racic pressure reduces the venous return,decreases the right and left ventricularpreload, and thus improves mechanics inan overloaded ventricle, whereas in dia-stole CPAP increases pericardial pressure,reduces transmural pressure, and thus de-creases afterload. Other mechanisms bywhich CPAP improves CPE include un-loading of respiratory muscles, preventingmicroatelectasis, decreasing dead space,and improving alveolar ventilation.

Pathogenetically, CPAP therapy thusbenefits only patients with systolic heartfailure by decreasing both preload and af-terload, whereas in patients with diastolicdysfunction the effects of positive pressuretherapy compromises venous return anddecreases left ventricular end diastolic vol-ume, further limiting stroke volume andhence cardiac output because of the steepcurve for left ventricular diastolic pressurein relation to volume with resultant deteri-oration in hemodynamics [4]. Hence cau-tion must be used because patients with di-astolic heart failure are sensitive to thepreload reduction and may develop hypo-tension or severe prerenal azotemia [5]. Infact it adds to the primary pathophysiologi-cal mechanism of diastolic heart failureand can worsen the pulmonary edema. Insuch patients NIPSV is theoretically likelyto be more beneficial because of differinginspiratory and expiratory pressure. Anoth-er factor by which positive pressure thera-py can act in patients with diastolic heartfailure is lung inflation with activation ofparasympathetic nervous system and resul-tant decrease in heart rate [6].

Thus one needs to be cautious whileinitiating noninvasive ventilation in pa-tients with diastolic heart failure. In thisgroup of patients treatment of the basiccause should be initiated as soon as possi-ble, and NIPSV should be used in prefer-ence to CPAP. Moreover, NIPSV should beused cautiously under strict experimentalconditions with the minimum pressure em-ployed that achieves physiological goalswith the potential of clinical deteriorationdue to CPAP per se being kept in mind.

References

1. Bellone A, Vettorello M, Monari A,Cortellaro F, Coen D (2005) Noninva-sive pressure support ventilation vs.continuous positive airway pressure inacute hypercapnic pulmonary edema.Intensive Care Med 31:807–811

2. Gandhi SK, Powers JC, Nomeir AM,Fowle K, Kitzman DW, Rankin KM,Little WC (2001) The pathogenesis of acute pulmonary edema associatedwith hypertension. N Engl J Med344:17–22

3. Gaasch WH, Zile MR (2004) Left ventricular diastolic dysfunction and diastolic heart failure. Annu Rev Med55:373–394

4. Agarwal R, Aggarwal AN, Gupta D,Jindal SK (2005) Evidence based re-view: noninvasive ventilation in acutecardiogenic pulmonary edema. Postgrad Med J (in press)

5. Aurigemma GP, Gaasch WH (2004) Diastolic heart failure. N Engl J Med351:1097–1105

6. Seals D, Suwarno O, Dempsey J (1990)Influence of lung volume on sympathet-ic nerve activity in normal humans. Circ Res 67:130–141

An author’s reply to this contribution isavailable at http://dx.doi.org/10.1007/s00134-005-2753-7

R. Agarwal (✉) · D. GuptaDepartment of Pulmonary Medicine,Postgraduate Institute of Medical Education and Research,Sector 12, 160012 Chandigarh, Indiae-mail: riteshpgi@gmail.com

Intensive Care Med (2005) 31:1451DOI 10.1007/s00134-005-2752-8 C O R R E S P O N D E N C E

Ritesh AgarwalDheeraj Gupta

What is the role of noninvasiveventilation in diastolic heartfailure?

Accepted: 1 July 2005Published online: 12 August 2005© Springer-Verlag 2005

We read with interest the contribution by Dr. Bellone et al. [1] reporting that non-invasive pressure support ventilation(NIPSV) is as effective as continuous posi-tive airway pressure (CPAP) in the treat-ment of patients with acute hypercapnicpulmonary edema but does not improveresolution time, defined by the authors asclinical improvement with a respiratoryrate less than 30 breaths/min and SpO2 ofat least 96%. The authors, however, men-tion no details of the echocardiographicfindings, and therefore it is not knownwhether the patients had suffered systolicor diastolic heart failure. This factor has aclear bearing on the outcome of patientswith acute cardiogenic pulmonary edema(CPE), and a significant proportion of pa-tients in their study had hypertension,which is the most important risk factor as-sociated with diastolic heart failure [2].

CPAP has a definite role in the manage-ment of acute CPE, and recently in a meta-analysis of ours we showed that CPAP de-creases the rate of intubation and improvessurvival in patients with acute CPE; thenumber of patients who need to be treatedto prevent one intubation and one deathwas six and eight, respectively [3]. Duringsystole CPAP-induced increase in intratho-