Sleep Related Breathing Disorders In Congestive Heart Failure

BY AHMAD YOUNES

PROFESSOR OF THORACIC MEDICINEMansoura 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 maneuverIn the Mallampati maneuver, , patients are instructed not to emit sounds but to open patients are instructed not to emit sounds but to open the mouth as wide as possible and protrude the tongue as far as possible. the mouth as wide as possible and protrude the tongue as far as possible. In the modified MallampatiIn the modified Mallampati, , the patient is instructed to open the mouth as wide as the patient is instructed to open the mouth as wide as possible without emitting sounds.possible without emitting sounds.

Symptoms of central sleep apnea syndrome

• 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 AHF4- 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• 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)

• 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.

Does the type of ventilator make any difference?

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 AHI-associated 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 3-minute 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 ResMed ASV auto SV Advanced SomnoVent CR

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)