient must have complete trust in the staff and requires constant reassurance to be weaned.MODES OF VENTILATION2
Continuous Positive Airway Pressure (CPAP)
Classification: Spontaneous breaths are pressure controlled; pressure, flow, or volume triggered; pressure limited; and pressure or flow cycled.
e begin our discussion with continuous positive airway pressure. CPAP is a mode of mechanical “support” rather than mechanical “ventilation”. It is included in this course because all mechanical ventilators today provide a CPAP mode for use. The ventilator is used to create the positive pressure needed for CPAP. However, no mechanical breaths are given. The patient breathes spontaneously and may or may not be intubated.
As mentioned earlier, normal ventilation creates a negative airway pressure on inspiration and mechanical ventilation creates a positive airway pressure on inspiration. CPAP is a mode of mechanical support where the patient is breathing spontaneously, yet the airway pressure remains positive throughout inspiration and expiration. A positive pressure is created at the mouth continuously and when the patient inhales they lower that pressure. However, airway pressure remains above atmospheric at all times.
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CONTINOUS POSITIVE AIRWAY PRESSURE
Time P R E S S U R E POS 0 NEG
The patient breathes spontaneously during CPAP but at an elevated (above atmospheric) baseline pressure.
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The patient is not being ventilated, so CPAP can be done with or without the use of a mechanical ventilator. CPAP is also provided with or without the use of an artificial airway by utilization of a face mask or nasal CPAP system. Adults can use a nasal CPAP mask, or a full face CPAP mask. (In infants, nasal prong CPAP is another possibility). If the patient cannot tolerate or does not respond to a mask CPAP system, BIPAP is an option to try. If both fail, the use of anartificial airway and mechanical ventilation is recommended.
CPAP is useful on patients who are hypoxemic and receiving toxic levels of inspired O2. CPAP
is considered when the PaO2 is 50 or below on greater than 60% FIO2. Such patients often have
a reduced number of alveoli participating in gas exchange. CPAP creates a continuous distending pressure and recruits additional alveoli into the gas exchange process. This increases the
functional residual capacity (FRC) and helps decrease resistance to breathing. The hopeful result is an increase in PaO2 and %saturation. FIO2 can then be lowered to less toxic levels.
CPAP is also a commonly used therapy for patients with obstructive sleep apnea (OSA). For this patient population, the CPAP pressure helps to “splint” the airway open, thus overcoming the upper airway obstruction. This results in improved sleep pattern, improved oxygenation, and decreasing problematic daytime symptoms like hypersomnolence.
Positive End-Expiratory Pressure (PEEP)
The “mode” of positive end-expiratory pressure (PEEP), is the same as CPAP, but is called PEEP when a rate of mechanical ventilation is applied. PEEP is used with many modes
including SIMV, A/C, PCV, or MMV. When PEEP is applied, the airway pressure never returns to atmospheric pressure, the same principle as CPAP. However, the patient also receives
positive pressure breaths, unlike CPAP. (You will recall that in CPAP airway pressure is always above atmospheric but the patient is breathing spontaneously). The moment a mode of
mechanical ventilation (SIMV, A/C, PCV, etc.) is instituted, CPAP becomes PEEP. PEEP is indicated for the same reasons as CPAP, with the added ventilatory support, and has the same effects. Namely, it recruits alveoli into gas exchange, prevents premature collapse, increases alveolar ventilation, and helps overcome resistance to breathing.
PEEP is considered when the current mode of therapy is insufficient to provide adequate
oxygenation on an acceptable FIO2. A PaO2 less than 50 mm Hg on an FIO2 greater than 60% is
a common indication for PEEP. The danger of venous stasis and pneumothorax increase proportionately with the institution of PEEP. Fluid status, blood pressure, cardiac output, and peak inspiratory pressure should be monitored closely. A low level of PEEP (approx. 3-5 cm H2O) is often used on all intubated patients. Intubation and recumbency lower a patient’s normal
FRC. A normal lung can lose 600-1200 cc just going from an upright to supine position. A minimal PEEP level is used to replace this volume loss.
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Pressure-Support Ventilation (PSV)
Classification: Pressure-controlled; patient-triggered; pressure-limited; and patient-cycled ventilation.
The mode of pressure support ventilation provides gas flow up to a preset pressure during the patient’s spontaneous inspiration. The pressure is limited to the preset pressure. PSV is used for several reasons including: to increase the tidal volume on spontaneous breaths, to decrease the work of breathing, and to assist in weaning. The level of pressure support can be increased to increase tidal volume and decrease the effort of breathing. The amount of pressure support can be decreased to facilitate weaning by allowing the patient to assume more of the effort of
breathing. Decreased pressure support generally decreases tidal volume on spontaneous breaths. Other desired effects of adding pressure support to spontaneous breaths are a lowered PaCO2,
and an increased PaO2. PSV can be utilized with non-invasive ventilation such as BIPAP
(discussed later), or with invasive ventilation in most modes except assist/control (A/C). PSV has some theoretical advantages of a more normal ventilatory pattern than conventional modes. It allows the patient to control many of the variables of breathing. This leads to increased patient comfort with PSV versus other modes.
PSV also allows one to titrate the amount of work the patient has to do to breathe. High PSV levels relieve most, if not all, of the work of spontaneous breathing. Low levels are used to merely overcome the added resistance of the artificial airway. The amount of work the patient does can be adjusted anywhere between these levels. This makes PSV especially useful for weaning. Normal initial levels of pressure support are +5 to +10 cm H2O. Up to +20 cm H2O is
also common when additional support is required on spontaneous breaths.
Another major advantage with PSV is that the patient is provided the same type and amount of work each breath. This is helpful when one is reconditioning respiratory muscles after prolonged PPV. Weaning and reconditioning using SIMV expose the patient to an “all or nothing” type of work pattern. The patient does “all” of the work on the spontaneous breaths and “none” of the work on the SIMV breaths. This type of exercise increases strength of a muscle. Lifting weights is an example of strength training and similar to SIMV weaning.
Breathing is more of endurance than a strength activity. One builds endurance by doing the same level of work for extended periods. PSV allows the patient to do the same amount and same type of work on every spontaneous breath. This develops cellular mitochondria in the muscle. Mitochondria are crucial to endurance. Gradually one decreases the PSV level thereby increasing patient work. Aerobics and jogging are examples of endurance training and similar to PSV weaning. Respiratory muscles benefit from endurance training rather than strength training after prolonged disuse.
Automatic Tube Compensation
Mallinckrodt, Inc., has available a new tube compensation (ATC) software option for its Puritan-Bennett 840 ventilator. This mode is also found on the Evita 4 and Drager ventilators. ATC is
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designed to provide improvement in spontaneous breathing while attached to an endotracheal or tracheostomy tube. ATC results in greater comfort for the ventilator patient. With the tube compensation software, a positive pressure is delivered to the patient that is proportional to the inspiratory flow and internal diameter of the endotracheal or tracheostomy tube, thus assisting with the patient's spontaneous breathing. The result is that the patient does not have toexperience the resistive work caused by the artificial airway.
Bilevel Positive Airway Pressure (BIPAP)
BIPAP ventilation is normally used as a non-invasive positive pressure ventilator. However, the newest BIPAP machines, including the BIPAP Vision® come with many of the controls, alarms and monitoring capabilities of traditional invasive mechanical ventilators. The BIPAP Vision® can be used with an intubated or tracheotomized patient, but close monitoring is advised.
BIPAP machines offer two levels of ventilation. The first is CPAP/PEEP, also called expiratory positive airway pressure (EPAP). The second is pressure support, also called inspiratory positive airway pressure (IPAP). The CPAP and PSV are indicated for the same conditions as
mentioned above, and offer the same benefits. The normal initial levels of IPAP and EPAP are the same as for PSV and CPAP/PEEP. For example, a patient on BIPAP can have initial orders for IPAP +10, EPAP +5. Additional oxygen can also be given in line through the BIPAP circuit. Some BIPAP machines have built-in oxygen blenders. With others, adapters are used to bleed in oxygen from another source. BIPAP is typically given with a nasal mask or full-face mask with a tight seal. Nasal prongs or nasal pillows can also be used.
BIPAP is sometimes used for patients who are unable to tolerate CPAP alone. Some patient’s report a sensation of suffocation or choking with CPAP alone, but once the IPAP is added, they report experiencing a greater level of comfort. BIPAP is also used for neuromuscular patients to increase their tidal volume and ease their work of breathing, either at night, or for short periods through the day. At times, BIPAP is tried prior to intubation on a patient who is breathing spontaneously, but has an increasing PaCO2, and a decreasing PaO2. In these cases BIPAP is an attempt to avoid intubation on patients who may only need the assisted ventilation for a short period of time.
Bi-level or BiPhasic Ventilation
Not to be confused with BiPAP, BiLevel ventilation, a Puritan-Bennett innovation is similar to airway pressure release ventilation (APRV), incorporates pressure support working in
synchronicity with pressure control. BiLevel is smart pressure control, or two levels of PEEP are set, allowing the patient to breathe spontaneously, which is not allowed with APRV, while remaining on pressure control. The ability to take spontaneous breaths at a high PEEP level and a low PEEP level is what makes it different that APRV. Bi-level was designed for patients who may have ARDS and be inclined to “fight” the ventilator. Typically they are ready for less sedation or paralysis. They feel more comfortable, and their thoracic pressures drop without compromising oxygenation.
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Synchronized Intermittent Mandatory Ventilation (SIMV)
Classification: Mandatory breaths during SIMV are pressure or volume controlled; machine or patient-triggered; and machine cycled. Spontaneous breaths are pressure controlled; patient-triggered; and patient-cycled.
The mode of synchronized intermittent mandatory ventilation (SIMV) is a combination of spontaneous breathing and mechanical ventilation. SIMV may be considered when CPAP is unsuccessful and the patient has an increased PaCO2 level. Increased PaCO2 means the patient
has ventilation problems. SIMV provides the patient with a set amount of mechanical breaths per minute to reduce PaCO2. However, the patient continues to breathe spontaneously between
the mechanical breaths. The amount of mandatory mechanical breaths the patient receives is based upon how much support they require. High mandatory rates provide maximum support and low rates provide minimal support.
Generally, one begins with a high SIMV rate that is gradually reduced as the patient improves their respiratory effort. As the rate of the assisted breath is decreased, the patient gradually assumes more of the work of breathing with increased, unassisted, spontaneous ventilation. SIMV is the most common method of weaning patients from PPV. When the patient is receiving 4 or less SIMV breaths per minute, they may be ready to be removed from the ventilator if other clinical signs are within normal limits. Parameters to evaluate include spontaneous respiratory rate, tidal volume, minute volume, negative inspiratory force (NIF), vital capacity, arterial blood gases, heart rate, and blood pressure.
Pressure support is often used in conjunction with SIMV to give support during spontaneous breaths. This will decrease the work of breathing, and increase tidal volumes during spontaneous breaths. A low pressure support level of +5 cmH2O can also be used to overcome the resistance
of breathing through the circuit.
SIMV was created for weaning, but is often the initial mode of PPV provided. In this way, “weaning” has already begun. SIMV is also useful for the patient with borderline cardiac status who is not tolerating the positive pressure of full mechanical support. The negative pressure generated by spontaneous breaths in SIMV aid venous return to the heart. This may offset the adverse effects of the positive pressure breaths. Volume replacement therapy to augment the blood pressure is more commonly used in this situation.
SIMV Pressure Control + Pressure Support (SIMV PC + PS)
The SIMV PC + PS mode is a combination mode where the ventilator delivers the set rate of mandatory breaths using the PC mode, and assists with spontaneous breaths with the PS mode. This mode helps to avoid high peak airway pressures while providing a guaranteed minimum number of controlled breaths at a constant pressure level during the entire inspiration. This mode delivers a high initial flow rate with the pressure constant at the “PC above PEEP” level during the entire inspiratory time. A decelerating flow pattern is used for both the mandatory and the spontaneous breaths.
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Pressure control is one alternative to volume control. Regular volume control VC ventilation can cause excessive airway pressures leading to barotrauma, volutrauma, and adverse hemodynamic effects. Pressure control (PC) limits excessive airway pressure. With PC, the high initial flow rate and constant inspiratory pressure improves gas distribution, and decreases work of breathing as compared to VC.A problem associated with PC includes the variable tidal volume as pulmonary mechanics change. The changes in tidal volume can be excessive as compliance improves. The changes in tidal volume can be inconsistent with changes in PIP or PEEP.
The minute volume alarms must be set appropriately. The inspiratory time must be set either as an exact time or as an I: E ratio. The maximum allowable inspiratory time is 80% of the
respiratory cycle. The ventilator will automatically shift to expiration if the inspiratory time exceeds 80% of inspiratory time as determined by the CMV setting. PS breaths terminate when the flow drops to 5% of the peak flow needed to deliver the breath.
The Pressure Control Level above PEEP must be set to the desired inspiratory pressure control level. The ventilator has a SIMV period and a spontaneous period calculated by parameters set by the clinician. If the patient triggers a breath during the spontaneous period, it can be a
pressure support breath or a purely spontaneous breath. If the patient triggers a breath during the SIMV period, it will be a breath according to set parameters. The SIMV cycle is made up of two parts: The SIMV period during which the mandatory or synchronized breath will occur, and the spontaneous period during which the patient can breathe a purely spontaneous breath or a pressure supported breath. The time in seconds for one SIMV cycle is 60 divided by the set SIMV rate. The SIMV period is set by the CMV rate. The time in seconds for the SIMV period is calculated as 60 divided by the CMV rate. If the patient has insufficient spontaneous
breathing, the maximum time between any two SIMV breaths is just over one cycle.
Potential Indications
SIMV PC + PS can be indicated for:
• Patients in who high peak airway pressures must be avoided.
• Patients in whom variations in lung pressures must be avoided.
• Patients who have some breathing capacity, but still need ventilatory support.
• Patients who require a decreased work of breathing.
• Patients needing a high initial flow rate in order to open up closed lung compartments.
• Patients needing set pressure during the entire inspiratory time, and a set inspiratory time.
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• During weaning.
Contraindications
SIMV PC + PS are not appropriate for patients in whom a specific set tidal volume is necessary. The tidal volume variations in this mode can be minor to significant according to changes in the patient’s lung/thorax resistance and compliance.
Assist-Control (A/C) or Volume Control (V/C)
The assist-control mode provides the patient with a mechanical breath of a specific volume, at a set frequency and flow, with every mandatory breath. Inspiration may be initiated by the patient (assist) or by the machine (control). Like SIMV, machine sensitivity is adjusted to the patient’s inspiratory effort. The difference between the two is that each time the patient inhales in the A/C mode; the machine delivers a predetermined volume. In SIMV, a predetermined volume is only delivered on the mandatory breaths.
If the patient has no spontaneous inspiratory effort, the ventilator delivers a minimum number of breaths set by the frequency control. If this occurs, the patient is in the control mode of support, the ventilator delivers tidal volume and respiratory rate is controlled. Rarely does parameter “control” ventilation on a patient. Most that are in a “control” mode are apneicor paralyzed.
ASSIST – CONTROL MODE
Time P R E S S U R E POS 0 NEG
Assisted mechanical breaths are triggered by the patient’s negative inspiratory effort. Controlled mechanical breaths are triggered by a timer.
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There are times when A/C is utilized to decrease the patient’s spontaneous respiratory rate. A/C can be tried if other means of meeting the patient’s ventilatory demands (such as increasing the flow rate or increasing the level of pressure support) are unsuccessful. The concept here is that larger tidal volumes delivered by the ventilator in the A/C mode will meet the patient’s “air hunger” needs, and slow their spontaneous respiratory rate.A patient may be in a control mode when it is crucial the minute volume be closely regulated. An example of this might be a head trauma patient. For head trauma, the physician will control cerebral blood flow via PaCO2 levels. The patient is given sedation or paralyzed to remove
spontaneous inspiratory effort. Then they are mechanically hyperventilated to decrease PaCO2
and cerebral blood flow. This minimizes cerebral edema.
A potential problem with A/C is that volume is closely controlled, but pressure is not. This results in compliant areas being exposed to high pressures and overdistention while
noncompliant areas are underdistended. The mode pressure control ventilation was established to deal with this problem. But pressure control ventilation has its own problems. In PCV the pressure is controlled, but volume fluctuates. To get the best of both modes, newer ventilators have a pressure regulated volume control (PRVC) mode. This allows pressure within the circuit to be regulated while ensuring an appropriate volume.
Pressure Regulated Volume Control (PRVC)
PRVC is a control mode of ventilation. The breaths are delivered at preset tidal volume, minute volume, and preset rate during preset inspiratory time. The ventilator automatically adjusts the inspiratory pressure control level to changes in the mechanical properties of the lung/thorax on a breath by breath basis. The ventilator always uses the lowest possible pressure level to deliver the preset tidal and minute volumes. The I: E ratio is controlled, and the inspiratory flow is decelerating. The patient can initiate breaths depending on the sensitivity setting, so it is important to adjust trigger sensitivity appropriately. The patient triggered breaths are delivered using the same preset parameters as the ventilator initiated breaths. This is a pressure-limited, time cycled mode.
The purpose of the PRVC mode is to deliver set tidal volumes at the minimum pressure level needed. Regular volume control ventilation has been a conventional mode of ventilation for decades. The main problem associated with regular volume control is the excessive airway pressure that can lead to barotrauma, volutrauma, and adverse hemodynamic effect. These problems can be minimized with PRVC.
The ventilator gives a test breath to the patient first, and after a few breaths the target volume will be given. The maximum available pressure level is 5 cm below the preset “Upper Pressure Limit”. It is important to set the “Upper Pressure Limit” as low as possible, while still assuring adequate tidal volumes. In PRVC, like VS, the upper pressure limit has two purposes. First, if the upper pressure limit is reached, the ventilator alarms, then immediately switches to expiration to avoid high airway pressures. Second, if the peak airway pressure reaches a point 5 cm H2O
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still delivered, but the tidal volume will be lower than the preset tidal volume. If the peak airway pressure starts to climb, or is sustained at a higher than expected level, one should evaluate the patient for lung compliance or resistance problems that lead to higher pressures to deliver the same tidal volume than prior to the problem.The ventilator automatically adjusts the inspiratory pressure to changes in the volume/pressure relationship on a breath by breath basis. Whenever the measured volume increases above preset tidal volume, the ventilator automatically adjusts inspiratory pressure support in increments of 1 to 3 cm H2O until the preset volume is attained. Likewise, if the measured volume decreases
below preset tidal volume, the ventilator automatically adjusts inspiratory pressure support in increments of 1 to 3 cm H2O until preset volumes are attained. While the ventilator is
automatically adjusting pressures, one may see a difference between the set and measured tidal volumes. When the ventilator detects measured tidal volumes correspond to preset values, the pressure level remains consistent.
Limitations of PRVC include:
• If the patient demand and effort increases, higher tidal volumes are produced, and pressure support level decreases. At times, this means the patient is getting less support when they may need more support.
• As the pressure support level decreases, mean airway pressure decreases, and hypoxemia can result.
Potential Indications
Patients who may be indicated for the PRVC mode include:
• Patients with no breathing capacity.
• Patients who need to have high airway pressures avoided.
• Patients needing high initial flow rates to open closed lung compartments.
• Patients with lung injury.
• Patients with asthma.
• Patients with chronic obstructive bronchitis.
• Postoperative patients with no respiratory drive.
• Pediatric patients.
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Contraindications
PRVC is not appropriate for patients with intact respiratory drive who are ready to be weaned from mechanical ventilation.
Pressure Control Ventilation (PC or PCV)
Classification: Pressure controlled; machine triggered; pressure limited; and machine cycled.
The mode of pressure control ventilation is an A/C type of mode based on pressure rather than volume. PCV provides a constant pressure on inspiration for a specific length of time upon patient demand. If the patient does not initiate inspiration, the machine provides a breath at the preset pressure for the preset time. Flow is maintained throughout inspiration to maintain the set pressure. Inspiratory flow and volume vary with the pressure used, patient compliance, and inspiratory effort of the patient.
PCV has been the common mode of PPV for infants for many years. In adults, its primary application is for ARDS, but can be utilized for most patients on mechanical ventilation, when peak pressures are a concern. The application of a steady pressure throughout inspiration allows more time for the pressure to equilibrate in all lung segments. Diseased, noncompliant areas are therefore ventilated. Pressure is limited so, hopefully, compliant areas are not overdistended.
Conventional volume-oriented ventilation modes only expose the lung to peak inflating pressures for a brief instant. The peak inflating pressure is only reached at the point where inspiration ends when the VT is delivered. Noncompliant areas may never be exposed to the peak inflating pressure. The bulk of the VT is delivered to compliant areas where it overdistends the alveoli. PCV increases ventilation to noncompliant areas and limits the maximum pressure reached in compliant areas. The result is improved gas exchange and less overdistention. This reduces alveolar distention stretch injury.
The pressure is limited to the preset pressure with PCV. Flow is provided to the patient as long as an inspiratory effort continues. The patient regulates respiratory rate and inspiratory time in this mode. The patient also influences/regulates inspiratory flow. Patient inspiratory effort, compliance, and the level of pressure support being used determine the tidal volume received.
Volume-Support Ventilation (VS)
Most of the newer ventilators have a volume support mode of ventilation. This is a pressure support mode in which the practitioner sets a tidal volume/minute volume. Like pressure support mode, the patient initiates all breaths. PSV by itself has no guarantee of tidal volume or minute volume; pressure is controlled but volume fluctuates. Volume support monitors volumes and adjusts the pressure support level to achieve a minimum volume.
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Auto-mode
Classification: All breaths are mandatory breaths that are time triggered; pressure limited; and time cycled.
The Auto-mode (available on the Siemens SV 300A), is a combination mode that automatically facilitates weaning at the earliest possible opportunity. When Automode is turned “ON”, and the patient triggers two consecutive spontaneous breaths, the ventilator detects the patient trigger efforts, and will automatically switch from a control mode to a support mode. The ventilator will remain in the support mode as long as the patient is spontaneously breathing. If the patient stops breathing spontaneously, the ventilator automatically switches back to a control mode of
ventilation.
The purpose of Automode is to facilitate weaning and increase patient comfort. The patient may display less fighting of the ventilator, since they are automatically switched to a more
comfortable mode of ventilation as soon as they start breathing. Automode may also decrease the length of time a patient remains on ventilation.
The combination modes include the control modes with corresponding support modes as follows:
• PRVC...and...VS
• VC...and...VS
• PC...and...PS
Each mode listed above is discussed in detail separately in this course.
Mandatory Minute Ventilation (MMV), or Augmented Minute Ventilation (AMV), or Extended Mandatory Minute Ventilation (EMMV)
The mode of mandatory minute volume ventilation has also been called extended or augmented mandatory ventilation. This mode is used primarily as a “back-up” mode of ventilation in case the patient’s minute volume is inadequate. In this mode exhaled minute volume is monitored and, if inadequate, mechanical breaths are provided. A minimum exhaled minute volume is set that must be exceeded by the patient. If not, the ventilator makes up the difference.
Conceivably, all ventilation could be spontaneous, mechanical, or any combination of the two. For example, if minimum minute volume is set at 10 lpm and the patient breathes 10 lpm or more, no mechanical breaths are given. If the patient becomes apneic, the entire 10 lpm will be mechanical breaths. Anything between the two extremes is possible.
High Frequency Positive Pressure Ventilation (HFPPV or HFV), High Frequency Jet Ventilation (HFJV) and High Frequency Oscillation (HFO)
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ventilation (HFPPV), high frequency jet ventilation (HFJV) and high frequency oscillation (HFO). HFPPV is conventional positive pressure ventilation at rates of 60-100 breaths per minute (bpm). HFJV delivers small “puffs” of gas through a jet in the ET tube or through the cricothyroid membrane. HFJV delivers approximately 100-350 breaths per minute. HFOoscillates a volume of gas in and out of the trachea at much higher frequencies, such as, 1200 per minute. HFO is the most popular of the three.
Generally, one does not consider “breaths per minute” in high-frequency ventilation. It’s equivalent is measured in “Hertz” (Hz), which is1 cycle/second (cps). One hertz = 60
cycles/min. An infantventilated at 10 hertz means there are 600 oscillations perminute (10 x 60).It is unknown how these high frequencies provide gas exchange. They are, however, capable of providing adequate gas exchange at lower peak airway pressures than conventional modes. For this reason, they are useful where a lowered peak airway pressure is desired. Lower peak pressures decrease the risk of barotrauma and decrease leakage through a bronchopleural fistula. (Mean airway pressures may or may not be lower on HFO versus other modes depending upon the clinical situation). High-frequency ventilation is much more commonly utilized for infants than adults. However HFV is undergoing trials, and gaining popularity as a mode of ventilation for ARDS patients. 2
Inverse Ratio Ventilation (IRV)
The mode of inverse ratio ventilation (IRV) is conventional positive pressure ventilation wherein inspiratory time exceeds expiratory time. Inspiratory to expiratory ratios of 2:1, 3:1, or 4:1 are used to trap air in the lung and increase oxygenation. (IRV works primarily by increasing auto-PEEP). Significant danger of decreased cardiac output, excessive auto-PEEP and barotrauma exist. These are particularly dangerous for the COPD patient. Patients must generally be heavily sedated or paralyzed to use IRV. It is a very abnormal ventilatory pattern and few will tolerate IRV without paralysis. “Extended ratio” ventilation is a term used when inspiratory time is longer than the traditional 1:2 I:E ratio. When extended ratio ventilation exceeds a 1:1 I:E ratio, it becomes IRV.
Airway Pressure Release Ventilation (APRV)
Classification: Mandatory breaths are pressure controlled; time triggered; pressure limited; and timed cycled. Spontaneous breaths are pressure controlled; pressure triggered; pressure limited; and pressure cycled.
APRV is designed to recruit collapsed alveoli while minimizing barotrauma, and optimizing ventilation. APRV is most often utilized to treat ARDS or acute lung injury (ALI), when other common modes of ventilation fail. APRV can be described as CPAP with the addition of regular, brief, intermittent releases in airway pressure. The elevated baseline improves oxygenation. The release phase facilitates CO2 removal and can be time cycled or patient
triggered. Similar to IRV, APRV uses increased inspiratory time to improve oxygenation. In APRV the inspiratory time is typically 4:1 or 5:1. Tidal volumes are delivered during transient
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decreases in intrathoracic pressure. In clinical trials, APRV was better tolerated by patients than IRV, gave lower peak airway pressures, and gave similar improvements in oxygenation. 2APRV is a time triggered, time cycled, pressure limited mode that allows spontaneous breathing throughout the ventilatory cycle. APRV can be used to augment ventilation in the patient with spontaneous breathing or to provide total ventilatory support for the apneic patient. The most common use of APRV is for patients with ARDS or ALI who need to have lower peak airway pressures while maintaining adequate oxygenation and ventilation. The lower airway pressures reduce the risk of barotrauma.
Example initial ventilator settingsfor APRV on an ARDS patient are as follows: 10 Rate...12
I:E Ratio...4:1 or 5:1
FIO2 ...80% - 90% (decrease to less toxic range as soon as clinically feasible)
P High...30 cmH2O
T High...Minimum of 4 seconds. Increase to 12 - 15 seconds as lung mechanics improve. P Low...0 cmH2O
T Low...0.5 to 1.0 seconds (typically 0.8 seconds) (P = Pressure, T = Time)
The goal is to maintain the peak airway pressure below 35 cmH2O, thus to decrease likelihood
of barotraumas. These initial setting will vary and must be changed according to institutional policy, patient response, ABG results, and other important patient monitoring parameters.
Independent Lung Ventilation (ILV)
The mode of independent lung ventilation is used in selected patients with unilateral lung disease and for various surgeries. This is particularly useful in surgery when an individual lung requires special procedures. Pulmonary contusion is probably the most common indication for
independent lung ventilation. Selective airway protection from secretions as a result of cavitary disease is another indication. ILV can also be useful for single lung transplantation, massive hemoptysis, and bronchopleural fistula. Each lung is selectively intubated with a double-lumen endotracheal tube and independently ventilated according to its physiologic characteristics. A normal lung with normal compliance and is ventilated with normal parameters. The lung with a contusion or other medical problem is ventilated according to the lung compliance and other characteristics of that lung. Ventilating each lung separately makes this possible and prevents overdistention of the normal lung.
Proportional Assist Ventilation (PAV)
Classification: Pressure controlled; patient-triggered; pressure limited; and flow cycled.
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The ventilator acts as an accessory muscle of inspiration. Flow and power are adapted on each breath to the patients’ needs. Proportional assist ventilation is not commonly used.INITIAL SET-UP GUIDELINES 2
nitial setup depends on the goal of providing mechanical support/ventilation to the patient. It may be as simple as providing continuous pressure, as in the CPAP mode. It may be to provide the entire minute volume to the patient, as in the Control mode. “Rules” are difficult to establish for ventilator settings, as each patient has different needs. The following serve as guidelines only and are intended for the adult patient population. The practitioner’s clinical experience, the disease state of the patient, and the policies of the institution all influence settings on an individual patient.
Basic ventilator management principles:
A. There are 3 common ways to change PaCO2 (alveolar volume must change to alter
PaCO2):
1. Tidal volume
2. Frequency and minute ventilation
3. Mode
B. There are 2 common ways to change PaO2:
1. FIO2
2. PEEP (when a shunt is present)
Mode - One of the first decisions to be made is the mode of support to be provided. If the patient has an adequate spontaneous minute volume, but requires a toxic level of FIO2 to
maintain adequate PaO2 blood gases levels, CPAP is considered. If it is felt that by providing a
minimum of mechanical support oxygenation will improve, SIMV with PEEP or PSV is
recommended. Likewise, if the patient has a minor CO2 retention problem, SIMV or PSV is the
mode of choice. If the entire minute volume needs to be altered in the patient, the assist/control mode is chosen. Institutional policy or physician order often dictates initial mode selection. In acute respiratory failure, it is wise to provide the patient with maximum mechanical support. Assist/Control mode should be chosen for this. As the patient improves, a change to SIMV should facilitate weaning. To support spontaneous breaths, PSV may be added. Before
extubation, the patient may be placed on a minimal CPAP level. Some patients may require the reverse of this sequence. Initially, CPAP is all that is necessary for adequate gas exchange. As the patient deteriorates, SIMV or PSV may be instituted. Eventually A/C may be required. The clinical status of the patient is the best guide for mode selection and management.
Tidal Volume/Minute Volume – In the past, the Radford nomogram was used to estimate tidal volume and rate on the basis of estimated body weight. In modern practice, acceptable tidal
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volume for mechanical ventilation can range from 5 to 15 mL/kg IBW. In general, for assist-control of SIMV mode, it’s suggested an initial tidal volume of 10 to 12 mL/kg with a rate of 10 to 12 breaths/min for most patients. After initiation of ventilation, the static or plateau pressure can be assessed, and tidal volume adjusted downward as needed, for maintenance of a plateau pressure less than 30 to 35 cm H2O. A larger tidal volume and lower rate (12-15 mL/kg and 6-10breaths/min) may be considered for maintaining lung volume for patients with neuromuscular disease or post-operative patients with normal lungs. A slightly smaller tidal volume (8-10 mL/kg IBW) has been suggested for patients with obstructive lung disease, including COPD and asthma, to allow for a shorter inspiratory time and longer expiratory time to avoid further air trapping. A smaller initial tidal volume (6-8 mL/kg IBW) is appropriate for patients with acute lung injury or ARDS
Some of the older model ventilators, such as the Servo 990c, have no VT control. Setting minute volume and frequency controls sets VT. In this situation, determine the VT and RR you wish the patient to receive and then multiply the two. For example, to give the patient a VT of 700 cc at a RR of 12, multiply 700 X 12 to get a minute volume of 8.4 liters. Setting minute volume at 8.4 liters and the RR at 12 bpm will give VT’s of 700 cc.
Adjustment of VT and minute volume are fairly straightforward. If there is a respiratory acidosis present, alveolar ventilation needs to be increased. Minute volume can be increased via an increase in the VT or RR. Generally, RR is increased. However, an increase in either will achieve the desired result. An exception exists if the increase in PaCO2 is related to a circulatory
defect (decreased perfusion of the alveoli). Changes in minute volume affect PaCO2 very little in
such cases. The reverse of all the above applies when there is a respiratory alkalosis. Minute volume must be decreased to correct respiratory alkalosis. VT or RR will have to be decreased.
Frequency - Normal adult spontaneous respiratory rate is 12-20 per minute. (Respiratory rate is used throughout this text to mean frequency of ventilation, not ml of O2 consumed per minute.)
If the patient has no spontaneous respirations, the range of 12 to 20 should be used. If the patient is “triggering” the machine a safe RR of 10-12 bpm should be used.
When the patient is being set-up in the SIMV mode the decision becomes more difficult. In this mode, the patient is encouraged to breathe in between ventilator breaths. Therefore, RR is usually set below the normal or “safe” rate of 10-12 bpm. A decision should be made as to how much work one wants the patient to do. A high RR, such as, 12-16 bpm, can accomplish
minimal work by the patient. On the other hand, if the bulk of the breathing is to be done by the patient, a low RR (4-6/min) may be appropriate.
To calculate settings for a specific PaCO2:
1. If you want to change the tidal volume:
Present VT x present PaCO2/desired PaCO2 = New VT
2. If you want to change the frequency:
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frequency3. If you want to change VE
Present VE x present PaCO2/desired PaCO2 = New VE
Note: The greatest accuracy occurs when the patient is in the controlled mode
FIO2- Setting of FIO2 depends on the patient’s previous PaO2 and FIO2. If the previous PaO2
was low, FIO2 was inadequate and should be increased. If the previous PaO2 was too high then
FIO2 should be decreased. (One should keep in mind that merely providing mechanical support
and reducing the work of breathing may increase the PaO2 with no change in FIO2). Clinical
experience is probably the most valuable determinant of what FIO2 to begin with. A safe starting
point is 40% for most situations. Further adjustment is based upon ABG, oximetry, and other clinical measurements. (Note: If the FIO2 is 60% or greater, an increase in CPAP or PEEP may
be indicated to minimize oxygen toxicity complications).
Sensitivity - Sensitivity is the control that determines how much negative pressure needs to be generated by the patient to receive a mechanical breath. Adjustments should be made so the creation of a negative one to two cm H2O pressure (below baseline pressure) results in the patient
receiving a breath. If the ventilator does not have sensitivity compensation for elevated baselines (PEEP or CPAP), the manometer needs to be carefully observed. (The overwhelming majority of ventilators in use today have sensitivity compensation). Sensitivity is adjusted so the machine delivers a breath when the patient creates a pressure 1-2 cm H2O below the baseline pressure. Flow Rate - If minute volume is constant, as in the Control mode, minimum flow rate can be calculated by multiplying minute volume by 3. This will provide an i:e ratio of 1:2. If the minute volume is not constant, flow rate is set by observation of the patient and pressure
manometer, along with measuring the i:e ratio. A normal spontaneous i:e ratio is 1:2.4. The i:e ratio of symptomatic asthmatics is 1:2.75 and for COPD patients 1:2.9. For most patients, an i:e ratio of 1:2 or 1:3 is recommended. The more expiratory resistance present, the longer
expiratory time must be.
Another flow rate calculation is:
Peak Flow (PF) = Exhaled Minute Volume (VE x (I + E)
As a starting point, initial flow rate may be set by the above calculation of minute volume X 3. Once the patient is connected, the manometer should be carefully observed for a smooth even rise to peak pressure. It should be neither too fast nor too slow or “hang up” at any point. Rise times that are too fast means the peak flow should be decreased, and too slow means it should be increased. Hanging up at any point means that patient inspiratory flow rate is exceeding
ventilator flow rate. If so, patients experience “air hunger”. Therefore, flow needs to be increased. Flow rate should always be set high enough to exceed, patient need, patient peak inspiratory flow rate to minimize patient work. In most instances, an i:e ratio of 1:2 is desired and flow should be adjusted to achieve this. A longer expiratory time is recommended for
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patients with obstructive airway disease.Observe the patient for signs they are comfortable and synchronized with the ventilator breaths. All breaths should be passive and smooth. This will take some clinical experience to master. Listening to the breath cycle of the ventilator can often be an indicator. To minimize turbulence and obtain an even distribution of the inspired gas with laminate flow, the lowest flow rate needed should be used. Keep in mind that the lowest flow rate for some patients may be very high and very low for others. Patients in distress and status asthmaticus initially require very high flow rates.
Flow rate is often ignored after the initial setting. One must continue to adjust flow based upon the patient’s condition. When minute volume demands are high, as in periods of acute distress, flow rate must be increased. As the distress subsides, flow rate is decreased accordingly. Most modern ventilators monitor and adjust flow automatically to a certain degree. This does not mean flow setting should be taken for granted. Observation of the patient is the only effective method of determining flow setting. Mechanical ventilators vary tremendously in how they provide and regulate flow to the patient, particularly between different modes. For example, in the PSV mode one ventilator terminates inspiration when flow in the circuit decreases to 25% of the original flow rate. Another ventilator will terminate inspiration when it reaches 1 lpm. On some ventilators, selecting a different flow pattern also changes the flow rate. The practitioner must know the characteristics of their particular ventilator.
PEEP/CPAP - One should select the lowest PEEP/CPAP level that achieves adequate oxygenation to minimize any effects on cardiac output. A generic safe starting point is 5 cm H2O. If this is not sufficient, 6 to 10 cm H2O may be tried. It this is not sufficient, it may be
wise to reconsider PEEP or perform an optimal PEEP determination. If PEEP/CPAP is felt to be indicated, there are several sophisticated methods of determining the proper level. These consist of determining optimal PEEP via static compliance, mixed venous PO2, cardiac output, or shunt
calculations. It is important to continue to monitor the optimal level so it may be adjusted
accordingly. Optimal PEEP is considered the level that provides the greatest tissue oxygenation. This is achieved by maximizing arterial oxygenation and oxygen transport by the cardiovascular system.
“Physiologic” PEEP is considered to be
