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TECHNICAL CORNER: DETERMINING RISE TIME AND OTHER PAP DEVICE
SETTINGS IN RELATION TO THE PATIENT'S RESPIRATORY CYCLE AND
PATHOPHYSIOLOGY By Will Eckhardt, BS, RST, RPSGT, CRT
T
he act of ventilation moves gas into and out of the alveoli
facilitating exchange of gases at the alveolar capillary
membrane and respiratory bronchioles. Without this gas exchange,
respiration (process of gas molecules moving at the cellular level)
would essentially not be possible. The respiratory cycle moves a
volume of air in and out of the airways and lungs; this volume is
one’s tidal volume. Achieving ventilation has a cost: the energy
required to ventilate the alveoli or work of breathing (WOB).
Two components of this workload are elastic work or compliance,
and resistive work due to the air molecules flowing through the
airways. This article will discuss what these components are and
how these forces along with disease process (pathophysiology)
of the patient determines how we might set respiratory cycle
parameters of the positive airway pressure (PAP) device used for
the patient.
Air flows from a region of high pressure to one of a lesser
pressure. Ventilation stops when alveolar gas pressure is equal to
the atmospheric pressure (e.g., at end expiration). During inhalation the muscles of ventilation cause the chest cavity to enlarge,
creating a greater degree of negative or subatmospheric intrathoracic pressure. Normally the lung (other than during exhalation)
is somewhat subatmospheric due to the forces of elastic recoil.
The lowering of intrathoracic pressure invites the expansion of the
alveoli making the exchange of gases possible, presuming the capillaries are filled with blood from a viable pulmonary circulation.
Upon end inspiration, normally the muscles of inspiration
relax and the elastic tissues of the lungs and thorax recoil causing
a positive pressure within. This pressure becomes greater than
atmospheric, expelling a quantity of the total lung volume termed
the tidal volume (VT). In some lung diseases active contraction of
expiratory muscles must be used, but in normal physiology exhalation is passive.
The term compliance is used to describe the forces produced by
the elastic properties of the lung and thorax. Compliance can be
decreased in the patient with lung disease. Decreasing compliance
causes an increase in the work of breathing (increasing muscular
work for adequate ventilation). Patients with reduced compliance
usually increase their respiratory rate to compensate for a decrease
in tidal volume.
Airway resistance is related to friction, whether it is between the
gas molecules as the gas flows through the airways and lungs or as
the molecules collide with the airway walls. When the airways are
unrestricted, the flow is usually laminar. Laminar flow is related
to the viscosity of the gas, the distance within the airways and
lungs, and inversely related to the radius of the lumen (size of the
tube). Turbulent flow, however, is proportional to the square of the
volume flow and the density of the gas and not related to viscosity. A smooth, straight tube will have turbulence only at high flow
rates. Acute and chronic conditions may exacerbate turbulence
within the airway; tumors, mucus, bronchoconstriction, airway
collapse and increased respiratory rate. When there is increased
airway resistance during expiration, the full tidal volume may not
have time to be completely exhaled; this will lead to an increas-
ing volume in the lungs at end expiration, thereby hampering gas
exchange. Giving more time for expiration will allow the return to
a normal expiratory volume. If not given this time, the patient may
exhibit a more active exhalation, increasing the work of breathing.
Increasing work of breathing will cost the patient in increased
oxygen consumption and possible ventilatory failure.
The act of ventilation (movement of gases during inspiration and
expiration) is a dynamic process aiding alveolar ventilation (volume
of oxygenated air entering the alveoli). If we breathe in a volume only
equal to that of the conducting airways, there would be no alveolar
ventilation. The air in the conducting airways is termed “dead
space” (dead space also includes unperfused alveoli). In the normal
adult, dead space is about 150 ml. This 150 ml is the first air to
reach the alveoli upon inspiration. If the tidal volume in a breath is
500ml and the dead space is 150 ml, the alveolar ventilation equals
350 ml. During expiration the first air leaving the body is the dead
space, followed by air that was actively used in respiration. Large
tidal volumes cause a larger volume to enter the alveoli, whereas
shallow breathing causes a smaller portion of the tidal volume to
enter the alveoli. This pulmonary ventilation must supply adequate
oxygen for the cells to use and remove the carbon dioxide produced by metabolic activity of the body.
Some parameters used in ventilation by some PAP devices are:
Respiratory Rate (RR), Tidal volume (VT), Rise Time, Inspiratory Time (Ti), Expiratory Time, I:E Ratio, and Pressure Support.
See Figure 1.
Respiratory rate settings are generally set a couple of breaths
lower than the patient’s normal respiratory rate. This enables
the machine to cycle when the time between breaths lengthens
beyond what the algorithm calculates is needed to maintain the
prescribed respiratory rate.
Rise time is the time it takes the pressure on a PAP device to
move from the expiratory PAP (EPAP) pressure to the inspiratory
PAP (IPAP) pressure; there would be no rise time on a CPAP
device as the pressure is constant. More on rise time to follow.
Inspiratory Time is the time over which the device is in the
inspiratory phase. Expiratory time is the time in which the device
is in the expiratory phase of a breath cycle. I:E Ratio is inspiratory
time plus the inspiratory pause time:expiration. In a normal adult
this is usually set to 1:2.
• I:E ratio
„„ = (inspiratory time + inspiratory pause time) :expiration
„„ usually set to 1:2 to mimic usual pattern of breathing
• In general longer inspiratory times:
„„ improve oxygenation by:
• increasing the mean airway pressure (longer period of high pressure increases mean airway pressure over the entire respiratory cycle)
• allowing re-distribution of gas from more compliant
alveoli to less compliant alveoli
„„ present potential problems such as:
• increased risk of gas trapping, intrinsic PEEP and
barotrauma due to reducing expiratory time
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• ventilation is less well tolerated by the patient,
necessitating a deeper level of sedation
• Pressure Support is determined by the difference between the
settings for IPAP and EPAP
FIGURE 1. POSITIVE AIRWAY PRESSURE (PAP) AND THE
RESPIRATORY CYCLE.
In patients with purely obstructive lung disease (e.g. COPD), resistive work increases without a change in elastic work. In purely
restrictive lung disease (e.g. Kyphoscoliosis), elastic work increases
with no change in resistive work. When setting PAP parameters,
we need to evaluate the patient’s respiratory cycle (see Figure 1)
and pathophysiology to the device settings available; one such
setting is rise time.
Rise time is the time it takes a device to change from EPAP
to IPAP. With a faster rise time, flow is greater at the beginning
of inspiration. A fast rise time can decrease dyspnea in patients
with a high respiratory drive, whereas increasing the rise time can
increase the work of breathing and decrease patient comfort. A
rise time that is too fast can cause turbulent air flow and cause
discomfort to the patient, hampering efforts toward compliance
with the therapy.
Adjustments to rise time are generally made for patient comfort. Rise time can be set to a minimum, creating a fast rise time;
or by increasing the rise time setting, we can increase the time it
takes for the pressure to go from EPAP to IPAP. In cases where
the patient has a high demand, the rise time can be set to the
minimum, giving the patient the fastest rise time. The rise time is
affected by the patient’s compliance, resistance and the difference
between the EPAP and the IPAP. The patient needs adequate
flows to prevent air hunger (the feeling of not getting adequate
ventilation as flow rates are too low); but this needs to be tempered
with decreasing the rise time and creating air turbulence causing
discomfort. An example of this setting would be settings in a
range of 1-6, with each increment corresponding to a tenth of a
second; such a setting of 3 would be 0.3 second rise time.
Gas trapping may occur with a rapid change to expiration as
the alveoli do not have time to empty before the start of the next
breath. Gas trapping may occur in COPD and asthma, and when
the setting for inspiratory time is long and therefore expiratory
time is shortened. An example of an inspiratory time setting
would be 0.5 to 3 seconds with increments of 0.1 seconds.
PAP devices trigger according to proprietary algorithms. Inspiratory positive airway pressure (IPAP) is delivered in response
to a trigger initiated by a spontaneous inspiratory effort. At end
inspiration, the equipment will cycle to expiratory positive airway
pressure (EPAP) according to the device’s algorithm.
Patients with obstructive lung disease such as COPD can
decrease the chance of barotraumas by using an expiratory time
that is somewhat protracted. In these patients, settings that
decrease minute ventilation and inspiratory time change the I:E
ratio, shortening the inspiratory time and thereby lengthening the
expiratory time (e.g., I:E ratio’s of 1:3 or 1:4). However, the effects
of this change will increase peak pressures and hypercapnia; these
side effects are usually well tolerated. VTs of 5-7 ml/kg and a faster
inspiratory flow (e.g., 80-100 L/min.) will tend to extend expiratory time and avoid breath staking or air trapping. A faster TiMax
setting allows a maximum inspiratory time that gives adequate time
for patients to exhale fully through their diseased airways.
For patients with restrictive disease (e.g., Amyotrophic Lateral
Sclerosis [ALS]), neuromuscular disorders, or deformity disorders
(e.g., Kyphoscoliosis), getting air in is more of the issue. With these
patients we can extend the inspiratory time, allowing the lungs to
more completely fill, minimizing the air hunger associated with
an abridged inhalation.
Airflow obstruction occurs in pathologies such as asthma and
COPD. To a lesser extent this is also seen in bronchiectasis, cystic
fibrosis, and bronchiolitis in which the small and large airways
often have obstructive processes. The narrowing of the airways
can diametrically increase airway resistance. The overload to the
respiratory pump muscles may cause ventilatory pump failure
with minute volumes unable to provide adequate spontaneous
minute ventilation, resulting in an inability to provide proper gas
exchange at the alveolar level. Another problem these patients
may face is air trapping caused by airway narrowing with some
alveolar regions within the patients’ lungs unable to properly
empty. The area unable to empty may overinflate upon subsequent
breaths. The best method of dealing with the hyperinflation is to
keep VT and pressures low. It is also recommended to lengthen
the expiratory time to deal with air trapping.
Getting it right for the patient is essential for compliance and
may take a number of adjustments. Patients requiring PAP therapies for ventilation issues are often not seen in a sleep laboratory
setting, giving the clinician less time to evaluate setting changes.
An understanding of how the parameters affect patients and how
differing pathophysiologies affect ventilation will make the clinician more comfortable with setting up PAP for ventilation.
PAP devices serve a more complex array of patients from ALS
and COPD to complex sleep apnea and obesity hypoventilation.
Patients often are affected by their medications (e.g., opioids), making
it difficult to adjust equipment to address patient comfort. The
individual who sets up patients in the home or long-term care environment needs to focus on the patients and interact with them to
accommodate their needs in relation to the equipment parameters.
ADDITIONAL READING
Comroe JH. The lung: clinical physiology and pulmonary function tests. Chicago: Year Book Medical Publishers; 1962.
Hlastala MP, Berger AJ. Physiology of respiration. New York:
Oxford University Press; 2001.
MacIntyre NR, Branson RD. Mechanical ventilation. St. Louis:
Saunders Elsevier; 2009.
Will Eckhardt, BS, RST, RPSGT, CRT, has been in the sleep field for
more than 20 years and is a clinical liaison for Genter Healthcare in
New Hampshire. 
A2 Zzz 21.2 | July 2012