Download Sleep Related Breathing Disorders in Congestive Heart Failure

Sleep Related Breathing Disorders In
Congestive Heart Failure
BY
AHMAD YOUNES
PROFESSOR OF THORACIC MEDICINE
Mansoura Faculty of Medicine
Monitoring of sleep and wake
• The standard parameters used to record sleep
and wake are electroencephalography (EEG),
electro-oculography (EOG), electromyography
(EMG), airflow measurement, respiratory effort
measurement, electrocardiography (ECG),
oxygen saturation, snoring monitor, and sleep
position evaluation.
• All these parameters are recorded in
polysomnography which is the gold standard
for diagnosis of Sleep disordered breathing .
Apnea: is defined as the drop in peak airflow by >90% of baseline for
10 seconds or longer and at least 90% of the event duration meet the
amplitude reduction.
• An obstructive apnea occurs when airflow is
absent or nearly absent, but ventilatory effort
persists. It is caused by complete, or near
complete, upper airway obstruction
A central apnea occurs when both airflow and ventilatory
effort are absent.
During a mixed apnea, there is an interval during which there is no
respiratory effort (ie, central apnea pattern) and an interval during
which there are obstructed respiratory efforts .
An epoch of Polysomnography
An epoch of Polysomnography
Hypopnea
• Hypopnea be scored when all of the following criteria
are met:
1- Airflow decreases at least 30 percent from baseline
2-There is diminished airflow lasting at least 10 seconds
3- at least 3 percent oxyhemoglobin desaturation .
• Apnea-hypopnea index (AHI) is the total number of
apneas and hypopneas per hour of sleep.
• Respiratory effort related arousal (RERA) is an event
characterized by increasing respiratory effort for 10
seconds or longer leading to an arousal from sleep but
does not fulfill the criteria for a hypopnea or apnea
• The respiratory disturbance index (RDI) is defined as the
number of obstructive apneas, hypopneas, and
respiratory event–related arousals (RERAs) per hour.
Types of SLEEP RELATED BREATHING DISORDES
1- Obstructive sleep apnea syndrome (OSA) in
adults is defined as either
• More than 15 apneas, hypopneas, per hour of
sleep ( AHI >15 events/hr) in an asymptomatic
patient
OR
• More than 5 apneas, hypopneas, per hour of sleep
(AHI >5 events per hour) in a patient with
symptoms (eg, sleepiness, fatigue and
inattention) or signs of disturbed sleep (snoring,
restless sleep, and respiratory pauses).
2- Central sleep apnea syndrome can defined as:
a. Study showing AHI > 5 events/hr. and
b. Central AHI > 50% of the total AHI, and
c. Central apneas or hypopneas >=5/hr., and
d. Symptoms of either excessive sleepiness or
disrupted sleep.
3- Sleep Hypoventilation Syndrome if either of the
below occur:
a-There is an increase in the arterial PaCO2 to a
value > 55 mm Hg for ≥ 10 minutes.
b. There is ≥ 10 mm Hg increase in PaCO2
during sleep (in comparison to an awake supine
value) to a value exceeding 50 mm Hg for ≥ 10
minutes.
OSA symptoms
OSA symptoms
OSA signs
The STOP-Bang scoring model.
In the Mallampati maneuver, patients are instructed not to emit sounds but to open
the mouth as wide as possible and protrude the tongue as far as possible.
In the modified Mallampati, the patient is instructed to open the mouth as wide as
possible without emitting sounds.
Symptoms of central sleep apnea syndrome
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Asymptomatic
Excessive sleepiness
Insomnia (repeated nocturnal awakenings)
Nocturnal sensation of dyspnea
Morning headaches
Inattention
Poor concentration
Different forms of CSAS
(1) Primary Central Sleep Apnea
(2) Central Sleep Apnea Due to Cheyne Stokes
Breathing Pattern
(3) Central Sleep Apnea Due to Medical Condition
Not Cheyne Stokes
(4) Central Sleep Apnea Due to High-Altitude
Periodic Breathing
(5) Central Sleep Apnea Due to Drug or Substance
(6) Primary Sleep Apnea of Infancy.
CSAS due to Cheyne Stokes Respiration
• Cheyne-Stokes respiration (CSR) is characterized by an
absence of air flow and respiratory effort followed by
hyperventilation in a crescendo-decrescendo pattern.
• CSR most often occurs in patients with congestive heart
failure (CHF).
• The prevalence is estimated to be approximately 30% to
40% in patients with CHF.
• This respiratory pattern can also be seen in patients with
stroke or renal failure.
• There is mounting evidence that CSAS/CSR may be an
indicator of higher morbidity and mortality in CHF patients.
• Effective treatment of CSAS/CSR might improve the
outcome of CHF patients with CSAS/CSR.
CSAS Due to Medical Condition Not Cheyne Stokes
• CSAS can occur in individuals with cardiac,
renal, and neurological disorders but without a
CSR pattern.
• This category is referred to CSAS Due to
Medical Condition Not Cheyne Stokes.
Complex sleep apnea
• CompSA is defined as a form of CSA identified
by the persistence or emergence of central
sleep apneas or hypopneas upon exposure to
CPAP or BPAP without a backup rate when
obstructive events have disappeared.
• These patients have predominantly obstructive
or mixed apneas during the diagnostic portion
of the study occurring 5/hr or more.
• With use of CPAP or BPAP without a backup
rate, they show a pattern of apneas and
hypopneas that meets the definition of CSA.
Clinical Classification of AHF
• The patient with AHF will usually present in one of six clinical
categories. Pulmonary oedema may or may not complicate the clinical
presentation.
1- Worsening or decompensated chronic HF (peripheral oedema /
congestion): there is usually a history of progressive worsening of
known chronic HF on treatment, and evidence of systemic and
pulmonary congestion. Low BP on admission is associated with a poor
prognosis.
2- Pulmonary oedema: patients present with severe respiratory distress,
tachypnoea, and orthopnoea with rales over the lung fields. SPo2 is
usually <90% on room air prior to treatment with oxygen.
3- Hypertensive HF: signs and symptoms of HF accompanied by high BP
and usually relatively preserved LV systolic function. There is evidence
of increased sympathetic tone with tachycardia and vasoconstriction.
The patients present frequently with signs of pulmonary congestion
without signs of systemic congestion. The response to appropriate
therapy is rapid, and hospital mortality is low.
Clinical Classification of AHF
4- Cardiogenic shock: is defined as evidence of tissue
hypoperfusion induced by HF after adequate correction
of preload and major arrhythmia. Typically, cardiogenic
shock is characterized by reduced systolic blood
pressure (SBP<90 mmHg or a drop of mean arterial
pressure >30 mmHg) and absent or low urine output (<
0.5 mL/kg/h). Evidence of organ hypoperfusion and
pulmonary congestion develop rapidly.
5- Isolated right HF: is characterized by a low output
syndrome in the absence of pulmonary congestion with
increased jugular venous pressure, with or without
hepatomegaly, and low LV filling pressures .
6- Acute coronary syndrome (ACS) and HF: Approximately
15% of patients with an ACS have signs and symptoms
of HF . Episodes of acute HF are frequently associated
with or precipitated by an arrhythmia (bradycardia, Atrial
fibrillation, Ventricular tachycardia).
Clinical classification of acute heart failure
Evaluation of patients with suspected AHF
Non-invasive ventilation In AHF
• NIV with positive end-expiratory pressure
(PEEP) should be considered as early as
possible in every patient with acute cardiogenic
pulmonary oedema and hypertensive AHF as it
improves clinical parameters including
respiratory distress.
• NIV with PEEP improves LV function by
reducing LV afterload.
• NIV should be used with caution in cardiogenic
shock and right ventricular failure.
Acute Cardiogenic Pulmonary Edema
• Acute cardiogenic pulmonary edema is the first
cause of acute respiratory distress worldwide.
• The initial management of patients with ACPE
address the ABCs (airways, breathing,
circulation).
• Oxygen should be adminstered to all patiients
to keep oxygen >90%.
• Any associated arrhythmia or infarction should
be treated appropriately .
Acute Cardiogenic Pulmonary Edema
Medical treatment of ACPE:
• Reduction of pulmonary venous return
(preload reduction)
• Reduction of systemic vascular resistance
(afterload reduction), and, in some cases ,
• Inotropic support
Acute Cardiogenic Pulmonary Edema
• Preload reduction decreases pulmonary capillary
hydrostatic pressure and reduces fluid transudation into
the pulmonary interstitium and alveoli.
• Afterload reduction increases cardiac output and
improves renal perfusion, which allows for diuresis in
the patient with fluid overload .
• Patients with severe LV dysfunction or acute valvular
disorders present with hypotension. These patients may
not tolerate medications to reduce their preload and
afterload. Therefore, inotropic support is necessary in
this subset of patients to maintain adequate blood
pressure .
• Patients who remain hypoxic despite supplemental
oxygenation and patients who have severe respiratory
distress require ventilatory support in addition to
maximal medical therapy .
Acute Cardiogenic Pulmonary Edema
• In patients with acute respiratory failure, standard
treatment, including diuretics, nitroglycerin,
morphine, and oxygen, may not be sufficient to
reduce respiratory distress.
• In this setting, noninvasive ventilation support
should be initiated rapidly, with the main goals to
1-Improve oxygenation,
2- Avoid invasive ventilation, and
3- Permit a sufficient period for medical therapy to
decrease pulmonary vascular congestion.
Acute Cardiogenic Pulmonary Edema
• Methods of oxygen delivery
1- Face mask
2- Noninvasive pressure-upport ventilation (which
includes BiPAP and CPAP), and
3- Intubation and mechanical ventilation
• Which method is used depends on the presence
of hypoxemia and acidosis and on the patient's
level of consciousness. For example, intubation
and mechanical ventilation may become
necessary in cases of persistent hypoxemia,
acidosis, or altered mental status .
What should be the interface?
oronasal masks -general advantage
• Best suited for less cooperative patients
• Better in patients with a higher severity of
illness
• Better for patients with mouth-breathing or
pursed-lips breathing
• Better in edentulous patients
• Generally more effective ventilation
oronasal masks -cautions, disadvantages
• Claustrophobic
• Hinder speaking and coughing
• Risk of aspiration with emesis
What should be the interface?
Nasal masks -general advantages
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Best suited for more cooperative patients
Better in patients with a lower severity of illness
Not claustrophobic
Allows speaking, drinking, coughing, and secretion
clearance
• Less aspiration risk with emesis
• Generally better tolerated
Nasal masks -cautions, disadvantages
• More leaks possible (eg, mouth-breathing or edentulous
patients)
• Effectiveness limited in patients with nasal deformities or
blocked nasal passages
What should be the interface?
• It cannot be said that any interface is clearly
superior to another in terms of important
outcomes such as intubation rate or mortality.
• An oro-nasal interface may be more effective and
better tolerated than the nasal interface for
patients with acute respiratory failure. Thus, a
sensible approach would be to start with an
oronasal mask for most patients with acute
respiratory failure, and switch to a nasal mask if
prolonged use is contemplated.
• Whichever mask is chosen, a comfortable fit is of
paramount importance, and thus using a mask of
proper size, not strapping the headgear too
tightly, and using wound care tape on the bridge
of the nose are important considerations to avoid
pressure ulcers.
Does the type of ventilator make any difference?
• NIV can be delivered through ventilators designed for
invasive mechanical ventilation (‘‘critical care
ventilators’’),and portable devices.
• Critical care ventilators are less leak tolerant and are
thus likely to sound alarms more inappropriately. But
the monitoring capabilities and presence of oxygen
blenders make it superior to portable devices.
• On the other hand, the portable ventilators are more
leak tolerant and less likely to sound alarms
inappropriately than the critical care ventilators.
However, they may promote rebreathing by virtue of
their single inspiratory and expiratory tubing
(minimized by assuring adequate expiratory pressure
and expiratory ports over the nasal bridge)
Does the type of ventilator make any difference?
• Most of the portable ventilators do not have an oxygen
blender and supplemental oxygen is usually given by
adding it into the mask or the circuit.
• Continuous pulse oximetry is required to monitor
oxygenation when using this device in patients with ACPE.
• Comparisons of the two devices show that the portable
device performs as well as the critical care ventilators.
• Recently, ventilators that deliver either invasive ventilation
or NIV have been designed. When in the non-invasive mode,
they are more leak tolerant and use only the alarms
essential for the operation of NIV.
• The choice of CPAP versus BPAP can be dictated by local
experience and patient preference, although BPAP may
have some additional benefit to those with hypercapnic
acidosis.
Where are these patients best treated?
• Patients with severe ACPE requiring NIV need to
be triaged to an environment with adequate
nurse-patient ratio, and continuous
electrocardiographic and pulse oximetry
monitoring facilities.
Do all patients with ACPE require NIV?
• Consider NIV early when treating patients with
severe ACPE.
• Several studies suggest that NIV is associated
with decreased length of stay in the ICU,
decreased need for mechanical ventilation, and
decreased hospital costs.
• A few clinical trials showed that early and
prehospital NIV treatment by paramedics is safe
and associated with faster improvement of
oxygen saturation.
• However, the mortality and the need for
intensive care did not differ between the
patients who were treated with NIV and those
who were treated with a Venturi face mask in
most of those studies.
Initial treatment algorithm in AHF
AHF treatment strategy according
to systolic blood pressure.
Venturi face mask (Air entrainment mask) The colour of the
device reflects the delivered oxygen concentration: 24%: blue;
28%: white; 31%: orange; 35%: yellow; 40%: red; 60%: green.
Do all patients with ACPE require NIV?
• Not all patients with ACPE require NIV.
• A large number of patients rapidly respond to medical
treatment and do not need additional intervention.
• NIV is likely to be beneficial in patients with more severe
forms of ACPE, especially those who present with a PH
< 7.35 ,Pao2/Fio2<200,respiratory rate > 24-30 /minute .
• Another approach is to give a trial of NIV in all patients
with ACPE who do not respond to initial medical
therapy.
• Patients should be carefully monitored and failure to
improve after 30 minutes on NIV should be an indication
for its withdrawal, with facilities for immediate
endotracheal intubation and mechanical ventilation
being readily available
CPAP and BPAP
• A randomized trial comparing CPAP, NIPPV, and
standard oxygen therapy in 1069 patients with ACPE
demonstrated no mortality benefit from noninvasive
ventilation, but improvements were seen in
symptomatology and oxygenation.
• CPAP be the preferred method employed when NIV is
used unless the patient has obstructive airway disease.
• PAP decreases the need for intubation and improves
respiratory parameters in acute respiratory failure
secondary to ACPE when compared with medical
therapy alone.
• PAP is now standard treatment for severe ACPE and is
usually initiated in the ambulance or emergency
department.
The proposed acute mechanisms for the
efficacy of PAP include:1. Increased lung volume and increased oxygen
availability
2. Reduced pulmonary atelectasis caused by edema
3. Increased intrathoracic pressure and reduced systolic
left ventricular transmural pressure, resulting in reduced
left ventricular afterload and mitral regurgitation and
increasing cardiac output
4. Bronchodilatation
5. Assistance to inspiratory muscles when inspiratory PAP
is greater than expiratory PAP (BPAP).
How should NIV be applied initially?
• The application of PAP (either CPAP or BPAP)
is an art of medicine.
• All physicians using PAP should personally
apply PAP to actually understand what the
patient is experiencing.
• You should not order a specific pressure level
for a given patient without first applying NIV and
assessing the patient’s tolerance to the device.
• Initial application of NIV requires careful
instruction of the patient, with a goal to gain the
patient’s confidence and acceptance of NIV.
How should NIV be applied initially?
• You must start with low pressures (5 cm H2o)
and the mask should be held and not strapped to
the patient’s face.
• As the patient accepts the NIV, pressures are
increased to reach the gas exchange goal, but
generally should not exceed 20–25 cm H2O to
minimize gastric distension and the risk of
vomiting.
• Although time consuming, the cost savings are
large compared with the alternative—that is,
invasive ventilation.
How to use non-invasive ventilation
Initiation
• A PEEP of 5–7.5 cmH2O should be applied first
and titrated to clinical response up to 10
cmH2O; FiO2 delivery should be >0.40.
Duration
• Usually 30 min/h until patient’s dyspnoea and
oxygen saturation remain improved without
CPAP
Potential adverse effects
• Worsening of severe right ventricular failure
• Drying of the mucous membranes with
prolonged, continuous use
• Hypercapnia
• Anxiety or claustrophobia
• Pneumothorax
• Aspiration
Initial BPAP ( IPAP/EPAP) settings
• Start at 10 cm water / 5 cm water
• Pressures < 8 cm water/4 cm water not advised as this may
be inadequate
• Increase IPAP and EPAP by 2 cm water if persistent
hypoxemia
• Increase IPAP by 2 cm water if persistent hypercapnia
• Maximal IPAP limited to 20-25 cm water (avoids gastric
distension, improves patient comfort)
• Maximal EPAP limited to 10-15 cm water
• FIO2 at 1.0 and adjust to lowest level with an acceptable
SPo2 from 90-92%
• Back up respiratory rate 12-16 breaths/minute
Predictors of success of NIV (1-2 h)
• Decrease in PaCO2 > 8 mm Hg
• Improvement in pH > 0.06
• Correction of hypoxemia and respiratory
acidosis
Predictors of failure
• Severity of illness
– Acidosis (pH < 7.25)
– Hypercapnia (>80 and pH < 7.25)
– Acute Physiology and Chronic Health Evaluation II
(APACHE II) score >20
• level of consciousness
– Neurologic score (stuporous, arousal only after vigorous
stimulation; inconsistently follows commands)
– Encephalopathy score (major confusion, daytime
sleepiness or agitation)
– Glasgo coma scale score < 8
• Failure of improvement within 12-24 hours of noninvasive
ventilation
Intubation guidelines
• Any 1 of the following:
– pH < 7.20
– pH 7.20–7.25 on 2 occasions 1 hour apart
– Hypercapnic coma (Glasgow Coma Scale
score < 8 and PaCO2 >60 mm Hg)
– PaO2 < 45 mm Hg
– Cardiopulmonary arrest
Intubation guidelines
• Two or more of the following in the context of
respiratory distress:
– Respiratory rate > 35 breaths/minute or < 6
breaths/minute
– Tidal volume < 5 mL/kg
– Blood pressure changes, with systolic < 90 mm Hg
– Oxygen desaturation to < 90% despite adequate
supplemental oxygen
– Hypercapnia (PaCO2 >10 mm increase) or acidosis
(pH decline >0.08) from baseline
– Obtundation
– Diaphoresis
– Abdominal paradox
CONCLUSIONS
• There is a strong evidence for the use of
CPAP by face mask in patients with ACPE,
and CPAP decreases the need for
endotracheal intubation and improves
survival.
• There is insufficient evidence to
recommend the use of BPAP, probably
the exception being patients with
hypercapnic ACPE.
Sleep Disordered Breathing
In Congestive Heart Failure
• Sleep-disordered breathing in CHF includes obstructive
(OSA) and central sleep apnea (CSA).
• The prevalence of SDB in patients with CHF is more than
tenfold that seen in the general community.
• Two large studies, one in Canada and the other in
Germany have reported SDB (AHI >15) in 60 to 70% of
CHF patients. In contrast, the incidence of SDB in the
general population has been reported to be 6% to 17%
(AHI >15 and >5, respectively).
• In the general community, OSA is the predominant form of
SDB, with CSA making up about 1% of cases. In CHF
populations, CSA is far more common.
Prevalence of sleep apnea (AHI >15/h) in 1250
consecutive patients with systolic heart failure
OSA in CHF
• Patients with OSA are at a 2.4-fold elevated risk
of self-reported CHF, which may occur as a
result of OSA-related hypertension and the
impact of OSA on left ventricular function.
• CHF may also augment a tendency toward OSA
by increasing upper airway edema leading to a
narrowing of the airway lumen, a factor
especially important in the supine position.
The adverse physiologic effects of OSA are thought to
be the consequence of
1. Recurrent arousal from sleep
2. Asphyxia and intermittent hypoxia
3. Negative intrathoracic pressure swings
4. Inflammatory endothelial injury due to
formation of oxygen radicals
5. Direct vibrational trauma.
Treatment of OSA in CHF with CPAP
• Treatment of OSA in CHF with CPAP ( after
manual titration) lowers sympathetic nervous
system activity, blood pressure, and heart rate,
reduces nocturnal ventricular arrhythmia, and
improves left ventricular function.
• Better survival in CHF patients without SDB or
treated OSA compared with those with
untreated OSA (AHI >15).
• Effective treatment of OSA in patients with CHF
results in improved outcomes.
Indications for BPAP Use
• Several studies comparing the effectiveness of BPAP
and CPAP, with and without coexisting respiratory
disorders, showed no differences in the improvement of
AHI, ESS, or sleep quality. Similarly, no differences have
been seen in adherence or comfort level among BPAP
and CPAP users in the treatment of OSA without
coexisting respiratory disorders.
• Some data suggest that a subset of patients with OSA
who have comorbid obesity and daytime hypercapnia
(OHS) prefer BPAP over CPAP in the treatment of OSA.
• Despite the overall lack of evidence, BPAP still tends to
be considered for OSA treatment, even in patients
without comorbid respiratory disorders, particularly
when they are or unable to tolerate CPAP because of a
high pressure requirement or have persistent OSA on
CPAP even at a pressure of 20 cm H2O.
CSA IN CHF
• CSA is rare in the general population, whereas it affects
28% to 38% of those with advanced CHF.
• Cheyne-Stokes respiration (CSR ) is characterized by
a crescendo-decrescendo pattern of ventilation followed
by a central apnea and is associated with mild hypoxemia,
modest hypocapnia, and an arousal at peak ventilation.
• CSR occurs more commonly in men than women with
similar degrees of CHF.
• CSR has a periodicity of 45 to 90 seconds and occurs
during non-rapid eye movement sleep stages 1 and 2 and
is often triggered by an arousal or state change.
• The predominant mechanism underlying CSA in patients
with CHF is an unstable negative feedback controlling
ventilation during sleep.
Pathophysiology of CSA
• Supplemental oxygen use in CHF can reduce
chemosensitivity and AHI.
• The carbonic anhydrase inhibitor and diuretic
acetazolamide has been found to reduce the severity of
CSA.
• Acetazolamide is considered to reduce peripheral
chemosensitivity and elevate central respiratory drive.
Acetazolamide increases the difference between resting
PaCO2 (eupnea) and the apneic threshold. In essence,
this increase in difference must represent a reduced
chemosensitivity; therefore, acetazolamide is likely to
ameliorate CSA via reduction in loop gain.
Pathophysiology of CSA
• Patients with CHF have a reduction in lung
volumes attributed to cardiomegaly, pleural
effusions, respiratory muscle weakness, and
pulmonary interstitial edema, which may vary to
differing degrees with sleeping position and
sleep state between patients.
• AHI in CHF-CSA patients are strongly
associated with the rate of arterial oxygen
desaturation during apnea, a factor strongly
influenced by lung volume.
Pathophysiology of CSA
• The lateral sleeping position strongly attenuated
the AHI by 50% to 71% compared with the
supine position, depending on sleep state.
• The lateral position attenuated the AHIassociated desaturation (4.7% vs 3.0%) with no
difference in event duration.
• This change in desaturation and the known
elevation in lung volume in the lateral position
are indirect evidence that lung volume might be
of major importance in the pathogenesis of
CSA.
Pathophysiology of CSA
• There is substantial evidence that pulmonary
congestion and interstitial edema may affect the
stability of respiratory control.
• Reduced
pulmonary
diffusing
capacity
measured with carbon monoxide (DLCO) in CSA
patients was associated with increased severity
of CSA as reflected by AHI.
• Elevated pulmonary capillary wedge pressure
(PCWP) was associated with hypocapnia (an
indication of elevated chemosensitivity) and
CSA frequency and severity.
TREATMENT OF CSA
• Optimizing management of the underlying CHF
• Significant improvements were observed in LVEF,
plasma catecholamines, overnight oxygen levels,
and AHI plus 6-minute walk distance with CPAP
treatment.
• The effect of CPAP on cardiac transplant-free
survival in patients who had CSA and CHF
showed no significant difference in transplant-free
survival, hospitalization, or quality of life was
detected between the 2 groups.
TREATMENT OF CSA
• CPAP has been found to be effective in
reducing AHI to <15 /h only in approximately
50% of patients with HF.
• The patients whose CSA does not resolve
with treatment are those with the most
unstable respiratory control or the highest
loop gain.
MECHANISMS OF ACTION OF CPAP IN CSA-CHF
• The effectiveness of CPAP on breathing stability
has long been attributed to the stabilization of
the upper airway by its action of splinting the
airway open.
• PAP has stabilizing effects that result from lung
inflation. Such effects are considered to result
from increasing O2 and CO2 stores and damping
oscillations in blood gases, which would
otherwise increase loop gain and precipitate
unstable breathing.
• CPAP did not alter the cycle duration of periodic
breathing; given that cycle duration is strongly
related to circulatory delay/ejection fraction,
Alternative Modes of PAP Therapy
• BPAP and adaptive pressure support servo-ventilation
(ASV) provide varying levels of PAP in the hope of
directly suppressing hypoventilation while providing the
benefits of low-level CPAP.
• BPAP (ST mode) has been shown to increase LVEF,
reduce AHI and arousals, and decrease sympathetic
outflow compared with medical therapy.
• Three months of BPAP (ST mode) increased LVEF by
8.5% compared with 0.5% for those treated with CPAP in
a study of 24 patients with CHF and OSA.
Alternative Modes of PAP Therapy
• ASV measures and aims to maintain a patient’s
ventilation at 90% of the prior 3-minute moving
average.
• ASV is designed to eliminate obstructive apneas
and hypopneas with a minimum level of
expiratory PAP and to modulate the inspiratory
PAP to eliminate central apneas and hypopneas.
• ASV provides a low level of expiratory PAP
(approximately 5 cm H2O) and an adaptive level
of inspiratory PAP (> 4 cm H2O). Inspiratory
PAP adapts to ventilatory effort; it increases as
inspiratory effort falls and reduces as
inspiratory effort increases.
Alternative Modes of PAP Therapy
• During central apneas, ASV provides inspiratory
support (5–8 cm H2O) at 15 breaths per minute,
sufficient to maintain ventilation at 90% of the prior 3minute average
• ASV during sleep causes an acute 1 to 2 mm Hg rise in
pCO2 levels, possibly by increasing slow-wave and
rapid-eye movement sleep and reducing arousals. This
may result in stabilization of ventilation.
• For, CPAP non-responsive patients and those who are
intolerant to CPAP, we recommend use of adaptive
pressure support servoventilators devices.
• ASV devices are effective in treating CSA and OSA,
Respironics
Weinmann
auto SV Advanced SomnoVent CR
ResMed ASV
Direct comparison treatment studies
with more than 2 treatment modalities
• All treatment devices (oxygen, CPAP, BPAP, and ASV)
significantly reduced AHI compared to baseline.
• ASV was significantly superior to all other treatment
devices.
• BPAP also was significantly better than CPAP .
• ASV performed almost equivalently to BPAP-ST for
patients with CSAS and equivalent to CPAP (and better
than BPAP-ST) for patients with CSAS/CSR.
• The following therapies have limited supporting evidence
but may be considered for the treatment of CSAS related to
CHF, after optimization of standard medical therapy, if PAP
therapy is not tolerated, and if accompanied by close
clinical follow-up: acetazolamide and theophylline.
(OPTION)
Conclusion
• Nocturnal oxygen therapy is indicated for the treatment
of CSAS related to CHF. (STANDARD)
• A CPAP therapy targeted to normalize the AHI is
indicated for the initial treatment of CSAS related to
CHF. (STANDARD)
• A BPAP therapy in a spontaneous timed (ST) mode
targeted to normalize the AHI may be considered for the
treatment of CSAS related to CHF only if there is no
response to adequate trials of CPAP, ASV, and oxygen
therapies. (OPTION)
• A Adaptive Servo-Ventilation (ASV) targeted to
normalize the AHI is indicated for the treatment of CSAS
related to CHF. (STANDARD)