International Journal of Cardiology 171 (2014) e104e105

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International Journal of Cardiology

journal homepage: www.elsevier.com/locate/ijcard

Letter to the Editor

Pressure-dependent hemodynamic effect of continuous positive airway

pressure in severe chronic heart failure: A case series
Nicolas Combes a,, Dany Jaffuel b, Guilhaume Cayla c, Mathieu Granier c, Jean Christian Borel d,e, Philipe Corne f,
Olivier Jonquet f, Samir Jaber g, Jean Marc Davy h, Jean Louis Ppin d,i
a
Cardiology Unit, Pasteur Clinic, 45 Avenue de Lombez, 31076 Toulouse Cedex 3, France
b
Polyclinic Saint-Privat, Pulmonary Disorders and Respiratory Sleep Disorders Unit, Rue de la Margeride, 34760 Boujan sur Libron, France
c
Cardiology Unit, Carremeau hospital, Chemin du Carreau de Lanes, 30000 Nmes, France
d
INSERM U 1042, HP2 Laboratory, Universit Joseph Fourier, Facult de Mdecine, 38043 Grenoble cedex 09, France
e
AGIRadom, Research and Development department, 38240 Meylan, France
f
Medical Intensive Care Unit, Gui de Chauliac Hospital, University of Montpellier 1, 80 avenue Augustin Fliche, 34295 Montpellier Cedex 5, France
g
Intensive Care Unit, Anesthesia and Critical Care Department B, Saint-Eloi Teaching Hospital, INSERM U1046, Montpellier 1 University, 80 Avenue Augustin Fliche, 34295 Montpellier Cedex 5,
France
h
Clinique du Cur et des Vaisseaux, CHU de Montpellier, Hpital Arnaud de Villeneuve, 37 avenue Gaston Giraud, 34295 Montpellier, France
i
CHU, Hpital A. Michallon, Ple Locomotion, Rducation et Physiologie, 38043 Grenoble cedex 09, France

a r t i c l e i n f o
Article history:
Received 17 September 2013
Accepted 8 December 2013
Available online 16 December 2013
Keywords:
Sleep apnea syndrome
Continuous positive airway pressure
Chronic heart failure
Echocardiography
Two third of stable severe Chronic Heart Failure (CHF) patients are
affected by central or obstructive sleep disordered breathing (SDB). Al-
though Continuous Positive Airway Pressure (CPAP) is a validated treat-
ment for obstructive sleep apnea (OSA) in CHF [1], its interest in central
sleep apnea (CSA) associated with CHF remains still controversial. The
CANPAP randomized controlled trial showed an increase in event
rates and mortality occurring during the rst months of CPAP initiation
[2]. It suggests that CPAP may have an early adverse effect in some CHF
patients suffering from CSA. Using CPAP in CHF patients, when lling
pressures are high, the cardiac output seems to increase, and when
pressures are low, it seems to decrease. Potentially, upward titration
of CPAP reduced cardiac output in some patients and may then be dele-
All authors take responsibility for all aspects of the reliability and freedom from bias of
the data presented and their discussed interpretation.
Corresponding author. Tel.: +33 562211607; fax: +33 562211641.
E-mail addresses: n.combes@clinique-pasteur.com (N. Combes),
dany.jaffuel@wanadoo.fr (D. Jaffuel), guilhaume.cayla@chu-nimes.fr (G. Cayla),
mathieu.granier@chu-nimes.fr (M. Granier), j.borel@agiradom.com (J.C. Borel),
p-corne@chu-montpellier.fr (P. Corne), o-jonquet@chu-montpellier.fr (O. Jonquet),
s-jaber@chu-montpellier.fr (S. Jaber), jm-davy@chu-montpellier.fr (J.M. Davy),
Jpepin@chu-grenoble.fr (J.L. Ppin).
terious [2]. As recently highlighted by a Task Force report [3], a clear lim-
itation of most of the studies in the eld is that CPAP therapy was not
titrated. In clinical practice, CPAP titration in CHF is mainly addressing
the correction of SDB but its impact on hemodynamic should probably
be included in the titration process in CHF patients [4]. A more careful
CPAP titration might avoid some adverse events.
To our knowledge, only one study has described in 1995 the hemo-
dynamic echocardiographic consequences of different level of CPAP in
15 patients with CHF [5], with a maximal level of CPAP of 10 cmH2O
and without 2000's optimal treatment of CHF.
The aim of the current case series was to describe a systematic and
standardized method for an echocardiographic hemodynamic evalua-
tion of different levels of CPAP (4, 8, 12, 16 cm H2O), in awake patients,
with severe stable CHF and optimal contemporary treatment.
Ten patients with severe stable cardiac heart failure were recruited
and underwent Brain Natriuretic Peptide (BNP), blood gazes and sleep
studies. Assessment was done in supine position with a 30 thorax incli-
nation. An upward CPAP titration was applied using a facial mask for
15 min at every single pressure level (0 with facial mask but without
connection with the CPAP device, 4, 8, 12 and 16 cm H2O). Echocardio-
graphic measures were performed during spontaneous ventilation and
at each level of CPAP after a steady state of 15 min was achieved.
SaO2, blood pressure, and ECG were monitored continuously through-
out the study. CPAP was discontinued if arrhythmia, fall in systolic
blood pressure superior to 10 mm Hg or oxygen saturation decrease
below 90% occurred. Results are given as mean SD. A Friedman test
was performed for variance analysis. Values of p b 0.05 were accepted
as statistically signicant. XLSTAT software (version 2012.2.3, Addinsoft,
Paris, France) was used for statistical analysis. For more detailed de-
scription of the methods, see electronic supplementary material.
The characteristics of the ten male patients included are depicted in
Table 1. All had symptomatic left heart failure (mean Left Ventricular
Ejection Fraction (LVEF) of 25.5 4.9%) and 50% had associated right
heart failure. Brain Natriuretic Peptide (BNP) was elevated in 90% of pa-
tients (1333 898 ng/ml). Aetiologies of CHF were ischemic (ICM) in

0167-5273/$ see front matter 2014 Elsevier Ireland. Ltd All rights reserved.
http://dx.doi.org/10.1016/j.ijcard.2013.12.007
 N. Combes et al. / International Journal of Cardiology 171 (2014) e104e105 e105

Table 1
Baseline characteristics of patients.

Patient Age, Rhythm Aetiology Pa02/PaC02, AHI total AHI central BMI Treatment NYHA BNP EF, LV/RV %
years mm Hg number/hour number/hour kg/m2 class ng/l

1 76 SR M 35/35 6 6 24 BB, ACE, LD 2 1373 30/45

2 47 AF ICM 80/36 4 4 21 BB. ACE. S, LD, CRT 3 455 25/60
3 63 SR ICM 9O/36 15 12 23 ACE, S, LO 3 2300 20/55
4 63 SR ICM 90/39 3 6 20 BB, LD, CRT 3 1596 25/13
5 79 SR DCM 87/36 10 8 19 BB, LD 3 671 25/20
6 67 SR ICM 84/36 6 4 18 BB. ACE. L 3 1280 20/20
7 67 AF DCM 37/37 5 3 21 BB, ARB, LD 2 156 30/60
8 77 SR ICM 87/36 17 14 22 ACE, LD 4 2993 35/20
9 52 SR DCM 88/39 16 13 24 ACE. S. LD 4 1450 20/30
10 35 SR DCM 33/36 12 10 24 BB, ACE, S, LD 4 557 25/60
Population AF (20%) DCM (50%) ACE (70%), ARB (10%),
characteristic ICM (50%) BB(70%), S (40%),
LD (100%). CRT (20%)
Mean (SD) 63(14) 85 (3.3)/36 (1.9) 9.6(48) 7.7(4) 21.6(2) 3(0.7) 1333(898) 25.5 (4.9)/
38 (18)

AF = atrial brillation, SR = sinus rhythm, ICM = ischemic cardiomyopathy, DCM = dilated cardiomyopathy, AHI = apnea hypopnea index, BMI = body mass index, CRT = cardiac
resynchronization, ACE = angiotensin inhibitor, ARB = angiotensin receptor blocker, BB = beta-blocker, LD = loop diuretic; S = spironolactone; BNP = brain natriuretic peptide;
EF = ejection fraction; LV = left ventricule; RV = right ventricule.

50% of patients and dilated (DCM) in the others. Only 20% of patients
were in atrial brillation. 20% of patients previously received cardiac
resynchronization (CRT). The mean total apnea hypopnea index (AHI)
was 9.6 4.8/h with 80% of central events. CPAP titration impact on
cardiac output (CO) is depicted in Fig. 1. Mean CO showed a nearly sys-
tematic biphasic evolution with an initial improvement and a secondary
decrease in CO with the increase in CPAP pressure (4 cm H2O versus
16 cm H2O, p = 0.004; 8 cm H2O versus 12 cm H2O, p = 0.005; 8 cm
H2O versus 16 cm H2O, p = 0.003). Moreover, an important inter indi-
vidual variation was found. Three patients (2, 5 and 9) have a constant
decrease of CO, two patients (7 and 10) have a constant increase of
CO. The other results are exhaustively listed in the Table 1 of the elec-
tronic supplementary material.
In this case series of ten non obese severe chronic heart failure pa-
tients with optimal medications and mild to moderate CSA, we ob-
served a patient dependent hemodynamic response to upward CPAP
titration. We have observed three different patterns of hemodynamic
effects (positive, negative and biphasic response to CPAP). On an indi-
vidual basis, it is then impossible to predict CPAP hemodynamic impact
on CO and a systematic hemodynamic titration should probably be
proposed to these patients. Only one study [5] has previously evaluated
with echocardiography the acute hemodynamic effect of CPAP titration
(0, 5, 7.5 and 10 cm H2O) on CHF patients (mean LVEF of 17.9 2.4%).
The authors reported no signicant difference in the mean cardiac
index (CI) but a considerable variation in the response, with approxi-
mately half of patients experiencing an increase and half of patients
experiencing a decrease in CI. However, individual data were not
Fig. 1. Cardiac output evolution during CPAP titration (individual data and mean).
shown, no predictive factors were evaluated, the study was performed
before the 2000's optimal treatment of CHF and the AHI indices of pa-
tients were not reported. Other with a SwanGanz catheter have also
demonstrated a fall in CO with CPAP at a single level of 10 cm H2O [6]
or at 5 and 10 cm H2O [7].
In the CPAP treatment of CSA in CHF, a post hoc analysis of the
CANPAP study has demonstrated that CPAP is effective only in subjects
who normalize their AHI [8]. However no recommendation is available
regarding the titration process and the safety of an upward titration
targeting AHI reduction. Considering our data and others [5,6], we can
assume that domiciliary nocturnal CPAP should not be prescribed in se-
vere CHF without rst determining the individual patient's cardiac re-
sponse to such intervention. Moreover, the use of too high pressure
may favor the perpetuating of central events. In order to optimize the
care of these patients, echocardiographic CPAP titration for safety can
be an accessible tool but remains to be validated prospectively in a larg-
er population.
Appendix A. Supplementary data
Supplementary data to this article can be found online at http://dx.
doi.org/10.1016/j.ijcard.2013.12.007.
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