Hospital Medicine

Supplement Editor:
Amir K. Jaffer, MD, FHM

Associate Editors:
David L. Hepner, MD, and Franklin A. Michota, MD, FHM

Contents

Public reporting and pay-for-performance programs in perioperative medicine
Peter Lindenauer, MD MSc

Cardiac risk stratification for noncardiac surgery: Update from the American College of Cardiology/American Heart Association 2007 guidelines
Lee A. Fleisher, MD

Perioperative care of the elderly patient: An update
Robert M. Palmer, MD, MPH

The role of testing in the preoperative evaluation
David L. Hepner, MD

Perioperative fluid management: Progress despite lingering controversies
Mark A. Hamilton, MBBS, MRCP, FRCA

Giving anesthesiologists what they want: How to write a useful preoperative consult
David Lubarsky, MD, MBA, and Keith Candiotti, MD

Perioperative management of warfarin and antiplatelet therapy
Amir K. Jaffer, MD, FHM

Prevention of venous thromboembolism after surgery
Franklin A. Michota, MD, FHM

Perioperative management of diabetes: Translating evidence into practice
Luigi F. Meneghini, MD, MBA

Postoperative pulmonary complications: An update on risk assessment and reduction
Gerald W. Smetana, MD

Postoperative gastrointestinal tract dysfunction: An overview of causes and management strategies
Michael G. (Monty) Mythen, MD

Case studies in perioperative management: Challenges, controversies, and common ground
Steven L. Cohn, MD, and BobbieJean Sweitzer, MD

Statins and noncardiac surgery: Current evidence and practical considerations
Don Poldermans, MD, PhD

The experts debate: perioperative beta-blockade for noncardiac surgery patients—proven safe or not?
Don Poldermans, MD, PhD, and P.J. Devereaux, MD, PhD

Perioperative considerations for patients with liver disease
Paul Martin, MD

Perioperative management of obstructive sleep apnea: Ready for prime time?
Shirin Shafazand, MD, MS

Nuts and bolts of preoperative clinics: The view from three institutions
Angela M. Bader, MD, MPH; BobbieJean Sweitzer, MD; and Ajay Kumar, MD

Perioperative management of anemia: Limits of blood transfusion and alternatives to it
Ajay Kumar, MD

Medicolegal issues in perioperative medicine: Lessons from real cases
Franklin A. Michota, MD, FHM, and Matthew J. Donnelly, Esq

Perioperative medication management: General principles and practical applications
Christopher Whinney, MD

Supplement Editor:
Amir K. Jaffer, MD, FHM

Associate Editors:
David L. Hepner, MD, and Franklin A. Michota, MD, FHM

Contents

Public reporting and pay-for-performance programs in perioperative medicine
Peter Lindenauer, MD MSc

Cardiac risk stratification for noncardiac surgery: Update from the American College of Cardiology/American Heart Association 2007 guidelines
Lee A. Fleisher, MD

Perioperative care of the elderly patient: An update
Robert M. Palmer, MD, MPH

The role of testing in the preoperative evaluation
David L. Hepner, MD

Perioperative fluid management: Progress despite lingering controversies
Mark A. Hamilton, MBBS, MRCP, FRCA

Giving anesthesiologists what they want: How to write a useful preoperative consult
David Lubarsky, MD, MBA, and Keith Candiotti, MD

Perioperative management of warfarin and antiplatelet therapy
Amir K. Jaffer, MD, FHM

Prevention of venous thromboembolism after surgery
Franklin A. Michota, MD, FHM

Perioperative management of diabetes: Translating evidence into practice
Luigi F. Meneghini, MD, MBA

Postoperative pulmonary complications: An update on risk assessment and reduction
Gerald W. Smetana, MD

Postoperative gastrointestinal tract dysfunction: An overview of causes and management strategies
Michael G. (Monty) Mythen, MD

Case studies in perioperative management: Challenges, controversies, and common ground
Steven L. Cohn, MD, and BobbieJean Sweitzer, MD

Statins and noncardiac surgery: Current evidence and practical considerations
Don Poldermans, MD, PhD

The experts debate: perioperative beta-blockade for noncardiac surgery patients—proven safe or not?
Don Poldermans, MD, PhD, and P.J. Devereaux, MD, PhD

Perioperative considerations for patients with liver disease
Paul Martin, MD

Perioperative management of obstructive sleep apnea: Ready for prime time?
Shirin Shafazand, MD, MS

Nuts and bolts of preoperative clinics: The view from three institutions
Angela M. Bader, MD, MPH; BobbieJean Sweitzer, MD; and Ajay Kumar, MD

Perioperative management of anemia: Limits of blood transfusion and alternatives to it
Ajay Kumar, MD

Medicolegal issues in perioperative medicine: Lessons from real cases
Franklin A. Michota, MD, FHM, and Matthew J. Donnelly, Esq

Perioperative medication management: General principles and practical applications
Christopher Whinney, MD

Supplement Editor:
Amir K. Jaffer, MD, FHM

Associate Editors:
David L. Hepner, MD, and Franklin A. Michota, MD, FHM

Contents

Public reporting and pay-for-performance programs in perioperative medicine
Peter Lindenauer, MD MSc

Cardiac risk stratification for noncardiac surgery: Update from the American College of Cardiology/American Heart Association 2007 guidelines
Lee A. Fleisher, MD

Perioperative care of the elderly patient: An update
Robert M. Palmer, MD, MPH

The role of testing in the preoperative evaluation
David L. Hepner, MD

Perioperative fluid management: Progress despite lingering controversies
Mark A. Hamilton, MBBS, MRCP, FRCA

Giving anesthesiologists what they want: How to write a useful preoperative consult
David Lubarsky, MD, MBA, and Keith Candiotti, MD

Perioperative management of warfarin and antiplatelet therapy
Amir K. Jaffer, MD, FHM

Prevention of venous thromboembolism after surgery
Franklin A. Michota, MD, FHM

Perioperative management of diabetes: Translating evidence into practice
Luigi F. Meneghini, MD, MBA

Postoperative pulmonary complications: An update on risk assessment and reduction
Gerald W. Smetana, MD

Postoperative gastrointestinal tract dysfunction: An overview of causes and management strategies
Michael G. (Monty) Mythen, MD

Case studies in perioperative management: Challenges, controversies, and common ground
Steven L. Cohn, MD, and BobbieJean Sweitzer, MD

Statins and noncardiac surgery: Current evidence and practical considerations
Don Poldermans, MD, PhD

The experts debate: perioperative beta-blockade for noncardiac surgery patients—proven safe or not?
Don Poldermans, MD, PhD, and P.J. Devereaux, MD, PhD

Perioperative considerations for patients with liver disease
Paul Martin, MD

Perioperative management of obstructive sleep apnea: Ready for prime time?
Shirin Shafazand, MD, MS

Nuts and bolts of preoperative clinics: The view from three institutions
Angela M. Bader, MD, MPH; BobbieJean Sweitzer, MD; and Ajay Kumar, MD

Perioperative management of anemia: Limits of blood transfusion and alternatives to it
Ajay Kumar, MD

Medicolegal issues in perioperative medicine: Lessons from real cases
Franklin A. Michota, MD, FHM, and Matthew J. Donnelly, Esq

Perioperative medication management: General principles and practical applications
Christopher Whinney, MD

Technologic advances and computerized control of mechanical ventilators have made it possible to deliver ventilatory assistance in new modes. Driving these innovations is the desire to prevent ventilator-induced lung injury, improve patient comfort, and liberate the patient from mechanical ventilation as soon as possible.

We call these innovations “alternative” modes to differentiate them from the plain volume-control and pressure-control modes. Some clinicians rarely use these new modes, but in some medical centers they have become the most common ones used, or are being used unknowingly (the operator misunderstands the mode name). The information we provide on these modes of ventilation is by no means an endorsement of their use, but rather a tool to help the clinician understand their physiologic, theoretical, and clinical effects.

We focused on two goals:

• Explain what the mode does
• Briefly review the theoretical benefits and the actual evidence supporting these alternative modes of ventilation.

STANDARD NOMENCLATURE NEEDED

Since its invention, mechanical ventilation has been plagued by multiple names being used to describe the same things. For example, volume-control ventilation is also called volume-cycled ventilation, assist-control ventilation, volume-limited ventilation, and controlled mechanical ventilation. Similarly, multiple abbreviations are used, each depending on the brand of ventilator, and new acronyms have been added in recent years as new modes have been developed. The vast number of names and modes can confuse even the most seasoned critical care physician.

Efforts to establish a common nomenclature are under way.¹

WHAT IS A MODE?

A mode of mechanical ventilation has three essential components:

• The control variable
• The breath sequence
• The targeting scheme.

Similar modes may require more detailed descriptions to distinguish them, but the basic function can be explained by these three components.

The control variable

In general, inspiration is an active process, driven by the patient’s effort, the ventilator, or both, while expiration is passive. For simplicity, in this article a mechanical breath means the inspiratory phase of the breath.

The machine can only control the volume (and flow) or the pressure given. The breaths can be further described on the basis of what triggers the breath, what limits it (the maximum value of a control variable), and what ends (cycles) it.

Therefore, a volume-controlled breath is triggered by the patient or by the machine, limited by flow, and cycled by volume (Figure 1). A pressure-controlled breath is triggered by the patient or the machine, limited by pressure, and cycled by time or flow (Figure 1).

The breath sequence

There are three possible breath sequences:

• 
  Continuous mandatory ventilation, in which all breaths are controlled by the machine (but can be triggered by the patient)
• Intermittent mandatory ventilation, in which the patient can take spontaneous breaths between mandatory breaths
• Continuous spontaneous ventilation, in which all breaths are spontaneous (Table 1).

The targeting scheme

The targeting or feedback scheme refers to the ventilator settings and programming that dictate its response to the patient’s lung compliance, lung resistance, and respiratory effort. The regulation can be as simple as controlling the pressure in pressure-control mode, or it can be based on a complicated algorithm.

In the sections that follow, we describe some of the available alternative modes of mechanical ventilation. We will explain only the targeting schemes in the modes reviewed (Table 1, Table 2), but more information on other targeting schemes can be found elsewhere.^1,2 We will focus on evidence generated in adult patients receiving invasive mechanical ventilation.

 

ADAPTIVE PRESSURE CONTROL

One of the concerns with pressure-control ventilation is that it cannot guarantee a minimum minute ventilation (the volume of air that goes in and out in 1 minute; the tidal volume × breaths per minute) in the face of changing lung mechanics or patient effort, or both. To solve this problem, in 1991 the Siemens Servo 300 ventilator (Siemens, Maquet Critical Care AB, Solna, Sweden) introduced Pressure Regulated Volume Control, a mode that delivers pressure-controlled breaths with a target tidal volume and that is otherwise known as adaptive pressure control (APC) (Figure 2).

Other names for adaptive pressure control

• Pressure Regulated Volume Control (Maquet Servo-i, Rastatt, Germany)
• AutoFlow (Dräger Medical AG, Lübeck, Germany)
• Adaptive Pressure Ventilation (Hamilton Galileo, Hamilton Medical AG, Bonaduz, Switzerland)
• Volume Control+ (Puritan Bennett, Tyco Healthcare; Mansfield, MA)
• Volume Targeted Pressure Control, Pressure Controlled Volume Guaranteed (Engström, General Electric, Madison, WI).

What does adaptive pressure control do?

The APC mode delivers pressure-controlled breaths with an adaptive targeting scheme (Table 2).

In pressure-control ventilation, tidal volumes depend on the lung’s physiologic mechanics (compliance and resistance) and patient effort (Figure 1). Therefore, the tidal volume varies with changes in lung physiology (ie, larger or smaller tidal volumes than targeted).

To overcome this effect, a machine in APC mode adjusts the inspiratory pressure to deliver the set minimal target tidal volume. If tidal volume increases, the machine decreases the inspiratory pressure, and if tidal volume decreases, the machine increases the inspiratory pressure. However, if the patient effort is large enough, the tidal volume will increase in spite of decreasing the inspiratory pressure (Figure 2). The adjustments to the inspiratory pressure occur after the tidal volume is off-target in a number of breaths.

Common sources of confusion with adaptive pressure control

First, APC is not a volume-control mode. In volume control, the tidal volume does not change; in APC the tidal volume can increase or decrease, and the ventilator will adjust the inflation pressure to achieve the target volume. Thus, APC guarantees an average minimum tidal volume but not a maximum tidal volume.

Second, a characteristic of pressure control (and hence, APC) is that the flow of gas varies to maintain constant airway pressure (ie, maintain the set inspiratory pressure). This characteristic allows a patient who generates an inspiratory effort to receive flow as demanded, which is likely more comfortable. This is essentially different from volume control, in which flow is set by the operator and hence is fixed. Thus, if the patient effort is strong enough (Figure 1), this leads to what is called flow asynchrony, in which the patient does not get the flow asked for in a breath.

Ventilator settings in adaptive pressure control

Ventilator settings in APC are:

• Tidal volume
• Time spent in inspiration (inspiratory time)
• Frequency
• Fraction of inspired oxygen (Fio₂)
• Positive end-expiratory pressure (PEEP).

Some ventilators also require setting the speed to reach the peak pressure (also known as slope percent or inspiratory rise time).

Clinical applications of adaptive pressure control

This mode is designed to maintain a consistent tidal volume during pressure-control ventilation and to promote inspiratory flow synchrony. It is a means of automatically reducing ventilatory support (ie, weaning) as the patient’s inspiratory effort becomes stronger, as in awakening from anesthesia.

APC may not be ideal for patients who have an inappropriately increased respiratory drive (eg, in severe metabolic acidosis), since the inspiratory pressure will decrease to maintain the targeted average tidal volume, inappropriately shifting the work of breathing onto the patient.

Theoretical benefits of adaptive pressure control

APC guarantees a minimum average tidal volume (unless the pressure alarm threshold is set too low, so that the target tidal volume is not delivered). Other theoretical benefits are flow synchrony, less ventilator manipulation by the operator, and automatic weaning of ventilator support.

Evidence of benefit of adaptive pressure control

Physiologic benefits. This mode has lower peak inspiratory pressures than does volume-control ventilation,^3,4 which is often reported as a positive finding. However, in volume-control mode (the usual comparator), the peak inspiratory pressure is a manifestation of both resistance and compliance. Hence, peak inspiratory pressure is expected to be higher but does not reflect actual lung-distending pressures. It is the plateau pressure, a manifestation of lung compliance, that is related to lung injury.

Patient comfort. APC may increase the work of breathing when using low tidal volume ventilation and when there is increased respiratory effort (drive).⁵ Interestingly, APC was less comfortable than pressure support ventilation in a small trial.⁶

Outcomes have not been studied.⁷

Adaptive pressure control: Bottom line

APC is widely available and widely used, sometimes unknowingly (eg, if the operator thinks it is volume control). It is relatively easy to use and to set; however, evidence of its benefit is scant.

 

ADAPTIVE SUPPORT VENTILATION

Adaptive support ventilation (ASV) evolved as a form of mandatory minute ventilation implemented with adaptive pressure control. Mandatory minute ventilation is a mode that allows the operator to preset a target minute ventilation, and the ventilator then supplies mandatory breaths, either volume- or pressure-controlled, if the patient’s spontaneous breaths generate a lower minute ventilation.

ASV automatically selects the appropriate tidal volume and frequency for mandatory breaths and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and target minute alveolar ventilation.

Described in 1994 by Laubscher et al,^8,9 ASV became commercially available in 1998 in Europe and in 2007 in the United States (Hamilton Galileo ventilator, Hamilton Medical AG). This is the first commercially available ventilator that uses an “optimal” targeting scheme (see below).

What does adaptive support ventilation do?

ASV delivers pressure-controlled breaths using an adaptive (optimal) scheme (Table 2). “Optimal,” in this context, means minimizing the mechanical work of breathing: the machine selects a tidal volume and frequency that the patient’s brain would presumably select if the patient were not connected to a ventilator. This pattern is assumed to encourage the patient to generate spontaneous breaths.

The ventilator calculates the normal required minute ventilation based on the patient’s ideal weight and estimated dead space volume (ie, 2.2 mL/kg). This calculation represents 100% of minute ventilation. The clinician at the bedside sets a target percent of minute ventilation that the ventilator will support—higher than 100% if the patient has increased requirements due, eg, to sepsis or increased dead space, or less than 100% during weaning.

The ventilator initially delivers test breaths, in which it measures the expiratory time constant for the respiratory system and then uses this along with the estimated dead space and normal minute ventilation to calculate an optimal breathing frequency in terms of mechanical work.

The optimal or target tidal volume is calculated as the normal minute ventilation divided by the optimal frequency. The target tidal volume is achieved by the use of APC (see above) (Figure 2). This means that the pressure limit is automatically adjusted to achieve an average delivered tidal volume equal to the target. The ventilator continuously monitors the respiratory system mechanics and adjusts its settings accordingly.

The ventilator adjusts its breaths to avoid air trapping by allowing enough time to exhale, to avoid hypoventilation by delivering tidal volume greater than the dead space, and to avoid volutrauma by avoiding large tidal volumes.

Ventilator settings in adaptive support ventilation

Ventilator settings in ASV are:

• Patient height (to calculate the ideal body weight)
• Sex
• Percent of normal predicted minute ventilation goal
• Fio₂
• PEEP.

Clinical applications of adaptive support ventilation

ASV is intended as a sole mode of ventilation, from initial support to weaning.

Theoretical benefits of adaptive support ventilation

In theory, ASV offers automatic selection of ventilator settings, automatic adaptation to changing patient lung mechanics, less need for human manipulation of the machine, improved synchrony, and automatic weaning.

Evidence of benefit of adaptive support ventilation

Physiologic benefits. Ventilator settings are adjusted automatically. ASV selects different tidal volume-respiratory rate combinations based on respiratory mechanics in passive and paralyzed patients.^10–12 In actively breathing patients, there was no difference in the ventilator settings chosen by ASV for different clinical scenarios (and lung physiology).¹⁰ Compared with pressure-controlled intermittent mandatory ventilation, with ASV, the inspiratory load is less and patient-ventilator interaction is better.¹³

Patient-ventilator synchrony and comfort have not been studied.

Outcomes. Two trials suggest that ASV may decrease time on mechanical ventilation.^14,15 However, in another trial,¹⁶ compared with a standard protocol, ASV led to fewer ventilator adjustments but achieved similar postsurgical weaning outcomes. The effect of this mode on the death rate has not been examined.^17,18

Adaptive support ventilation: Bottom line

ASV is the first commercially available mode that automatically selects all the ventilator settings except PEEP and Fio₂. These seem appropriate for different clinical scenarios in patients with poor respiratory effort or in paralyzed patients. Evidence of the effect in actively breathing patients and on outcomes such as length of stay or death is still lacking.

PROPORTIONAL ASSIST VENTILATION

Patients who have normal respiratory drive but who have difficulty sustaining adequate spontaneous ventilation are often subjected to pressure support ventilation (PSV), in which the ventilator generates a constant pressure throughout inspiration regardless of the intensity of the patient’s effort.

In 1992, Younes and colleagues^19,20 developed proportional assist ventilation (PAV) as an alternative in which the ventilator generates pressure in proportion to the patient’s effort. PAV became commercially available in Europe in 1999 and was approved in the United States in 2006, available on the Puritan Bennett 840 ventilator (Puritan Bennett Co, Boulder, CO). PAV has also been used for noninvasive ventilation, but this is not available in the United States.

Other names for proportional assist ventilation

Proportional Pressure Support (Dräger Medical; not yet available in the United States).

 

 

What does proportional assist ventilation do?

This mode delivers pressure-controlled breaths with a servo control scheme (Table 2).

To better understand PAV, we can compare it with PSV. With PSV, the pressure applied by the ventilator rises to a preset level that is held constant (a set-point scheme) until a cycling criterion (a percent of the maximum inspiratory flow value) is reached. The inspiratory flow and tidal volume are the result of the patient’s inspiratory effort, the level of pressure applied, and the respiratory system mechanics.

In contrast, during PAV, the pressure applied is a function of patient effort: the greater the inspiratory effort, the greater the increase in applied pressure (servo targeting scheme) (Figure 3). The operator sets the percentage of support to be delivered by the ventilator. The ventilator intermittently measures the compliance and resistance of the patient’s respiratory system and the instantaneous patient-generated flow and volume, and on the basis of these it delivers a proportional amount of inspiratory pressure.

In PAV, as in PSV, all breaths are spontaneous (Table 1). The patient controls the timing and size of the breath. There are no preset pressure, flow, or volume goals, but safety limits on the volume and pressure delivered can be set.

Ventilator settings in proportional assist ventilation

Ventilator settings in PAV are:

• Airway type (endotracheal tube, tracheostomy)
• Airway size (inner diameter)
• Percentage of work supported (assist range 5%–95%)
• Tidal volume limit
• Pressure limit
• Expiratory sensitivity (normally, as inspiration ends, flow should stop; this parameter tells the ventilator at what flow to end inspiration).

Caution when assessing the literature. Earlier ventilator versions, ie, Dräger and Manitoba (University of Manitoba, Winnipeg, MB, Canada), which are not available in the United States, required the repeated calculation of the respiratory system mechanics and the manual setting of flow and volume assists (amplification factors) independently. To overcome this limitation, new software automatically adjusts the flow and volume amplification to support the loads imposed by the automatically measured values of resistance and elastance (inverse of compliance) of the respiratory system.²¹ This software is included in the model (Puritan Bennett) available in the United States.

Clinical applications of proportional assist ventilation

The PAV mode is indicated for maximizing ventilator patient synchrony for assisted spontaneous ventilation.

PAV is contraindicated in patients with respiratory depression (bradypnea) or large air leaks (eg, bronchopleural fistulas). It should be used with caution in patients with severe hyperinflation, in which the patient may still be exhaling but the ventilator doesn’t recognize it. Another group in which PAV should be used with caution is those with high ventilatory drives, in which the ventilator overestimates respiratory system mechanics. This situation can lead to overassistance due to the “runaway phenomenon,” in which the ventilator continues to provide support even if the patient has stopped inspiration.²²

Theoretical benefits of proportional assist ventilation

In theory, PAV should reduce the work of breathing, improve synchrony, automatically adapt to changing patient lung mechanics and effort, decrease the need for ventilator intervention and manipulation, decrease the need for sedation, and improve sleep.

Evidence of benefit of proportional assist ventilation

Physiologic benefits. PAV reduces the work of breathing better than PSV,²¹ even in the face of changing respiratory mechanics or increased respiratory demand (hypercapnia).^23–25 The hemodynamic profile is similar to that in PSV. Tidal volumes are variable; however, in recent reports the tidal volumes were within the lung-protective range (6–8 mL/kg, plateau pressure < 30 cm H₂0).^26,27

Comfort. PAV entails less patient effort and discomfort that PSV does.^23,25 PAV significantly reduces asynchrony,²⁷ which in turn may favorably affect sleep in critically ill patients. ²⁸

Outcomes. The probability of spontaneous breathing without assistance was significantly better in critically ill patients ventilated with PAV than with PSV. No trial has reported the effect of PAV on deaths.^27,29

Proportional assist ventilation: Bottom line

Extensive basic research has been done with PAV in different forms of respiratory failure, such as obstructive lung disease, acute respiratory distress syndrome (ARDS), and chronic respiratory failure. It fulfills its main goal, which is to improve patient-ventilator synchrony. Clinical experience with PAV in the United States is limited, as it was only recently approved.

 

AIRWAY PRESSURE-RELEASE VENTILATION AND BIPHASIC POSITIVE AIRWAY PRESSURE

Airway pressure-release ventilation (APRV) was described in 1987 by Stock et al³⁰ as a mode for delivering ventilation in acute lung injury while avoiding high airway pressures. APRV combines high constant positive airway pressure (improving oxygenation and promoting alveolar recruitment) with intermittent releases (causing exhalation).

In 1989, Baum et al³¹ described biphasic positive airway pressure ventilation as a mode in which spontaneous ventilation could be achieved at any point in the mechanical ventilation cycle—inspiration or exhalation (Figure 4). The goal was to allow unrestricted spontaneous breathing to reduce sedation and promote weaning. These modes are conceptually the same, the main difference being that the time spent in low pressure (T_low; see below) is less than 1.5 seconds for APRV. Otherwise, they have identical characteristics, thus allowing any ventilator with the capability of delivering APRV to deliver biphasic positive airway pressure, and vice versa. Machines with these modes became commercially available in the mid 1990s.

Other names for biphasic positive airway pressure

Other names for biphasic positive airway pressure are:

• BiLevel (Puritan Bennett)
• BIPAP (Dräger Europe)
• Bi Vent (Siemens)
• BiPhasic (Avea, Cardinal Health, Inc, Dublin, OH)
• PCV+ (Dräger Medical)
• DuoPAP (Hamilton).

Caution—name confusion. In North America, BiPAP (Respironics, Murrysville, PA) and BiLevel are used to refer to noninvasive modes of ventilation.

APRV has no other name.

What do these modes do?

These modes deliver pressure-controlled, time-triggered, and time-cycled breaths using a set-point targeting scheme (Table 2). This means that the ventilator maintains a constant pressure (set point) even in the face of spontaneous breaths.

Caution—source of confusion. The term continuous positive airway pressure (CPAP) is often used to describe this mode. However, CPAP is pressure that is applied continuously at the same level; the patient generates all the work to maintain ventilation (“pressure-controlled continuous spontaneous ventilation” in the current nomenclature). In APRV, the airway pressure is intermittently released and reapplied, generating a tidal volume that supports ventilation. In other words, this is a pressure-controlled breath with a very prolonged inspiratory time and a short expiratory time in which spontaneous ventilation is possible at any point (“pressure-controlled intermittent mandatory ventilation” in the current nomenclature).

How these modes are set in the ventilator may also be a source of confusion. To describe the time spent in high and low airway pressures, we use the terms T_high and T_low, respectively. By convention, the difference between APRV and biphasic mode is the duration of T_low (< 1.5 sec for APRV).

Similarly, P_high and P_low are used to describe the high and low airway pressure. To better understand this concept, you can create the same mode in conventional pressure-control ventilation by thinking of the T_high as the inspiratory time, the T_low as the expiratory time, the P_high as inspiratory pressure, and the P_low as PEEP.

Hence, APRV is an extreme form of inverse ratio ventilation, with an inspiration-to-expiration ratio of 4:1. This means a patient spends most of the time in P_high and T_high, and exhalations are short (T_low and P_low). In contrast, the biphasic mode uses conventional inspiration-expiration ratios (Figure 4).

As with any form of pressure control, the tidal volume is generated by airway pressure rising above baseline (ie, the end-expiratory value). Hence, to ensure an increase in minute ventilation, the mandatory breath rate must be increased (ie, decreasing T_high, T_low, or both) or the tidal volume must be increased (ie, increasing the difference between P_high and P_low). This means that in APRV the T_low has to happen more often (by increasing the number of breaths) or be more prolonged (allowing more air to exhale). Because unrestricted spontaneous breaths are permitted at any point of the cycle, the patient contributes to the total minute ventilation (usually 10%–40%).

In APRV and biphasic mode, the operator’s set time and pressure in inspiration and expiration will be delivered regardless of the patient’s breathing efforts—the patient’s spontaneous breath does not trigger a mechanical breath. Some ventilators have automatic adjustments to improve the trigger synchrony.

Ventilator settings in APRV and biphasic mode

These modes require the setting of two pressure levels (P_high and P_low) and two time durations (T_high and T_low). One can add pressure support or automatic tube compensation to assist spontaneous breaths. The difference in T_low generates differences in the T_high:T_low ratio: APRV has a short T_low (an inspiration-expiration ratio of 4:1). Biphasic mode has a conventional inspiration-expiration ratio of 1:1 to 1:4.

Clinical applications

APRV is used in acute lung injury and ARDS. This mode should be used with caution or not at all in patients with obstructive lung disease or inappropriately increased respiratory drive.^32–35

Biphasic mode is intended for both ventilation and weaning. In a patient who has poor respiratory effort or who is paralyzed, biphasic is identical to pressure-control/continuous mandatory ventilation.

Theoretical benefits of APRV and biphasic mode

Multiple benefits have been ascribed to these modes. In theory, APRV will maximize and maintain alveolar recruitment, improve oxygenation, lower inflation pressures, and decrease overinflation. Both APRV and biphasic, by preserving spontaneous breathing, will improve ventilation-perfusion matching and gas diffusion, improve the hemodynamic profile (less need for vasopressors, higher cardiac output, reduced ventricular workload, improved organ perfusion), and improve synchrony (decrease the work of breathing and the need for sedation).

Evidence of benefit of APRV and biphasic mode

APRV and biphasic are different modes. However studies evaluating their effects are combined. This is in part the result of the nomenclature confusion and different practice in different countries.³⁶

Physiologic benefits. In studies, spontaneous breaths contributed to 10% to 40% of minute ventilation,^37,38 improved ventilation of dependent areas of the lung, improved ventilation-perfusion match and recruitment,³⁹ and improved hemodynamic profile.⁴⁰

Patient comfort. These modes are thought to decrease the need for analgesia and sedation,³⁸ but a recent trial showed no difference with pressure-controlled intermittent mandatory ventilation.⁴¹ Patient ventilator synchrony and comfort have not been studied.^32,42

Outcomes. In small trials, these modes made no difference in terms of deaths, but they may decrease the length of mechanical ventilation.^38,41,43,44

APRV and biphasic mode: Bottom line

Maintaining spontaneous breathing while on mechanical ventilation has hemodynamic and ventilatory benefits.

APRV and biphasic mode are not the same thing. APRV’s main goal is to maximize mean airway pressure and, hence, lung recruitment, whereas the main goal of the biphasic mode is synchrony.

There is a plethora of ventilator settings and questions related to physiologic effects.^33,34,36

Although these modes are widely used in some centers, there is no evidence yet that they are superior to conventional volume- or pressure-control ventilation with low tidal volume for ARDS and acute lung injury. There is no conclusive evidence that these modes improve synchrony, time to weaning, or patient comfort.

 

HIGH-FREQUENCY OSCILLATORY VENTILATION

High-frequency oscillatory ventilation (HFOV) was first described and patented in 1952 by Emerson and was clinically developed in the early 1970s by Lunkenheimer.⁴⁵

The goal of HFOV is to minimize lung injury; its characteristics (discussed below) make it useful in patients with severe ARDS. The US Food and Drug Administration approved it for infants in 1991 and for children in 1995. The adult model has been available since 1993, but it was not approved until 2001 (SensorMedics 3100B, Cardinal Health, Inc).

Other names for high-frequency oscillatory ventilation

While HFOV has no alternative names, the following acronyms describe similar modes:

• HFPPV (high-frequency positive pressure ventilation)
• HFJV (high-frequency jet ventilation)
• HFFI (high-frequency flow interruption)
• HFPV (high-frequency percussive ventilation)
• HFCWO (high-frequency chest wall oscillation).

All of these modes require different specialized ventilators.

What does high-frequency oscillatory ventilation do?

Conceptually, HFOV is a form of pressure-controlled intermittent mandatory ventilation with a set-point control scheme. In contrast to conventional pressure-controlled intermittent mandatory ventilation, in which relatively small spontaneous breaths may be superimposed on relatively large mandatory breaths, HFOV superimposes very small mandatory breaths (oscillations) on top of spontaneous breaths.

HFOV can be delivered only with a special ventilator. The ventilator delivers a constant flow (bias flow), while a valve creates resistance to maintain airway pressure, on top of which a piston pump oscillates at frequencies of 3 to 15 Hz (160–900 breaths/minute). This creates a constant airway pressure with small oscillations (Figure 5); often, clinicians at the bedside look for the “chest wiggle” to assess the appropriate amplitude settings, although this has not been systematically studied.

Adult patients are usually paralyzed or deeply sedated, since deep spontaneous breathing will trigger alarms and affect ventilator performance.

To manage ventilation (CO₂ clearance), one or several of the following maneuvers can be done: decrease the oscillation frequency, increase the amplitude of the oscillations, increase the inspiratory time, or increase bias flow (while allowing an endotracheal tube cuff leak). Oxygenation adjustments are controlled by manipulating the mean airway pressure and the Fio₂.

Ventilator settings in high-frequency oscillatory ventilation

Ventilator settings in HFOV are⁴⁶:

• Airway pressure amplitude (delta P or power)
• Mean airway pressure
• Percent inspiration
• Inspiratory bias flow
• Fio₂.

Clinical applications of high-frequency oscillatory ventilation

This mode is usually reserved for ARDS patients for whom conventional ventilation is failing. A recently published protocol⁴⁶ suggests considering HFOV when there is oxygenation failure (Fio₂ ≥ 0.7 and PEEP ≥ 14 cm H₂O) or ventilation failure (pH < 7.25 with tidal volume ≥ 6 mL/kg predicted body weight and plateau airway pressure ≥ 30 cm H₂O).

This mode is contraindicated when there is known severe airflow obstruction or intracranial hypertension.

Theoretical benefits of high-frequency oscillatory ventilation

Conceptually, HFOV can provide the highest mean airway pressure paired with the lowest tidal volume of any mode. These benefits might make HFOV the ideal lung-protective ventilation strategy.

Evidence of benefit of high-frequency oscillatory ventilation

Physiologic benefits. Animal models have shown less histologic damage and lung inflammation with HFOV than with high-tidal-volume conventional ventilation^47,48 and low-tidal-volume conventional ventilation.⁴⁹

Patient comfort has not been studied. However, current technology does impose undue work of breathing in spontaneously breathing patients.⁵⁰

Outcomes. Several retrospective case series have described better oxygenation with HFOV as rescue therapy for severe ARDS than with conventional mechanical ventilation. Two randomized controlled trials have studied HFOV vs high-tidal-volume conventional mechanical ventilation for early severe ARDS; HFOV was safe but made no difference in terms of deaths.^42,51–54

High-frequency oscillatory ventilation: Bottom line

In theory, HFOV provides all the benefits of an ideal lung-protective strategy, at least for paralyzed or deeply sedated patients. Animal studies support these concepts. In human adults, HFOV has been shown to be safe and to provide better oxygenation but no improvement in death rates compared with conventional mechanical ventilation. Currently, HFOV is better reserved for patients with severe ARDS for whom conventional mechanical ventilation is failing.

Technologic advances and computerized control of mechanical ventilators have made it possible to deliver ventilatory assistance in new modes. Driving these innovations is the desire to prevent ventilator-induced lung injury, improve patient comfort, and liberate the patient from mechanical ventilation as soon as possible.

We call these innovations “alternative” modes to differentiate them from the plain volume-control and pressure-control modes. Some clinicians rarely use these new modes, but in some medical centers they have become the most common ones used, or are being used unknowingly (the operator misunderstands the mode name). The information we provide on these modes of ventilation is by no means an endorsement of their use, but rather a tool to help the clinician understand their physiologic, theoretical, and clinical effects.

We focused on two goals:

• Explain what the mode does
• Briefly review the theoretical benefits and the actual evidence supporting these alternative modes of ventilation.

STANDARD NOMENCLATURE NEEDED

Since its invention, mechanical ventilation has been plagued by multiple names being used to describe the same things. For example, volume-control ventilation is also called volume-cycled ventilation, assist-control ventilation, volume-limited ventilation, and controlled mechanical ventilation. Similarly, multiple abbreviations are used, each depending on the brand of ventilator, and new acronyms have been added in recent years as new modes have been developed. The vast number of names and modes can confuse even the most seasoned critical care physician.

Efforts to establish a common nomenclature are under way.¹

WHAT IS A MODE?

A mode of mechanical ventilation has three essential components:

• The control variable
• The breath sequence
• The targeting scheme.

Similar modes may require more detailed descriptions to distinguish them, but the basic function can be explained by these three components.

The control variable

In general, inspiration is an active process, driven by the patient’s effort, the ventilator, or both, while expiration is passive. For simplicity, in this article a mechanical breath means the inspiratory phase of the breath.

The machine can only control the volume (and flow) or the pressure given. The breaths can be further described on the basis of what triggers the breath, what limits it (the maximum value of a control variable), and what ends (cycles) it.

Therefore, a volume-controlled breath is triggered by the patient or by the machine, limited by flow, and cycled by volume (Figure 1). A pressure-controlled breath is triggered by the patient or the machine, limited by pressure, and cycled by time or flow (Figure 1).

The breath sequence

There are three possible breath sequences:

• 
  Continuous mandatory ventilation, in which all breaths are controlled by the machine (but can be triggered by the patient)
• Intermittent mandatory ventilation, in which the patient can take spontaneous breaths between mandatory breaths
• Continuous spontaneous ventilation, in which all breaths are spontaneous (Table 1).

The targeting scheme

The targeting or feedback scheme refers to the ventilator settings and programming that dictate its response to the patient’s lung compliance, lung resistance, and respiratory effort. The regulation can be as simple as controlling the pressure in pressure-control mode, or it can be based on a complicated algorithm.

In the sections that follow, we describe some of the available alternative modes of mechanical ventilation. We will explain only the targeting schemes in the modes reviewed (Table 1, Table 2), but more information on other targeting schemes can be found elsewhere.^1,2 We will focus on evidence generated in adult patients receiving invasive mechanical ventilation.

 

ADAPTIVE PRESSURE CONTROL

One of the concerns with pressure-control ventilation is that it cannot guarantee a minimum minute ventilation (the volume of air that goes in and out in 1 minute; the tidal volume × breaths per minute) in the face of changing lung mechanics or patient effort, or both. To solve this problem, in 1991 the Siemens Servo 300 ventilator (Siemens, Maquet Critical Care AB, Solna, Sweden) introduced Pressure Regulated Volume Control, a mode that delivers pressure-controlled breaths with a target tidal volume and that is otherwise known as adaptive pressure control (APC) (Figure 2).

Other names for adaptive pressure control

• Pressure Regulated Volume Control (Maquet Servo-i, Rastatt, Germany)
• AutoFlow (Dräger Medical AG, Lübeck, Germany)
• Adaptive Pressure Ventilation (Hamilton Galileo, Hamilton Medical AG, Bonaduz, Switzerland)
• Volume Control+ (Puritan Bennett, Tyco Healthcare; Mansfield, MA)
• Volume Targeted Pressure Control, Pressure Controlled Volume Guaranteed (Engström, General Electric, Madison, WI).

What does adaptive pressure control do?

The APC mode delivers pressure-controlled breaths with an adaptive targeting scheme (Table 2).

In pressure-control ventilation, tidal volumes depend on the lung’s physiologic mechanics (compliance and resistance) and patient effort (Figure 1). Therefore, the tidal volume varies with changes in lung physiology (ie, larger or smaller tidal volumes than targeted).

To overcome this effect, a machine in APC mode adjusts the inspiratory pressure to deliver the set minimal target tidal volume. If tidal volume increases, the machine decreases the inspiratory pressure, and if tidal volume decreases, the machine increases the inspiratory pressure. However, if the patient effort is large enough, the tidal volume will increase in spite of decreasing the inspiratory pressure (Figure 2). The adjustments to the inspiratory pressure occur after the tidal volume is off-target in a number of breaths.

Common sources of confusion with adaptive pressure control

First, APC is not a volume-control mode. In volume control, the tidal volume does not change; in APC the tidal volume can increase or decrease, and the ventilator will adjust the inflation pressure to achieve the target volume. Thus, APC guarantees an average minimum tidal volume but not a maximum tidal volume.

Second, a characteristic of pressure control (and hence, APC) is that the flow of gas varies to maintain constant airway pressure (ie, maintain the set inspiratory pressure). This characteristic allows a patient who generates an inspiratory effort to receive flow as demanded, which is likely more comfortable. This is essentially different from volume control, in which flow is set by the operator and hence is fixed. Thus, if the patient effort is strong enough (Figure 1), this leads to what is called flow asynchrony, in which the patient does not get the flow asked for in a breath.

Ventilator settings in adaptive pressure control

Ventilator settings in APC are:

• Tidal volume
• Time spent in inspiration (inspiratory time)
• Frequency
• Fraction of inspired oxygen (Fio₂)
• Positive end-expiratory pressure (PEEP).

Some ventilators also require setting the speed to reach the peak pressure (also known as slope percent or inspiratory rise time).

Clinical applications of adaptive pressure control

This mode is designed to maintain a consistent tidal volume during pressure-control ventilation and to promote inspiratory flow synchrony. It is a means of automatically reducing ventilatory support (ie, weaning) as the patient’s inspiratory effort becomes stronger, as in awakening from anesthesia.

APC may not be ideal for patients who have an inappropriately increased respiratory drive (eg, in severe metabolic acidosis), since the inspiratory pressure will decrease to maintain the targeted average tidal volume, inappropriately shifting the work of breathing onto the patient.

Theoretical benefits of adaptive pressure control

APC guarantees a minimum average tidal volume (unless the pressure alarm threshold is set too low, so that the target tidal volume is not delivered). Other theoretical benefits are flow synchrony, less ventilator manipulation by the operator, and automatic weaning of ventilator support.

Evidence of benefit of adaptive pressure control

Physiologic benefits. This mode has lower peak inspiratory pressures than does volume-control ventilation,^3,4 which is often reported as a positive finding. However, in volume-control mode (the usual comparator), the peak inspiratory pressure is a manifestation of both resistance and compliance. Hence, peak inspiratory pressure is expected to be higher but does not reflect actual lung-distending pressures. It is the plateau pressure, a manifestation of lung compliance, that is related to lung injury.

Patient comfort. APC may increase the work of breathing when using low tidal volume ventilation and when there is increased respiratory effort (drive).⁵ Interestingly, APC was less comfortable than pressure support ventilation in a small trial.⁶

Outcomes have not been studied.⁷

Adaptive pressure control: Bottom line

APC is widely available and widely used, sometimes unknowingly (eg, if the operator thinks it is volume control). It is relatively easy to use and to set; however, evidence of its benefit is scant.

 

ADAPTIVE SUPPORT VENTILATION

Adaptive support ventilation (ASV) evolved as a form of mandatory minute ventilation implemented with adaptive pressure control. Mandatory minute ventilation is a mode that allows the operator to preset a target minute ventilation, and the ventilator then supplies mandatory breaths, either volume- or pressure-controlled, if the patient’s spontaneous breaths generate a lower minute ventilation.

ASV automatically selects the appropriate tidal volume and frequency for mandatory breaths and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and target minute alveolar ventilation.

Described in 1994 by Laubscher et al,^8,9 ASV became commercially available in 1998 in Europe and in 2007 in the United States (Hamilton Galileo ventilator, Hamilton Medical AG). This is the first commercially available ventilator that uses an “optimal” targeting scheme (see below).

What does adaptive support ventilation do?

ASV delivers pressure-controlled breaths using an adaptive (optimal) scheme (Table 2). “Optimal,” in this context, means minimizing the mechanical work of breathing: the machine selects a tidal volume and frequency that the patient’s brain would presumably select if the patient were not connected to a ventilator. This pattern is assumed to encourage the patient to generate spontaneous breaths.

The ventilator calculates the normal required minute ventilation based on the patient’s ideal weight and estimated dead space volume (ie, 2.2 mL/kg). This calculation represents 100% of minute ventilation. The clinician at the bedside sets a target percent of minute ventilation that the ventilator will support—higher than 100% if the patient has increased requirements due, eg, to sepsis or increased dead space, or less than 100% during weaning.

The ventilator initially delivers test breaths, in which it measures the expiratory time constant for the respiratory system and then uses this along with the estimated dead space and normal minute ventilation to calculate an optimal breathing frequency in terms of mechanical work.

The optimal or target tidal volume is calculated as the normal minute ventilation divided by the optimal frequency. The target tidal volume is achieved by the use of APC (see above) (Figure 2). This means that the pressure limit is automatically adjusted to achieve an average delivered tidal volume equal to the target. The ventilator continuously monitors the respiratory system mechanics and adjusts its settings accordingly.

The ventilator adjusts its breaths to avoid air trapping by allowing enough time to exhale, to avoid hypoventilation by delivering tidal volume greater than the dead space, and to avoid volutrauma by avoiding large tidal volumes.

Ventilator settings in adaptive support ventilation

Ventilator settings in ASV are:

• Patient height (to calculate the ideal body weight)
• Sex
• Percent of normal predicted minute ventilation goal
• Fio₂
• PEEP.

Clinical applications of adaptive support ventilation

ASV is intended as a sole mode of ventilation, from initial support to weaning.

Theoretical benefits of adaptive support ventilation

In theory, ASV offers automatic selection of ventilator settings, automatic adaptation to changing patient lung mechanics, less need for human manipulation of the machine, improved synchrony, and automatic weaning.

Evidence of benefit of adaptive support ventilation

Physiologic benefits. Ventilator settings are adjusted automatically. ASV selects different tidal volume-respiratory rate combinations based on respiratory mechanics in passive and paralyzed patients.^10–12 In actively breathing patients, there was no difference in the ventilator settings chosen by ASV for different clinical scenarios (and lung physiology).¹⁰ Compared with pressure-controlled intermittent mandatory ventilation, with ASV, the inspiratory load is less and patient-ventilator interaction is better.¹³

Patient-ventilator synchrony and comfort have not been studied.

Outcomes. Two trials suggest that ASV may decrease time on mechanical ventilation.^14,15 However, in another trial,¹⁶ compared with a standard protocol, ASV led to fewer ventilator adjustments but achieved similar postsurgical weaning outcomes. The effect of this mode on the death rate has not been examined.^17,18

Adaptive support ventilation: Bottom line

ASV is the first commercially available mode that automatically selects all the ventilator settings except PEEP and Fio₂. These seem appropriate for different clinical scenarios in patients with poor respiratory effort or in paralyzed patients. Evidence of the effect in actively breathing patients and on outcomes such as length of stay or death is still lacking.

PROPORTIONAL ASSIST VENTILATION

Patients who have normal respiratory drive but who have difficulty sustaining adequate spontaneous ventilation are often subjected to pressure support ventilation (PSV), in which the ventilator generates a constant pressure throughout inspiration regardless of the intensity of the patient’s effort.

In 1992, Younes and colleagues^19,20 developed proportional assist ventilation (PAV) as an alternative in which the ventilator generates pressure in proportion to the patient’s effort. PAV became commercially available in Europe in 1999 and was approved in the United States in 2006, available on the Puritan Bennett 840 ventilator (Puritan Bennett Co, Boulder, CO). PAV has also been used for noninvasive ventilation, but this is not available in the United States.

Other names for proportional assist ventilation

Proportional Pressure Support (Dräger Medical; not yet available in the United States).

 

 

What does proportional assist ventilation do?

This mode delivers pressure-controlled breaths with a servo control scheme (Table 2).

To better understand PAV, we can compare it with PSV. With PSV, the pressure applied by the ventilator rises to a preset level that is held constant (a set-point scheme) until a cycling criterion (a percent of the maximum inspiratory flow value) is reached. The inspiratory flow and tidal volume are the result of the patient’s inspiratory effort, the level of pressure applied, and the respiratory system mechanics.

In contrast, during PAV, the pressure applied is a function of patient effort: the greater the inspiratory effort, the greater the increase in applied pressure (servo targeting scheme) (Figure 3). The operator sets the percentage of support to be delivered by the ventilator. The ventilator intermittently measures the compliance and resistance of the patient’s respiratory system and the instantaneous patient-generated flow and volume, and on the basis of these it delivers a proportional amount of inspiratory pressure.

In PAV, as in PSV, all breaths are spontaneous (Table 1). The patient controls the timing and size of the breath. There are no preset pressure, flow, or volume goals, but safety limits on the volume and pressure delivered can be set.

Ventilator settings in proportional assist ventilation

Ventilator settings in PAV are:

• Airway type (endotracheal tube, tracheostomy)
• Airway size (inner diameter)
• Percentage of work supported (assist range 5%–95%)
• Tidal volume limit
• Pressure limit
• Expiratory sensitivity (normally, as inspiration ends, flow should stop; this parameter tells the ventilator at what flow to end inspiration).

Caution when assessing the literature. Earlier ventilator versions, ie, Dräger and Manitoba (University of Manitoba, Winnipeg, MB, Canada), which are not available in the United States, required the repeated calculation of the respiratory system mechanics and the manual setting of flow and volume assists (amplification factors) independently. To overcome this limitation, new software automatically adjusts the flow and volume amplification to support the loads imposed by the automatically measured values of resistance and elastance (inverse of compliance) of the respiratory system.²¹ This software is included in the model (Puritan Bennett) available in the United States.

Clinical applications of proportional assist ventilation

The PAV mode is indicated for maximizing ventilator patient synchrony for assisted spontaneous ventilation.

PAV is contraindicated in patients with respiratory depression (bradypnea) or large air leaks (eg, bronchopleural fistulas). It should be used with caution in patients with severe hyperinflation, in which the patient may still be exhaling but the ventilator doesn’t recognize it. Another group in which PAV should be used with caution is those with high ventilatory drives, in which the ventilator overestimates respiratory system mechanics. This situation can lead to overassistance due to the “runaway phenomenon,” in which the ventilator continues to provide support even if the patient has stopped inspiration.²²

Theoretical benefits of proportional assist ventilation

In theory, PAV should reduce the work of breathing, improve synchrony, automatically adapt to changing patient lung mechanics and effort, decrease the need for ventilator intervention and manipulation, decrease the need for sedation, and improve sleep.

Evidence of benefit of proportional assist ventilation

Physiologic benefits. PAV reduces the work of breathing better than PSV,²¹ even in the face of changing respiratory mechanics or increased respiratory demand (hypercapnia).^23–25 The hemodynamic profile is similar to that in PSV. Tidal volumes are variable; however, in recent reports the tidal volumes were within the lung-protective range (6–8 mL/kg, plateau pressure < 30 cm H₂0).^26,27

Comfort. PAV entails less patient effort and discomfort that PSV does.^23,25 PAV significantly reduces asynchrony,²⁷ which in turn may favorably affect sleep in critically ill patients. ²⁸

Outcomes. The probability of spontaneous breathing without assistance was significantly better in critically ill patients ventilated with PAV than with PSV. No trial has reported the effect of PAV on deaths.^27,29

Proportional assist ventilation: Bottom line

Extensive basic research has been done with PAV in different forms of respiratory failure, such as obstructive lung disease, acute respiratory distress syndrome (ARDS), and chronic respiratory failure. It fulfills its main goal, which is to improve patient-ventilator synchrony. Clinical experience with PAV in the United States is limited, as it was only recently approved.

 

AIRWAY PRESSURE-RELEASE VENTILATION AND BIPHASIC POSITIVE AIRWAY PRESSURE

Airway pressure-release ventilation (APRV) was described in 1987 by Stock et al³⁰ as a mode for delivering ventilation in acute lung injury while avoiding high airway pressures. APRV combines high constant positive airway pressure (improving oxygenation and promoting alveolar recruitment) with intermittent releases (causing exhalation).

In 1989, Baum et al³¹ described biphasic positive airway pressure ventilation as a mode in which spontaneous ventilation could be achieved at any point in the mechanical ventilation cycle—inspiration or exhalation (Figure 4). The goal was to allow unrestricted spontaneous breathing to reduce sedation and promote weaning. These modes are conceptually the same, the main difference being that the time spent in low pressure (T_low; see below) is less than 1.5 seconds for APRV. Otherwise, they have identical characteristics, thus allowing any ventilator with the capability of delivering APRV to deliver biphasic positive airway pressure, and vice versa. Machines with these modes became commercially available in the mid 1990s.

Other names for biphasic positive airway pressure

Other names for biphasic positive airway pressure are:

• BiLevel (Puritan Bennett)
• BIPAP (Dräger Europe)
• Bi Vent (Siemens)
• BiPhasic (Avea, Cardinal Health, Inc, Dublin, OH)
• PCV+ (Dräger Medical)
• DuoPAP (Hamilton).

Caution—name confusion. In North America, BiPAP (Respironics, Murrysville, PA) and BiLevel are used to refer to noninvasive modes of ventilation.

APRV has no other name.

What do these modes do?

These modes deliver pressure-controlled, time-triggered, and time-cycled breaths using a set-point targeting scheme (Table 2). This means that the ventilator maintains a constant pressure (set point) even in the face of spontaneous breaths.

Caution—source of confusion. The term continuous positive airway pressure (CPAP) is often used to describe this mode. However, CPAP is pressure that is applied continuously at the same level; the patient generates all the work to maintain ventilation (“pressure-controlled continuous spontaneous ventilation” in the current nomenclature). In APRV, the airway pressure is intermittently released and reapplied, generating a tidal volume that supports ventilation. In other words, this is a pressure-controlled breath with a very prolonged inspiratory time and a short expiratory time in which spontaneous ventilation is possible at any point (“pressure-controlled intermittent mandatory ventilation” in the current nomenclature).

How these modes are set in the ventilator may also be a source of confusion. To describe the time spent in high and low airway pressures, we use the terms T_high and T_low, respectively. By convention, the difference between APRV and biphasic mode is the duration of T_low (< 1.5 sec for APRV).

Similarly, P_high and P_low are used to describe the high and low airway pressure. To better understand this concept, you can create the same mode in conventional pressure-control ventilation by thinking of the T_high as the inspiratory time, the T_low as the expiratory time, the P_high as inspiratory pressure, and the P_low as PEEP.

Hence, APRV is an extreme form of inverse ratio ventilation, with an inspiration-to-expiration ratio of 4:1. This means a patient spends most of the time in P_high and T_high, and exhalations are short (T_low and P_low). In contrast, the biphasic mode uses conventional inspiration-expiration ratios (Figure 4).

As with any form of pressure control, the tidal volume is generated by airway pressure rising above baseline (ie, the end-expiratory value). Hence, to ensure an increase in minute ventilation, the mandatory breath rate must be increased (ie, decreasing T_high, T_low, or both) or the tidal volume must be increased (ie, increasing the difference between P_high and P_low). This means that in APRV the T_low has to happen more often (by increasing the number of breaths) or be more prolonged (allowing more air to exhale). Because unrestricted spontaneous breaths are permitted at any point of the cycle, the patient contributes to the total minute ventilation (usually 10%–40%).

In APRV and biphasic mode, the operator’s set time and pressure in inspiration and expiration will be delivered regardless of the patient’s breathing efforts—the patient’s spontaneous breath does not trigger a mechanical breath. Some ventilators have automatic adjustments to improve the trigger synchrony.

Ventilator settings in APRV and biphasic mode

These modes require the setting of two pressure levels (P_high and P_low) and two time durations (T_high and T_low). One can add pressure support or automatic tube compensation to assist spontaneous breaths. The difference in T_low generates differences in the T_high:T_low ratio: APRV has a short T_low (an inspiration-expiration ratio of 4:1). Biphasic mode has a conventional inspiration-expiration ratio of 1:1 to 1:4.

Clinical applications

APRV is used in acute lung injury and ARDS. This mode should be used with caution or not at all in patients with obstructive lung disease or inappropriately increased respiratory drive.^32–35

Biphasic mode is intended for both ventilation and weaning. In a patient who has poor respiratory effort or who is paralyzed, biphasic is identical to pressure-control/continuous mandatory ventilation.

Theoretical benefits of APRV and biphasic mode

Multiple benefits have been ascribed to these modes. In theory, APRV will maximize and maintain alveolar recruitment, improve oxygenation, lower inflation pressures, and decrease overinflation. Both APRV and biphasic, by preserving spontaneous breathing, will improve ventilation-perfusion matching and gas diffusion, improve the hemodynamic profile (less need for vasopressors, higher cardiac output, reduced ventricular workload, improved organ perfusion), and improve synchrony (decrease the work of breathing and the need for sedation).

Evidence of benefit of APRV and biphasic mode

APRV and biphasic are different modes. However studies evaluating their effects are combined. This is in part the result of the nomenclature confusion and different practice in different countries.³⁶

Physiologic benefits. In studies, spontaneous breaths contributed to 10% to 40% of minute ventilation,^37,38 improved ventilation of dependent areas of the lung, improved ventilation-perfusion match and recruitment,³⁹ and improved hemodynamic profile.⁴⁰

Patient comfort. These modes are thought to decrease the need for analgesia and sedation,³⁸ but a recent trial showed no difference with pressure-controlled intermittent mandatory ventilation.⁴¹ Patient ventilator synchrony and comfort have not been studied.^32,42

Outcomes. In small trials, these modes made no difference in terms of deaths, but they may decrease the length of mechanical ventilation.^38,41,43,44

APRV and biphasic mode: Bottom line

Maintaining spontaneous breathing while on mechanical ventilation has hemodynamic and ventilatory benefits.

APRV and biphasic mode are not the same thing. APRV’s main goal is to maximize mean airway pressure and, hence, lung recruitment, whereas the main goal of the biphasic mode is synchrony.

There is a plethora of ventilator settings and questions related to physiologic effects.^33,34,36

Although these modes are widely used in some centers, there is no evidence yet that they are superior to conventional volume- or pressure-control ventilation with low tidal volume for ARDS and acute lung injury. There is no conclusive evidence that these modes improve synchrony, time to weaning, or patient comfort.

 

HIGH-FREQUENCY OSCILLATORY VENTILATION

High-frequency oscillatory ventilation (HFOV) was first described and patented in 1952 by Emerson and was clinically developed in the early 1970s by Lunkenheimer.⁴⁵

The goal of HFOV is to minimize lung injury; its characteristics (discussed below) make it useful in patients with severe ARDS. The US Food and Drug Administration approved it for infants in 1991 and for children in 1995. The adult model has been available since 1993, but it was not approved until 2001 (SensorMedics 3100B, Cardinal Health, Inc).

Other names for high-frequency oscillatory ventilation

While HFOV has no alternative names, the following acronyms describe similar modes:

• HFPPV (high-frequency positive pressure ventilation)
• HFJV (high-frequency jet ventilation)
• HFFI (high-frequency flow interruption)
• HFPV (high-frequency percussive ventilation)
• HFCWO (high-frequency chest wall oscillation).

All of these modes require different specialized ventilators.

What does high-frequency oscillatory ventilation do?

Conceptually, HFOV is a form of pressure-controlled intermittent mandatory ventilation with a set-point control scheme. In contrast to conventional pressure-controlled intermittent mandatory ventilation, in which relatively small spontaneous breaths may be superimposed on relatively large mandatory breaths, HFOV superimposes very small mandatory breaths (oscillations) on top of spontaneous breaths.

HFOV can be delivered only with a special ventilator. The ventilator delivers a constant flow (bias flow), while a valve creates resistance to maintain airway pressure, on top of which a piston pump oscillates at frequencies of 3 to 15 Hz (160–900 breaths/minute). This creates a constant airway pressure with small oscillations (Figure 5); often, clinicians at the bedside look for the “chest wiggle” to assess the appropriate amplitude settings, although this has not been systematically studied.

Adult patients are usually paralyzed or deeply sedated, since deep spontaneous breathing will trigger alarms and affect ventilator performance.

To manage ventilation (CO₂ clearance), one or several of the following maneuvers can be done: decrease the oscillation frequency, increase the amplitude of the oscillations, increase the inspiratory time, or increase bias flow (while allowing an endotracheal tube cuff leak). Oxygenation adjustments are controlled by manipulating the mean airway pressure and the Fio₂.

Ventilator settings in high-frequency oscillatory ventilation

Ventilator settings in HFOV are⁴⁶:

• Airway pressure amplitude (delta P or power)
• Mean airway pressure
• Percent inspiration
• Inspiratory bias flow
• Fio₂.

Clinical applications of high-frequency oscillatory ventilation

This mode is usually reserved for ARDS patients for whom conventional ventilation is failing. A recently published protocol⁴⁶ suggests considering HFOV when there is oxygenation failure (Fio₂ ≥ 0.7 and PEEP ≥ 14 cm H₂O) or ventilation failure (pH < 7.25 with tidal volume ≥ 6 mL/kg predicted body weight and plateau airway pressure ≥ 30 cm H₂O).

This mode is contraindicated when there is known severe airflow obstruction or intracranial hypertension.

Theoretical benefits of high-frequency oscillatory ventilation

Conceptually, HFOV can provide the highest mean airway pressure paired with the lowest tidal volume of any mode. These benefits might make HFOV the ideal lung-protective ventilation strategy.

Evidence of benefit of high-frequency oscillatory ventilation

Physiologic benefits. Animal models have shown less histologic damage and lung inflammation with HFOV than with high-tidal-volume conventional ventilation^47,48 and low-tidal-volume conventional ventilation.⁴⁹

Patient comfort has not been studied. However, current technology does impose undue work of breathing in spontaneously breathing patients.⁵⁰

Outcomes. Several retrospective case series have described better oxygenation with HFOV as rescue therapy for severe ARDS than with conventional mechanical ventilation. Two randomized controlled trials have studied HFOV vs high-tidal-volume conventional mechanical ventilation for early severe ARDS; HFOV was safe but made no difference in terms of deaths.^42,51–54

High-frequency oscillatory ventilation: Bottom line

In theory, HFOV provides all the benefits of an ideal lung-protective strategy, at least for paralyzed or deeply sedated patients. Animal studies support these concepts. In human adults, HFOV has been shown to be safe and to provide better oxygenation but no improvement in death rates compared with conventional mechanical ventilation. Currently, HFOV is better reserved for patients with severe ARDS for whom conventional mechanical ventilation is failing.

Technologic advances and computerized control of mechanical ventilators have made it possible to deliver ventilatory assistance in new modes. Driving these innovations is the desire to prevent ventilator-induced lung injury, improve patient comfort, and liberate the patient from mechanical ventilation as soon as possible.

We call these innovations “alternative” modes to differentiate them from the plain volume-control and pressure-control modes. Some clinicians rarely use these new modes, but in some medical centers they have become the most common ones used, or are being used unknowingly (the operator misunderstands the mode name). The information we provide on these modes of ventilation is by no means an endorsement of their use, but rather a tool to help the clinician understand their physiologic, theoretical, and clinical effects.

We focused on two goals:

• Explain what the mode does
• Briefly review the theoretical benefits and the actual evidence supporting these alternative modes of ventilation.

STANDARD NOMENCLATURE NEEDED

Since its invention, mechanical ventilation has been plagued by multiple names being used to describe the same things. For example, volume-control ventilation is also called volume-cycled ventilation, assist-control ventilation, volume-limited ventilation, and controlled mechanical ventilation. Similarly, multiple abbreviations are used, each depending on the brand of ventilator, and new acronyms have been added in recent years as new modes have been developed. The vast number of names and modes can confuse even the most seasoned critical care physician.

Efforts to establish a common nomenclature are under way.¹

WHAT IS A MODE?

A mode of mechanical ventilation has three essential components:

• The control variable
• The breath sequence
• The targeting scheme.

Similar modes may require more detailed descriptions to distinguish them, but the basic function can be explained by these three components.

The control variable

In general, inspiration is an active process, driven by the patient’s effort, the ventilator, or both, while expiration is passive. For simplicity, in this article a mechanical breath means the inspiratory phase of the breath.

The machine can only control the volume (and flow) or the pressure given. The breaths can be further described on the basis of what triggers the breath, what limits it (the maximum value of a control variable), and what ends (cycles) it.

Therefore, a volume-controlled breath is triggered by the patient or by the machine, limited by flow, and cycled by volume (Figure 1). A pressure-controlled breath is triggered by the patient or the machine, limited by pressure, and cycled by time or flow (Figure 1).

The breath sequence

There are three possible breath sequences:

• 
  Continuous mandatory ventilation, in which all breaths are controlled by the machine (but can be triggered by the patient)
• Intermittent mandatory ventilation, in which the patient can take spontaneous breaths between mandatory breaths
• Continuous spontaneous ventilation, in which all breaths are spontaneous (Table 1).

The targeting scheme

The targeting or feedback scheme refers to the ventilator settings and programming that dictate its response to the patient’s lung compliance, lung resistance, and respiratory effort. The regulation can be as simple as controlling the pressure in pressure-control mode, or it can be based on a complicated algorithm.

In the sections that follow, we describe some of the available alternative modes of mechanical ventilation. We will explain only the targeting schemes in the modes reviewed (Table 1, Table 2), but more information on other targeting schemes can be found elsewhere.^1,2 We will focus on evidence generated in adult patients receiving invasive mechanical ventilation.

 

ADAPTIVE PRESSURE CONTROL

One of the concerns with pressure-control ventilation is that it cannot guarantee a minimum minute ventilation (the volume of air that goes in and out in 1 minute; the tidal volume × breaths per minute) in the face of changing lung mechanics or patient effort, or both. To solve this problem, in 1991 the Siemens Servo 300 ventilator (Siemens, Maquet Critical Care AB, Solna, Sweden) introduced Pressure Regulated Volume Control, a mode that delivers pressure-controlled breaths with a target tidal volume and that is otherwise known as adaptive pressure control (APC) (Figure 2).

Other names for adaptive pressure control

• Pressure Regulated Volume Control (Maquet Servo-i, Rastatt, Germany)
• AutoFlow (Dräger Medical AG, Lübeck, Germany)
• Adaptive Pressure Ventilation (Hamilton Galileo, Hamilton Medical AG, Bonaduz, Switzerland)
• Volume Control+ (Puritan Bennett, Tyco Healthcare; Mansfield, MA)
• Volume Targeted Pressure Control, Pressure Controlled Volume Guaranteed (Engström, General Electric, Madison, WI).

What does adaptive pressure control do?

The APC mode delivers pressure-controlled breaths with an adaptive targeting scheme (Table 2).

In pressure-control ventilation, tidal volumes depend on the lung’s physiologic mechanics (compliance and resistance) and patient effort (Figure 1). Therefore, the tidal volume varies with changes in lung physiology (ie, larger or smaller tidal volumes than targeted).

To overcome this effect, a machine in APC mode adjusts the inspiratory pressure to deliver the set minimal target tidal volume. If tidal volume increases, the machine decreases the inspiratory pressure, and if tidal volume decreases, the machine increases the inspiratory pressure. However, if the patient effort is large enough, the tidal volume will increase in spite of decreasing the inspiratory pressure (Figure 2). The adjustments to the inspiratory pressure occur after the tidal volume is off-target in a number of breaths.

Common sources of confusion with adaptive pressure control

First, APC is not a volume-control mode. In volume control, the tidal volume does not change; in APC the tidal volume can increase or decrease, and the ventilator will adjust the inflation pressure to achieve the target volume. Thus, APC guarantees an average minimum tidal volume but not a maximum tidal volume.

Second, a characteristic of pressure control (and hence, APC) is that the flow of gas varies to maintain constant airway pressure (ie, maintain the set inspiratory pressure). This characteristic allows a patient who generates an inspiratory effort to receive flow as demanded, which is likely more comfortable. This is essentially different from volume control, in which flow is set by the operator and hence is fixed. Thus, if the patient effort is strong enough (Figure 1), this leads to what is called flow asynchrony, in which the patient does not get the flow asked for in a breath.

Ventilator settings in adaptive pressure control

Ventilator settings in APC are:

• Tidal volume
• Time spent in inspiration (inspiratory time)
• Frequency
• Fraction of inspired oxygen (Fio₂)
• Positive end-expiratory pressure (PEEP).

Some ventilators also require setting the speed to reach the peak pressure (also known as slope percent or inspiratory rise time).

Clinical applications of adaptive pressure control

This mode is designed to maintain a consistent tidal volume during pressure-control ventilation and to promote inspiratory flow synchrony. It is a means of automatically reducing ventilatory support (ie, weaning) as the patient’s inspiratory effort becomes stronger, as in awakening from anesthesia.

APC may not be ideal for patients who have an inappropriately increased respiratory drive (eg, in severe metabolic acidosis), since the inspiratory pressure will decrease to maintain the targeted average tidal volume, inappropriately shifting the work of breathing onto the patient.

Theoretical benefits of adaptive pressure control

APC guarantees a minimum average tidal volume (unless the pressure alarm threshold is set too low, so that the target tidal volume is not delivered). Other theoretical benefits are flow synchrony, less ventilator manipulation by the operator, and automatic weaning of ventilator support.

Evidence of benefit of adaptive pressure control

Physiologic benefits. This mode has lower peak inspiratory pressures than does volume-control ventilation,^3,4 which is often reported as a positive finding. However, in volume-control mode (the usual comparator), the peak inspiratory pressure is a manifestation of both resistance and compliance. Hence, peak inspiratory pressure is expected to be higher but does not reflect actual lung-distending pressures. It is the plateau pressure, a manifestation of lung compliance, that is related to lung injury.

Patient comfort. APC may increase the work of breathing when using low tidal volume ventilation and when there is increased respiratory effort (drive).⁵ Interestingly, APC was less comfortable than pressure support ventilation in a small trial.⁶

Outcomes have not been studied.⁷

Adaptive pressure control: Bottom line

APC is widely available and widely used, sometimes unknowingly (eg, if the operator thinks it is volume control). It is relatively easy to use and to set; however, evidence of its benefit is scant.

 

ADAPTIVE SUPPORT VENTILATION

Adaptive support ventilation (ASV) evolved as a form of mandatory minute ventilation implemented with adaptive pressure control. Mandatory minute ventilation is a mode that allows the operator to preset a target minute ventilation, and the ventilator then supplies mandatory breaths, either volume- or pressure-controlled, if the patient’s spontaneous breaths generate a lower minute ventilation.

ASV automatically selects the appropriate tidal volume and frequency for mandatory breaths and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and target minute alveolar ventilation.

Described in 1994 by Laubscher et al,^8,9 ASV became commercially available in 1998 in Europe and in 2007 in the United States (Hamilton Galileo ventilator, Hamilton Medical AG). This is the first commercially available ventilator that uses an “optimal” targeting scheme (see below).

What does adaptive support ventilation do?

ASV delivers pressure-controlled breaths using an adaptive (optimal) scheme (Table 2). “Optimal,” in this context, means minimizing the mechanical work of breathing: the machine selects a tidal volume and frequency that the patient’s brain would presumably select if the patient were not connected to a ventilator. This pattern is assumed to encourage the patient to generate spontaneous breaths.

The ventilator calculates the normal required minute ventilation based on the patient’s ideal weight and estimated dead space volume (ie, 2.2 mL/kg). This calculation represents 100% of minute ventilation. The clinician at the bedside sets a target percent of minute ventilation that the ventilator will support—higher than 100% if the patient has increased requirements due, eg, to sepsis or increased dead space, or less than 100% during weaning.

The ventilator initially delivers test breaths, in which it measures the expiratory time constant for the respiratory system and then uses this along with the estimated dead space and normal minute ventilation to calculate an optimal breathing frequency in terms of mechanical work.

The optimal or target tidal volume is calculated as the normal minute ventilation divided by the optimal frequency. The target tidal volume is achieved by the use of APC (see above) (Figure 2). This means that the pressure limit is automatically adjusted to achieve an average delivered tidal volume equal to the target. The ventilator continuously monitors the respiratory system mechanics and adjusts its settings accordingly.

The ventilator adjusts its breaths to avoid air trapping by allowing enough time to exhale, to avoid hypoventilation by delivering tidal volume greater than the dead space, and to avoid volutrauma by avoiding large tidal volumes.

Ventilator settings in adaptive support ventilation

Ventilator settings in ASV are:

• Patient height (to calculate the ideal body weight)
• Sex
• Percent of normal predicted minute ventilation goal
• Fio₂
• PEEP.

Clinical applications of adaptive support ventilation

ASV is intended as a sole mode of ventilation, from initial support to weaning.

Theoretical benefits of adaptive support ventilation

In theory, ASV offers automatic selection of ventilator settings, automatic adaptation to changing patient lung mechanics, less need for human manipulation of the machine, improved synchrony, and automatic weaning.

Evidence of benefit of adaptive support ventilation

Physiologic benefits. Ventilator settings are adjusted automatically. ASV selects different tidal volume-respiratory rate combinations based on respiratory mechanics in passive and paralyzed patients.^10–12 In actively breathing patients, there was no difference in the ventilator settings chosen by ASV for different clinical scenarios (and lung physiology).¹⁰ Compared with pressure-controlled intermittent mandatory ventilation, with ASV, the inspiratory load is less and patient-ventilator interaction is better.¹³

Patient-ventilator synchrony and comfort have not been studied.

Outcomes. Two trials suggest that ASV may decrease time on mechanical ventilation.^14,15 However, in another trial,¹⁶ compared with a standard protocol, ASV led to fewer ventilator adjustments but achieved similar postsurgical weaning outcomes. The effect of this mode on the death rate has not been examined.^17,18

Adaptive support ventilation: Bottom line

ASV is the first commercially available mode that automatically selects all the ventilator settings except PEEP and Fio₂. These seem appropriate for different clinical scenarios in patients with poor respiratory effort or in paralyzed patients. Evidence of the effect in actively breathing patients and on outcomes such as length of stay or death is still lacking.

PROPORTIONAL ASSIST VENTILATION

Patients who have normal respiratory drive but who have difficulty sustaining adequate spontaneous ventilation are often subjected to pressure support ventilation (PSV), in which the ventilator generates a constant pressure throughout inspiration regardless of the intensity of the patient’s effort.

In 1992, Younes and colleagues^19,20 developed proportional assist ventilation (PAV) as an alternative in which the ventilator generates pressure in proportion to the patient’s effort. PAV became commercially available in Europe in 1999 and was approved in the United States in 2006, available on the Puritan Bennett 840 ventilator (Puritan Bennett Co, Boulder, CO). PAV has also been used for noninvasive ventilation, but this is not available in the United States.

Other names for proportional assist ventilation

Proportional Pressure Support (Dräger Medical; not yet available in the United States).

 

 

What does proportional assist ventilation do?

This mode delivers pressure-controlled breaths with a servo control scheme (Table 2).

To better understand PAV, we can compare it with PSV. With PSV, the pressure applied by the ventilator rises to a preset level that is held constant (a set-point scheme) until a cycling criterion (a percent of the maximum inspiratory flow value) is reached. The inspiratory flow and tidal volume are the result of the patient’s inspiratory effort, the level of pressure applied, and the respiratory system mechanics.

In contrast, during PAV, the pressure applied is a function of patient effort: the greater the inspiratory effort, the greater the increase in applied pressure (servo targeting scheme) (Figure 3). The operator sets the percentage of support to be delivered by the ventilator. The ventilator intermittently measures the compliance and resistance of the patient’s respiratory system and the instantaneous patient-generated flow and volume, and on the basis of these it delivers a proportional amount of inspiratory pressure.

In PAV, as in PSV, all breaths are spontaneous (Table 1). The patient controls the timing and size of the breath. There are no preset pressure, flow, or volume goals, but safety limits on the volume and pressure delivered can be set.

Ventilator settings in proportional assist ventilation

Ventilator settings in PAV are:

• Airway type (endotracheal tube, tracheostomy)
• Airway size (inner diameter)
• Percentage of work supported (assist range 5%–95%)
• Tidal volume limit
• Pressure limit
• Expiratory sensitivity (normally, as inspiration ends, flow should stop; this parameter tells the ventilator at what flow to end inspiration).

Caution when assessing the literature. Earlier ventilator versions, ie, Dräger and Manitoba (University of Manitoba, Winnipeg, MB, Canada), which are not available in the United States, required the repeated calculation of the respiratory system mechanics and the manual setting of flow and volume assists (amplification factors) independently. To overcome this limitation, new software automatically adjusts the flow and volume amplification to support the loads imposed by the automatically measured values of resistance and elastance (inverse of compliance) of the respiratory system.²¹ This software is included in the model (Puritan Bennett) available in the United States.

Clinical applications of proportional assist ventilation

The PAV mode is indicated for maximizing ventilator patient synchrony for assisted spontaneous ventilation.

PAV is contraindicated in patients with respiratory depression (bradypnea) or large air leaks (eg, bronchopleural fistulas). It should be used with caution in patients with severe hyperinflation, in which the patient may still be exhaling but the ventilator doesn’t recognize it. Another group in which PAV should be used with caution is those with high ventilatory drives, in which the ventilator overestimates respiratory system mechanics. This situation can lead to overassistance due to the “runaway phenomenon,” in which the ventilator continues to provide support even if the patient has stopped inspiration.²²

Theoretical benefits of proportional assist ventilation

In theory, PAV should reduce the work of breathing, improve synchrony, automatically adapt to changing patient lung mechanics and effort, decrease the need for ventilator intervention and manipulation, decrease the need for sedation, and improve sleep.

Evidence of benefit of proportional assist ventilation

Physiologic benefits. PAV reduces the work of breathing better than PSV,²¹ even in the face of changing respiratory mechanics or increased respiratory demand (hypercapnia).^23–25 The hemodynamic profile is similar to that in PSV. Tidal volumes are variable; however, in recent reports the tidal volumes were within the lung-protective range (6–8 mL/kg, plateau pressure < 30 cm H₂0).^26,27

Comfort. PAV entails less patient effort and discomfort that PSV does.^23,25 PAV significantly reduces asynchrony,²⁷ which in turn may favorably affect sleep in critically ill patients. ²⁸

Outcomes. The probability of spontaneous breathing without assistance was significantly better in critically ill patients ventilated with PAV than with PSV. No trial has reported the effect of PAV on deaths.^27,29

Proportional assist ventilation: Bottom line

Extensive basic research has been done with PAV in different forms of respiratory failure, such as obstructive lung disease, acute respiratory distress syndrome (ARDS), and chronic respiratory failure. It fulfills its main goal, which is to improve patient-ventilator synchrony. Clinical experience with PAV in the United States is limited, as it was only recently approved.

 

AIRWAY PRESSURE-RELEASE VENTILATION AND BIPHASIC POSITIVE AIRWAY PRESSURE

Airway pressure-release ventilation (APRV) was described in 1987 by Stock et al³⁰ as a mode for delivering ventilation in acute lung injury while avoiding high airway pressures. APRV combines high constant positive airway pressure (improving oxygenation and promoting alveolar recruitment) with intermittent releases (causing exhalation).

In 1989, Baum et al³¹ described biphasic positive airway pressure ventilation as a mode in which spontaneous ventilation could be achieved at any point in the mechanical ventilation cycle—inspiration or exhalation (Figure 4). The goal was to allow unrestricted spontaneous breathing to reduce sedation and promote weaning. These modes are conceptually the same, the main difference being that the time spent in low pressure (T_low; see below) is less than 1.5 seconds for APRV. Otherwise, they have identical characteristics, thus allowing any ventilator with the capability of delivering APRV to deliver biphasic positive airway pressure, and vice versa. Machines with these modes became commercially available in the mid 1990s.

Other names for biphasic positive airway pressure

Other names for biphasic positive airway pressure are:

• BiLevel (Puritan Bennett)
• BIPAP (Dräger Europe)
• Bi Vent (Siemens)
• BiPhasic (Avea, Cardinal Health, Inc, Dublin, OH)
• PCV+ (Dräger Medical)
• DuoPAP (Hamilton).

Caution—name confusion. In North America, BiPAP (Respironics, Murrysville, PA) and BiLevel are used to refer to noninvasive modes of ventilation.

APRV has no other name.

What do these modes do?

These modes deliver pressure-controlled, time-triggered, and time-cycled breaths using a set-point targeting scheme (Table 2). This means that the ventilator maintains a constant pressure (set point) even in the face of spontaneous breaths.

Caution—source of confusion. The term continuous positive airway pressure (CPAP) is often used to describe this mode. However, CPAP is pressure that is applied continuously at the same level; the patient generates all the work to maintain ventilation (“pressure-controlled continuous spontaneous ventilation” in the current nomenclature). In APRV, the airway pressure is intermittently released and reapplied, generating a tidal volume that supports ventilation. In other words, this is a pressure-controlled breath with a very prolonged inspiratory time and a short expiratory time in which spontaneous ventilation is possible at any point (“pressure-controlled intermittent mandatory ventilation” in the current nomenclature).

How these modes are set in the ventilator may also be a source of confusion. To describe the time spent in high and low airway pressures, we use the terms T_high and T_low, respectively. By convention, the difference between APRV and biphasic mode is the duration of T_low (< 1.5 sec for APRV).

Similarly, P_high and P_low are used to describe the high and low airway pressure. To better understand this concept, you can create the same mode in conventional pressure-control ventilation by thinking of the T_high as the inspiratory time, the T_low as the expiratory time, the P_high as inspiratory pressure, and the P_low as PEEP.

Hence, APRV is an extreme form of inverse ratio ventilation, with an inspiration-to-expiration ratio of 4:1. This means a patient spends most of the time in P_high and T_high, and exhalations are short (T_low and P_low). In contrast, the biphasic mode uses conventional inspiration-expiration ratios (Figure 4).

As with any form of pressure control, the tidal volume is generated by airway pressure rising above baseline (ie, the end-expiratory value). Hence, to ensure an increase in minute ventilation, the mandatory breath rate must be increased (ie, decreasing T_high, T_low, or both) or the tidal volume must be increased (ie, increasing the difference between P_high and P_low). This means that in APRV the T_low has to happen more often (by increasing the number of breaths) or be more prolonged (allowing more air to exhale). Because unrestricted spontaneous breaths are permitted at any point of the cycle, the patient contributes to the total minute ventilation (usually 10%–40%).

In APRV and biphasic mode, the operator’s set time and pressure in inspiration and expiration will be delivered regardless of the patient’s breathing efforts—the patient’s spontaneous breath does not trigger a mechanical breath. Some ventilators have automatic adjustments to improve the trigger synchrony.

Ventilator settings in APRV and biphasic mode

These modes require the setting of two pressure levels (P_high and P_low) and two time durations (T_high and T_low). One can add pressure support or automatic tube compensation to assist spontaneous breaths. The difference in T_low generates differences in the T_high:T_low ratio: APRV has a short T_low (an inspiration-expiration ratio of 4:1). Biphasic mode has a conventional inspiration-expiration ratio of 1:1 to 1:4.

Clinical applications

APRV is used in acute lung injury and ARDS. This mode should be used with caution or not at all in patients with obstructive lung disease or inappropriately increased respiratory drive.^32–35

Biphasic mode is intended for both ventilation and weaning. In a patient who has poor respiratory effort or who is paralyzed, biphasic is identical to pressure-control/continuous mandatory ventilation.

Theoretical benefits of APRV and biphasic mode

Multiple benefits have been ascribed to these modes. In theory, APRV will maximize and maintain alveolar recruitment, improve oxygenation, lower inflation pressures, and decrease overinflation. Both APRV and biphasic, by preserving spontaneous breathing, will improve ventilation-perfusion matching and gas diffusion, improve the hemodynamic profile (less need for vasopressors, higher cardiac output, reduced ventricular workload, improved organ perfusion), and improve synchrony (decrease the work of breathing and the need for sedation).

Evidence of benefit of APRV and biphasic mode

APRV and biphasic are different modes. However studies evaluating their effects are combined. This is in part the result of the nomenclature confusion and different practice in different countries.³⁶

Physiologic benefits. In studies, spontaneous breaths contributed to 10% to 40% of minute ventilation,^37,38 improved ventilation of dependent areas of the lung, improved ventilation-perfusion match and recruitment,³⁹ and improved hemodynamic profile.⁴⁰

Patient comfort. These modes are thought to decrease the need for analgesia and sedation,³⁸ but a recent trial showed no difference with pressure-controlled intermittent mandatory ventilation.⁴¹ Patient ventilator synchrony and comfort have not been studied.^32,42

Outcomes. In small trials, these modes made no difference in terms of deaths, but they may decrease the length of mechanical ventilation.^38,41,43,44

APRV and biphasic mode: Bottom line

Maintaining spontaneous breathing while on mechanical ventilation has hemodynamic and ventilatory benefits.

APRV and biphasic mode are not the same thing. APRV’s main goal is to maximize mean airway pressure and, hence, lung recruitment, whereas the main goal of the biphasic mode is synchrony.

There is a plethora of ventilator settings and questions related to physiologic effects.^33,34,36

Although these modes are widely used in some centers, there is no evidence yet that they are superior to conventional volume- or pressure-control ventilation with low tidal volume for ARDS and acute lung injury. There is no conclusive evidence that these modes improve synchrony, time to weaning, or patient comfort.

 

HIGH-FREQUENCY OSCILLATORY VENTILATION

High-frequency oscillatory ventilation (HFOV) was first described and patented in 1952 by Emerson and was clinically developed in the early 1970s by Lunkenheimer.⁴⁵

The goal of HFOV is to minimize lung injury; its characteristics (discussed below) make it useful in patients with severe ARDS. The US Food and Drug Administration approved it for infants in 1991 and for children in 1995. The adult model has been available since 1993, but it was not approved until 2001 (SensorMedics 3100B, Cardinal Health, Inc).

Other names for high-frequency oscillatory ventilation

While HFOV has no alternative names, the following acronyms describe similar modes:

• HFPPV (high-frequency positive pressure ventilation)
• HFJV (high-frequency jet ventilation)
• HFFI (high-frequency flow interruption)
• HFPV (high-frequency percussive ventilation)
• HFCWO (high-frequency chest wall oscillation).

All of these modes require different specialized ventilators.

What does high-frequency oscillatory ventilation do?

Conceptually, HFOV is a form of pressure-controlled intermittent mandatory ventilation with a set-point control scheme. In contrast to conventional pressure-controlled intermittent mandatory ventilation, in which relatively small spontaneous breaths may be superimposed on relatively large mandatory breaths, HFOV superimposes very small mandatory breaths (oscillations) on top of spontaneous breaths.

HFOV can be delivered only with a special ventilator. The ventilator delivers a constant flow (bias flow), while a valve creates resistance to maintain airway pressure, on top of which a piston pump oscillates at frequencies of 3 to 15 Hz (160–900 breaths/minute). This creates a constant airway pressure with small oscillations (Figure 5); often, clinicians at the bedside look for the “chest wiggle” to assess the appropriate amplitude settings, although this has not been systematically studied.

Adult patients are usually paralyzed or deeply sedated, since deep spontaneous breathing will trigger alarms and affect ventilator performance.

To manage ventilation (CO₂ clearance), one or several of the following maneuvers can be done: decrease the oscillation frequency, increase the amplitude of the oscillations, increase the inspiratory time, or increase bias flow (while allowing an endotracheal tube cuff leak). Oxygenation adjustments are controlled by manipulating the mean airway pressure and the Fio₂.

Ventilator settings in high-frequency oscillatory ventilation

Ventilator settings in HFOV are⁴⁶:

• Airway pressure amplitude (delta P or power)
• Mean airway pressure
• Percent inspiration
• Inspiratory bias flow
• Fio₂.

Clinical applications of high-frequency oscillatory ventilation

This mode is usually reserved for ARDS patients for whom conventional ventilation is failing. A recently published protocol⁴⁶ suggests considering HFOV when there is oxygenation failure (Fio₂ ≥ 0.7 and PEEP ≥ 14 cm H₂O) or ventilation failure (pH < 7.25 with tidal volume ≥ 6 mL/kg predicted body weight and plateau airway pressure ≥ 30 cm H₂O).

This mode is contraindicated when there is known severe airflow obstruction or intracranial hypertension.

Theoretical benefits of high-frequency oscillatory ventilation

Conceptually, HFOV can provide the highest mean airway pressure paired with the lowest tidal volume of any mode. These benefits might make HFOV the ideal lung-protective ventilation strategy.

Evidence of benefit of high-frequency oscillatory ventilation

Physiologic benefits. Animal models have shown less histologic damage and lung inflammation with HFOV than with high-tidal-volume conventional ventilation^47,48 and low-tidal-volume conventional ventilation.⁴⁹

Patient comfort has not been studied. However, current technology does impose undue work of breathing in spontaneously breathing patients.⁵⁰

Outcomes. Several retrospective case series have described better oxygenation with HFOV as rescue therapy for severe ARDS than with conventional mechanical ventilation. Two randomized controlled trials have studied HFOV vs high-tidal-volume conventional mechanical ventilation for early severe ARDS; HFOV was safe but made no difference in terms of deaths.^42,51–54

High-frequency oscillatory ventilation: Bottom line

In theory, HFOV provides all the benefits of an ideal lung-protective strategy, at least for paralyzed or deeply sedated patients. Animal studies support these concepts. In human adults, HFOV has been shown to be safe and to provide better oxygenation but no improvement in death rates compared with conventional mechanical ventilation. Currently, HFOV is better reserved for patients with severe ARDS for whom conventional mechanical ventilation is failing.

Telemetry—from the Greek words tele (remote) and metron (measure)—for cardiac monitoring was developed in the mid-1960s by Spacelabs Medical for use in spaceflight.¹ The system was later adopted in hospitals to detect life-threatening arrhythmias.

Guidelines for the use of telemetry were published in 1991 by the American College of Cardiology (ACC)² in response to concerns raised by its increasing use in noncritical care settings during the 30 years after its introduction to clinical medicine. The latest revision of the guidelines was published in 2004 by the American Heart Association (AHA).³

However, the guidelines are based largely on expert opinion and on research data in electrocardiography. Few clinical trials of telemetry have been published, and they were either retrospective or nonrandomized. In fact, there were no published randomized trials at the time the 2004 guidelines were written. Moreover, very few of these studies evaluated the impact of cardiac telemetry monitoring on physician management decisions.

We reviewed the literature to find out how cardiac telemetry is being used in clinical practice and how it might be used more selectively. The literature search was performed using Ovid MEDLINE (1996 to present) and PubMed Central using the key search terms “cardiac monitoring,” “telemetry monitoring,” “telemetry,” and “inpatient.” References from articles identified using Ovid MEDLINE (1996 to present) and PubMed Central that were relevant to our review were also included.

THREE CLASSES OF RISK

Both the ACC and the AHA guidelines divide patients into three classes on the basis of clinical conditions.^2,3

• 
  Class I consists of patients at significant risk of an immediate life-threatening arrhythmia, and cardiac monitoring is indicated for almost all of them (Table 1).
• Class II consists of patients for whom cardiac monitoring may be of benefit in some cases but is not essential for all (Table 2).
• 
  Class III consists of patients at low risk or otherwise unlikely to benefit from cardiac monitoring, and for whom it is not indicated (Table 3).

PATIENTS AT LOW RISK DO NOT BENEFIT

Telemetry monitoring has become an essential and commonly used clinical tool in most hospital systems. However, physicians do not seem to be using the risk stratification guidelines routinely or appropriately. The result is that many patients are being monitored needlessly, because telemetric monitoring neither affects how patients at low risk are managed nor improves their clinical outcomes.

Saleem et al⁴ reported that, of 105 patients at low risk who presented with chest pain and were admitted to a telemetry unit, none experienced a cardiac event or arrhythmia warranting changes in management while in the hospital.

Durairaj et al⁵ conducted a prospective cohort study of 1,033 patients admitted consecutively from an emergency department to an inpatient telemetry unit from July 1998 to January 1999. Patients were initially stratified according to a prediction model proposed by Goldman et al⁶ into groups at high, moderate, low, and very low risk. The risk groups were substratified according to the presence or absence of chest pain. The outcomes measured were transfer to an intensive care unit and a major cardiac complication, which included acute myocardial infarction, cardiac arrest, ventricular fibrillation, temporary pacemaker implantation, cardiogenic shock, emergency cardioversion, use of an intraaortic balloon assist device, intubation, and recurrent ischemic pain requiring coronary revascularization within 72 hours after admission or requiring cardiac catheterization followed by coronary revascularization before discharge from the hospital. The subgroup of patients who were classified as being at very low risk and who did not have chest pain (n = 318) did not experience any major cardiac complication.

Sivaram and colleagues⁷ studied the role of telemetric monitoring in the management of patients with class I, II, and III indications for telemetric monitoring outside of critical care units. The class was assigned at the time of discharge for the purpose of the study. A total of 297 telemetry events were noted during the study, but only 12 (4%) of the events led to changes in patient management: a change in medication in 8 patients, cardioversion for unstable atrial flutter in 1 patient, insertion of a pacemaker for sinus pause in 1, and electrophysiology studies in 2 patients.

Estrada et al⁸ examined the clinical outcomes of 2,240 patients admitted to a non-intensive care unit. The physicians perceived telemetric monitoring as helpful in 283 (12.6%) of the patients. However, data obtained from telemetry monitoring directly affected management decisions in only 156 patients (7% of the original study population). The researchers concluded that physicians may overestimate the role of telemetry in guiding patient management.

Hollander et al⁹ examined the outcomes of 261 patients admitted because of chest pain who had normal or nonspecific findings on electrocardiography on presentation. Only 4 patients (1.5%) experienced arrhythmias. The authors concluded that the policy of admitting patients at low risk to monitored beds should be reevaluated.

Snider et al¹⁰ showed that patients presenting with atypical chest pain and normal electrocardiographic findings were at low risk of arrhythmias and did not benefit from telemetric monitoring.

Schull and Redelmeier¹¹ performed a 5-year observational study in which they reviewed all telemetry admissions (N = 8,932) to a tertiary care facility. Twenty patients experienced cardiac arrest during the study period, but telemetric monitoring was in use at the time in only 16 of the 20. Furthermore, the telemetry monitors signalled the onset of cardiac arrest in only 9 of these 16 patients. Three of the patients whose hearts stopped beating survived until discharge: two in whom telemetry actually signalled the onset of cardiac arrest and one in whom it did not.

 

TELEMETRY CAN GIVE FALSE-POSITIVE ALARMS

Inappropriate use of telemetric monitoring increases the chance of artifacts or false-positive rhythms being misinterpreted as dysrhythmias and can potentially lead to errors in management.

Cases have been reported of patients undergoing invasive procedures because of artifacts seen during telemetric monitoring. Knight et al¹² described 12 patients who underwent unnecessary diagnostic or therapeutic interventions as a result of misdiagnosis of artifacts as ventricular tachycardia.

We did not discover in our review any data correlating the frequency of false-positive telemetric monitoring findings to management errors. On the other hand, it is also not possible to discern from these studies how often cardiac telemetric monitoring reaffirmed the clinical impression and facilitated ongoing therapy.

TELEMETRY IS EXPENSIVE

Telemetry requires specialized equipment and trained personnel, making it both costly and labor-intensive. The additional costs and cost-effectiveness of telemetry remain uncertain. Studies of its medical costs have found wide variations across different hospital systems. Sivaram et al,⁷ in an observational study published in 1998, estimated the cost per patient at $683. At our hospital, the current cost of telemetric monitoring is at least $1,400 per patient per 24 hours.

Whatever the true cost, inappropriate use of telemetry creates a financial burden on the health care system and adds to unnecessary costs incurred by patients.

POTENTIAL BARRIERS TO APPROPRIATE USE OF TELEMETRY

A number of factors contribute to the inappropriate use of telemetry. Possible causes for its overuse may be a lack of awareness of the ACC and AHA guidelines, nonadherence to the guidelines, or a combination of factors.

Even when physicians are aware of these guidelines, adherence may be suboptimal for a variety of reasons (reviewed by Mehta¹³). Adams et al¹⁴ revealed that most studies evaluating adherence were biased by overreporting, since the levels of adherence were self-reported.

OUR RECOMMENDATIONS

To improve on the appropriate use of telemetry, we recommend that several strategies be implemented.

Current guidelines for in-hospital cardiac monitoring need to be updated, particularly since the recommendations were based on evidence that is several decades old. Also, medical care has improved since the publication of the last guidelines, justifying an update in the guidelines.

Guidelines for cardiac monitoring should be incorporated into the curriculum for physician education to increase awareness of the guidelines. Hospitals should ensure that the emergency medicine staff is educated with regard to ensuring appropriateness of admissions to telemetry units.

Finally, the implementation of predictive models similar to that developed by Goldman et al⁶ and implemented in the study by Durairaj⁵ could help to ensure that cardiac telemetry is reserved for patients who will benefit from it the most.

Telemetry—from the Greek words tele (remote) and metron (measure)—for cardiac monitoring was developed in the mid-1960s by Spacelabs Medical for use in spaceflight.¹ The system was later adopted in hospitals to detect life-threatening arrhythmias.

Guidelines for the use of telemetry were published in 1991 by the American College of Cardiology (ACC)² in response to concerns raised by its increasing use in noncritical care settings during the 30 years after its introduction to clinical medicine. The latest revision of the guidelines was published in 2004 by the American Heart Association (AHA).³

However, the guidelines are based largely on expert opinion and on research data in electrocardiography. Few clinical trials of telemetry have been published, and they were either retrospective or nonrandomized. In fact, there were no published randomized trials at the time the 2004 guidelines were written. Moreover, very few of these studies evaluated the impact of cardiac telemetry monitoring on physician management decisions.

We reviewed the literature to find out how cardiac telemetry is being used in clinical practice and how it might be used more selectively. The literature search was performed using Ovid MEDLINE (1996 to present) and PubMed Central using the key search terms “cardiac monitoring,” “telemetry monitoring,” “telemetry,” and “inpatient.” References from articles identified using Ovid MEDLINE (1996 to present) and PubMed Central that were relevant to our review were also included.

THREE CLASSES OF RISK

Both the ACC and the AHA guidelines divide patients into three classes on the basis of clinical conditions.^2,3

• 
  Class I consists of patients at significant risk of an immediate life-threatening arrhythmia, and cardiac monitoring is indicated for almost all of them (Table 1).
• Class II consists of patients for whom cardiac monitoring may be of benefit in some cases but is not essential for all (Table 2).
• 
  Class III consists of patients at low risk or otherwise unlikely to benefit from cardiac monitoring, and for whom it is not indicated (Table 3).

PATIENTS AT LOW RISK DO NOT BENEFIT

Telemetry monitoring has become an essential and commonly used clinical tool in most hospital systems. However, physicians do not seem to be using the risk stratification guidelines routinely or appropriately. The result is that many patients are being monitored needlessly, because telemetric monitoring neither affects how patients at low risk are managed nor improves their clinical outcomes.

Saleem et al⁴ reported that, of 105 patients at low risk who presented with chest pain and were admitted to a telemetry unit, none experienced a cardiac event or arrhythmia warranting changes in management while in the hospital.

Durairaj et al⁵ conducted a prospective cohort study of 1,033 patients admitted consecutively from an emergency department to an inpatient telemetry unit from July 1998 to January 1999. Patients were initially stratified according to a prediction model proposed by Goldman et al⁶ into groups at high, moderate, low, and very low risk. The risk groups were substratified according to the presence or absence of chest pain. The outcomes measured were transfer to an intensive care unit and a major cardiac complication, which included acute myocardial infarction, cardiac arrest, ventricular fibrillation, temporary pacemaker implantation, cardiogenic shock, emergency cardioversion, use of an intraaortic balloon assist device, intubation, and recurrent ischemic pain requiring coronary revascularization within 72 hours after admission or requiring cardiac catheterization followed by coronary revascularization before discharge from the hospital. The subgroup of patients who were classified as being at very low risk and who did not have chest pain (n = 318) did not experience any major cardiac complication.

Sivaram and colleagues⁷ studied the role of telemetric monitoring in the management of patients with class I, II, and III indications for telemetric monitoring outside of critical care units. The class was assigned at the time of discharge for the purpose of the study. A total of 297 telemetry events were noted during the study, but only 12 (4%) of the events led to changes in patient management: a change in medication in 8 patients, cardioversion for unstable atrial flutter in 1 patient, insertion of a pacemaker for sinus pause in 1, and electrophysiology studies in 2 patients.

Estrada et al⁸ examined the clinical outcomes of 2,240 patients admitted to a non-intensive care unit. The physicians perceived telemetric monitoring as helpful in 283 (12.6%) of the patients. However, data obtained from telemetry monitoring directly affected management decisions in only 156 patients (7% of the original study population). The researchers concluded that physicians may overestimate the role of telemetry in guiding patient management.

Hollander et al⁹ examined the outcomes of 261 patients admitted because of chest pain who had normal or nonspecific findings on electrocardiography on presentation. Only 4 patients (1.5%) experienced arrhythmias. The authors concluded that the policy of admitting patients at low risk to monitored beds should be reevaluated.

Snider et al¹⁰ showed that patients presenting with atypical chest pain and normal electrocardiographic findings were at low risk of arrhythmias and did not benefit from telemetric monitoring.

Schull and Redelmeier¹¹ performed a 5-year observational study in which they reviewed all telemetry admissions (N = 8,932) to a tertiary care facility. Twenty patients experienced cardiac arrest during the study period, but telemetric monitoring was in use at the time in only 16 of the 20. Furthermore, the telemetry monitors signalled the onset of cardiac arrest in only 9 of these 16 patients. Three of the patients whose hearts stopped beating survived until discharge: two in whom telemetry actually signalled the onset of cardiac arrest and one in whom it did not.

 

TELEMETRY CAN GIVE FALSE-POSITIVE ALARMS

Inappropriate use of telemetric monitoring increases the chance of artifacts or false-positive rhythms being misinterpreted as dysrhythmias and can potentially lead to errors in management.

Cases have been reported of patients undergoing invasive procedures because of artifacts seen during telemetric monitoring. Knight et al¹² described 12 patients who underwent unnecessary diagnostic or therapeutic interventions as a result of misdiagnosis of artifacts as ventricular tachycardia.

We did not discover in our review any data correlating the frequency of false-positive telemetric monitoring findings to management errors. On the other hand, it is also not possible to discern from these studies how often cardiac telemetric monitoring reaffirmed the clinical impression and facilitated ongoing therapy.

TELEMETRY IS EXPENSIVE

Telemetry requires specialized equipment and trained personnel, making it both costly and labor-intensive. The additional costs and cost-effectiveness of telemetry remain uncertain. Studies of its medical costs have found wide variations across different hospital systems. Sivaram et al,⁷ in an observational study published in 1998, estimated the cost per patient at $683. At our hospital, the current cost of telemetric monitoring is at least $1,400 per patient per 24 hours.

Whatever the true cost, inappropriate use of telemetry creates a financial burden on the health care system and adds to unnecessary costs incurred by patients.

POTENTIAL BARRIERS TO APPROPRIATE USE OF TELEMETRY

A number of factors contribute to the inappropriate use of telemetry. Possible causes for its overuse may be a lack of awareness of the ACC and AHA guidelines, nonadherence to the guidelines, or a combination of factors.

Even when physicians are aware of these guidelines, adherence may be suboptimal for a variety of reasons (reviewed by Mehta¹³). Adams et al¹⁴ revealed that most studies evaluating adherence were biased by overreporting, since the levels of adherence were self-reported.

OUR RECOMMENDATIONS

To improve on the appropriate use of telemetry, we recommend that several strategies be implemented.

Current guidelines for in-hospital cardiac monitoring need to be updated, particularly since the recommendations were based on evidence that is several decades old. Also, medical care has improved since the publication of the last guidelines, justifying an update in the guidelines.

Guidelines for cardiac monitoring should be incorporated into the curriculum for physician education to increase awareness of the guidelines. Hospitals should ensure that the emergency medicine staff is educated with regard to ensuring appropriateness of admissions to telemetry units.

Finally, the implementation of predictive models similar to that developed by Goldman et al⁶ and implemented in the study by Durairaj⁵ could help to ensure that cardiac telemetry is reserved for patients who will benefit from it the most.

Telemetry—from the Greek words tele (remote) and metron (measure)—for cardiac monitoring was developed in the mid-1960s by Spacelabs Medical for use in spaceflight.¹ The system was later adopted in hospitals to detect life-threatening arrhythmias.

Guidelines for the use of telemetry were published in 1991 by the American College of Cardiology (ACC)² in response to concerns raised by its increasing use in noncritical care settings during the 30 years after its introduction to clinical medicine. The latest revision of the guidelines was published in 2004 by the American Heart Association (AHA).³

However, the guidelines are based largely on expert opinion and on research data in electrocardiography. Few clinical trials of telemetry have been published, and they were either retrospective or nonrandomized. In fact, there were no published randomized trials at the time the 2004 guidelines were written. Moreover, very few of these studies evaluated the impact of cardiac telemetry monitoring on physician management decisions.

We reviewed the literature to find out how cardiac telemetry is being used in clinical practice and how it might be used more selectively. The literature search was performed using Ovid MEDLINE (1996 to present) and PubMed Central using the key search terms “cardiac monitoring,” “telemetry monitoring,” “telemetry,” and “inpatient.” References from articles identified using Ovid MEDLINE (1996 to present) and PubMed Central that were relevant to our review were also included.

THREE CLASSES OF RISK

Both the ACC and the AHA guidelines divide patients into three classes on the basis of clinical conditions.^2,3

• 
  Class I consists of patients at significant risk of an immediate life-threatening arrhythmia, and cardiac monitoring is indicated for almost all of them (Table 1).
• Class II consists of patients for whom cardiac monitoring may be of benefit in some cases but is not essential for all (Table 2).
• 
  Class III consists of patients at low risk or otherwise unlikely to benefit from cardiac monitoring, and for whom it is not indicated (Table 3).

PATIENTS AT LOW RISK DO NOT BENEFIT

Telemetry monitoring has become an essential and commonly used clinical tool in most hospital systems. However, physicians do not seem to be using the risk stratification guidelines routinely or appropriately. The result is that many patients are being monitored needlessly, because telemetric monitoring neither affects how patients at low risk are managed nor improves their clinical outcomes.

Saleem et al⁴ reported that, of 105 patients at low risk who presented with chest pain and were admitted to a telemetry unit, none experienced a cardiac event or arrhythmia warranting changes in management while in the hospital.

Durairaj et al⁵ conducted a prospective cohort study of 1,033 patients admitted consecutively from an emergency department to an inpatient telemetry unit from July 1998 to January 1999. Patients were initially stratified according to a prediction model proposed by Goldman et al⁶ into groups at high, moderate, low, and very low risk. The risk groups were substratified according to the presence or absence of chest pain. The outcomes measured were transfer to an intensive care unit and a major cardiac complication, which included acute myocardial infarction, cardiac arrest, ventricular fibrillation, temporary pacemaker implantation, cardiogenic shock, emergency cardioversion, use of an intraaortic balloon assist device, intubation, and recurrent ischemic pain requiring coronary revascularization within 72 hours after admission or requiring cardiac catheterization followed by coronary revascularization before discharge from the hospital. The subgroup of patients who were classified as being at very low risk and who did not have chest pain (n = 318) did not experience any major cardiac complication.

Sivaram and colleagues⁷ studied the role of telemetric monitoring in the management of patients with class I, II, and III indications for telemetric monitoring outside of critical care units. The class was assigned at the time of discharge for the purpose of the study. A total of 297 telemetry events were noted during the study, but only 12 (4%) of the events led to changes in patient management: a change in medication in 8 patients, cardioversion for unstable atrial flutter in 1 patient, insertion of a pacemaker for sinus pause in 1, and electrophysiology studies in 2 patients.

Estrada et al⁸ examined the clinical outcomes of 2,240 patients admitted to a non-intensive care unit. The physicians perceived telemetric monitoring as helpful in 283 (12.6%) of the patients. However, data obtained from telemetry monitoring directly affected management decisions in only 156 patients (7% of the original study population). The researchers concluded that physicians may overestimate the role of telemetry in guiding patient management.

Hollander et al⁹ examined the outcomes of 261 patients admitted because of chest pain who had normal or nonspecific findings on electrocardiography on presentation. Only 4 patients (1.5%) experienced arrhythmias. The authors concluded that the policy of admitting patients at low risk to monitored beds should be reevaluated.

Snider et al¹⁰ showed that patients presenting with atypical chest pain and normal electrocardiographic findings were at low risk of arrhythmias and did not benefit from telemetric monitoring.

Schull and Redelmeier¹¹ performed a 5-year observational study in which they reviewed all telemetry admissions (N = 8,932) to a tertiary care facility. Twenty patients experienced cardiac arrest during the study period, but telemetric monitoring was in use at the time in only 16 of the 20. Furthermore, the telemetry monitors signalled the onset of cardiac arrest in only 9 of these 16 patients. Three of the patients whose hearts stopped beating survived until discharge: two in whom telemetry actually signalled the onset of cardiac arrest and one in whom it did not.

 

TELEMETRY CAN GIVE FALSE-POSITIVE ALARMS

Inappropriate use of telemetric monitoring increases the chance of artifacts or false-positive rhythms being misinterpreted as dysrhythmias and can potentially lead to errors in management.

Cases have been reported of patients undergoing invasive procedures because of artifacts seen during telemetric monitoring. Knight et al¹² described 12 patients who underwent unnecessary diagnostic or therapeutic interventions as a result of misdiagnosis of artifacts as ventricular tachycardia.

We did not discover in our review any data correlating the frequency of false-positive telemetric monitoring findings to management errors. On the other hand, it is also not possible to discern from these studies how often cardiac telemetric monitoring reaffirmed the clinical impression and facilitated ongoing therapy.

TELEMETRY IS EXPENSIVE

Telemetry requires specialized equipment and trained personnel, making it both costly and labor-intensive. The additional costs and cost-effectiveness of telemetry remain uncertain. Studies of its medical costs have found wide variations across different hospital systems. Sivaram et al,⁷ in an observational study published in 1998, estimated the cost per patient at $683. At our hospital, the current cost of telemetric monitoring is at least $1,400 per patient per 24 hours.

Whatever the true cost, inappropriate use of telemetry creates a financial burden on the health care system and adds to unnecessary costs incurred by patients.

POTENTIAL BARRIERS TO APPROPRIATE USE OF TELEMETRY

A number of factors contribute to the inappropriate use of telemetry. Possible causes for its overuse may be a lack of awareness of the ACC and AHA guidelines, nonadherence to the guidelines, or a combination of factors.

Even when physicians are aware of these guidelines, adherence may be suboptimal for a variety of reasons (reviewed by Mehta¹³). Adams et al¹⁴ revealed that most studies evaluating adherence were biased by overreporting, since the levels of adherence were self-reported.

OUR RECOMMENDATIONS

To improve on the appropriate use of telemetry, we recommend that several strategies be implemented.

Current guidelines for in-hospital cardiac monitoring need to be updated, particularly since the recommendations were based on evidence that is several decades old. Also, medical care has improved since the publication of the last guidelines, justifying an update in the guidelines.

Guidelines for cardiac monitoring should be incorporated into the curriculum for physician education to increase awareness of the guidelines. Hospitals should ensure that the emergency medicine staff is educated with regard to ensuring appropriateness of admissions to telemetry units.

Finally, the implementation of predictive models similar to that developed by Goldman et al⁶ and implemented in the study by Durairaj⁵ could help to ensure that cardiac telemetry is reserved for patients who will benefit from it the most.

 

Supplement Editors:
Deepak L. Bhatt, MD, MPH, and W. Frank Peacock, MD

Contents

Importance of platelets and platelet response in acute coronary syndromes
Kandice Kottke-Marchant, MD, PhD

Novel antiplatelet strategies in acute coronary syndromes
Marc S. Sabatine, MD, MPH

The current state of antiplatelet therapy in acute coronary syndromes: The data and the real word
John H. Alexander, MD, MHSc

Platelet response in practice: Applying new insights and tools for testing and treatment
Deepak L. Bhatt, MD, MPH; Kandice Kottke-Marchant, MD, PhD; John H. Alexander, MD, MHSc; W. Frank Peacock, MD; and Marc S. Sabatine, MD, MPH

 

Supplement Editors:
Deepak L. Bhatt, MD, MPH, and W. Frank Peacock, MD

Contents

Importance of platelets and platelet response in acute coronary syndromes
Kandice Kottke-Marchant, MD, PhD

Novel antiplatelet strategies in acute coronary syndromes
Marc S. Sabatine, MD, MPH

The current state of antiplatelet therapy in acute coronary syndromes: The data and the real word
John H. Alexander, MD, MHSc

Platelet response in practice: Applying new insights and tools for testing and treatment
Deepak L. Bhatt, MD, MPH; Kandice Kottke-Marchant, MD, PhD; John H. Alexander, MD, MHSc; W. Frank Peacock, MD; and Marc S. Sabatine, MD, MPH

 

Supplement Editors:
Deepak L. Bhatt, MD, MPH, and W. Frank Peacock, MD

Contents

Importance of platelets and platelet response in acute coronary syndromes
Kandice Kottke-Marchant, MD, PhD

Novel antiplatelet strategies in acute coronary syndromes
Marc S. Sabatine, MD, MPH

The current state of antiplatelet therapy in acute coronary syndromes: The data and the real word
John H. Alexander, MD, MHSc

Platelet response in practice: Applying new insights and tools for testing and treatment
Deepak L. Bhatt, MD, MPH; Kandice Kottke-Marchant, MD, PhD; John H. Alexander, MD, MHSc; W. Frank Peacock, MD; and Marc S. Sabatine, MD, MPH